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El Niño–Southern Oscillation

El Niño–Southern Oscillation ( ENSO ) is a global climate phenomenon that emerges from variations in winds and sea surface temperatures over the tropical Pacific Ocean . Those variations have an irregular pattern but do have some semblance of cycles. The occurrence of ENSO is not predictable. It affects the climate of much of the tropics and subtropics , and has links ( teleconnections ) to higher-latitude regions of the world. The warming phase of the sea surface temperature is known as El Niño and the cooling phase as La Niña . The Southern Oscillation is the accompanying atmospheric component, which is coupled with the sea temperature change. El Niño is associated with higher than normal air sea level pressure over Indonesia, Australia and across the Indian Ocean to the Atlantic . La Niña has roughly the reverse pattern: high pressure over the central and eastern Pacific and lower pressure through much of the rest of the tropics and subtropics. The two phenomena last a year or so each and typically occur every two to seven years with varying intensity, with neutral periods of lower intensity interspersed. El Niño events can be more intense but La Niña events may repeat and last longer. A key mechanism of ENSO is the Bjerknes feedback (named after Jacob Bjerknes in 1969) in which the atmospheric changes alter the sea temperatures that in turn alter the atmospheric winds in a positive feedback. Weaker easterly trade winds result in a surge of warm surface waters to the east and reduced ocean upwelling on the equator . In turn, this leads to warmer sea surface temperatures (called El Niño), a weaker Walker circulation (an east-west overturning circulation in the atmosphere) and even weaker trade winds. Ultimately the warm waters in the western tropical Pacific are depleted enough so that conditions return to normal. The exact mechanisms that cause the oscillation are unclear and are being studied. Each country that monitors the ENSO has a different threshold for what constitutes an El Niño or La Niña event, which is tailored to their specific interests. El Niño and La Niña affect the global climate and disrupt normal weather patterns, which as a result can lead to intense storms in some places and droughts in others. El Niño events cause short-term (approximately 1 year in length) spikes in global average surface temperature while La Niña events cause short term surface cooling. Therefore, the relative frequency of El Niño compared to La Niña events can affect global temperature trends on timescales of around ten years. The countries most affected by ENSO are developing countries that are bordering the Pacific Ocean and are dependent on agriculture and fishing. In climate change science, ENSO is known as one of the internal climate variability phenomena. : 23 Future trends in ENSO due to climate change are uncertain, although climate change exacerbates the effects of droughts and floods. The IPCC Sixth Assessment Report summarized the scientific knowledge in 2021 for the future of ENSO as follows: "In the long term, it is very likely that the precipitation variance related to El Niño–Southern Oscillation will increase". : 113 The scientific consensus is also that "it is very likely that rainfall variability related to changes in the strength and spatial extent of ENSO teleconnections will lead to significant changes at regional scale". : 114The El Niño–Southern Oscillation is a single climate phenomenon that periodically fluctuates between three phases: Neutral, La Niña or El Niño. La Niña and El Niño are opposite phases in the oscillation which are deemed to occur when specific ocean and atmospheric conditions are reached or exceeded. An early recorded mention of the term "El Niño" ("The Boy" in Spanish) to refer to climate occurred in 1892, when Captain Camilo Carrillo told the geographical society congress in Lima that Peruvian sailors named the warm south-flowing current "El Niño" because it was most noticeable around Christmas. Although pre-Columbian societies were certainly aware of the phenomenon, the indigenous names for it have been lost to history. The capitalized term El Niño refers to the Christ child , Jesus, because periodic warming in the Pacific near South America is usually noticed around Christmas . Originally, the term El Niño applied to an annual weak warm ocean current that ran southwards along the coast of Peru and Ecuador at about Christmas time. However, over time the term has evolved and now refers to the warm and negative phase of the El Niño–Southern Oscillation (ENSO). The original phrase, El Niño de Navidad , arose centuries ago, when Peruvian fishermen named the weather phenomenon after the newborn Christ. La Niña ("The Girl" in Spanish) is the colder counterpart of El Niño, as part of the broader ENSO climate pattern . In the past, it was also called an anti-El Niño and El Viejo, meaning "the old man." A negative phase exists when atmospheric pressure over Indonesia and the west Pacific is abnormally high and pressure over the east Pacific is abnormally low, during El Niño episodes, and a positive phase is when the opposite occurs during La Niña episodes, and pressure over Indonesia is low and over the west Pacific is high. On average, the temperature of the ocean surface in the tropical East Pacific is roughly 8–10 °C (14–18 °F) cooler than in the tropical West Pacific . The sea surface temperature (SST) of the West Pacific northeast of Australia averages around 28–30 °C (82–86 °F) . SSTs in the East Pacific off the western coast of South America are closer to 20 °C (68 °F) . Strong trade winds near the equator push water away from the East Pacific and towards the West Pacific. [lower-alpha 1] This water is slowly warmed by the Sun as it moves west along the equator. The ocean surface near Indonesia is typically around 0.5 m (1.5 ft) higher than near Peru because of the buildup of water in the West Pacific. [ clarification needed ] The thermocline , or the transitional zone between the warmer waters near the ocean surface and the cooler waters of the deep ocean , is pushed downwards in the West Pacific due to this water accumulation. [lower-alpha 2] Consequently, the thermocline is tilted across the tropical Pacific, rising from an average depth of about 140 m (450 ft) in the West Pacific to a depth of about 30 m (90 ft) in the East Pacific. Cooler deep ocean water takes the place of the outgoing surface waters in the East Pacific, rising to the ocean surface in a process called upwelling . [lower-alpha 1] This process cools the East Pacific because the thermocline is closer to the ocean surface, leaving relatively little separation between the deeper cold water and the ocean surface. Additionally, the northward-flowing Humboldt Current carries colder water from the Southern Ocean to the tropics in the East Pacific . The combination of the Humboldt Current and upwelling maintains an area of cooler ocean waters off the coast of Peru. The West Pacific lacks a cold ocean current and has less upwelling as the trade winds are usually weaker than in the East Pacific, allowing the West Pacific to reach warmer temperatures. These warmer waters provide energy for the upward movement of air . As a result, the warm West Pacific has on average more cloudiness and rainfall than the cool East Pacific. ENSO describes a quasi-periodic change of both oceanic and atmospheric conditions over the tropical Pacific Ocean. These changes affect weather patterns across much of the Earth. The tropical Pacific is said to be in one of three states of ENSO (also called "phases") depending on the atmospheric and oceanic conditions. When the tropical Pacific roughly reflects the average conditions, the state of ENSO is said to be in the neutral phase. However, the tropical Pacific experiences occasional shifts away from these average conditions. If trade winds are weaker than average, the effect of upwelling in the East Pacific and the flow of warmer ocean surface waters towards the West Pacific lessen. This results in a cooler West Pacific and a warmer East Pacific, leading to a shift of cloudiness and rainfall towards the East Pacific. This situation is called El Niño. The opposite occurs if trade winds are stronger than average, leading to a warmer West Pacific and an cooler East Pacific. This situation is called La Niña and is associated with increased cloudiness and rainfall over the West Pacific. The close relationship between ocean temperatures and the strength of the trade winds was first identified by Jacob Bjerknes in 1969. Bjerknes also hypothesized that ENSO was a positive feedback system where the associated changes in one component of the climate system (the ocean or atmosphere) tend to reinforce changes in the other. : 86 For example, during El Niño, the reduced contrast in ocean temperatures across the Pacific results in weaker trade winds, further reinforcing the El Niño state. This process is known as Bjerknes feedback . Although these associated changes in the ocean and atmosphere often occur together, the state of the atmosphere may resemble a different ENSO phase than the state of the ocean or vice versa. Because their states are closely linked, the variations of ENSO may arise from changes in both the ocean and atmosphere and not necessarily from an initial change of exclusively one or the other. Conceptual models explaining how ENSO operates generally accept the Bjerknes feedback hypothesis. However, ENSO would perpetually remain in one phase if Bjerknes feedback were the only process occurring. : 88 Several theories have been proposed to explain how ENSO can change from one state to the next, despite the positive feedback. These explanations broadly fall under two categories. In one view, the Bjerknes feedback naturally triggers negative feedbacks [ clarification needed ] that end and reverse the abnormal state of the tropical Pacific. This perspective implies that the processes that lead to El Niño and La Niña also eventually bring about their end, making ENSO a self-sustaining [ clarification needed ] process. : 88 Other theories view the state of ENSO as being changed by irregular and external phenomena such as the Madden–Julian oscillation , tropical instability waves , and westerly wind bursts . : 90 The three phases of ENSO relate to the Walker circulation, which was named after Gilbert Walker who discovered the Southern Oscillation during the early twentieth century. The Walker circulation is an east-west overturning circulation in the vicinity of the equator in the Pacific. Upward air is associated with high sea temperatures, convection and rainfall, while the downward branch occurs over cooler sea surface temperatures in the east. During El Niño, as the sea surface temperatures change so does the Walker Circulation. Warming in the eastern tropical Pacific weakens or reverses the downward branch, while cooler conditions in the west lead to less rain and downward air, so the Walker Circulation first weakens and may reverse. : 185 The Southern Oscillation is the atmospheric component of ENSO. This component is an oscillation in surface air pressure between the tropical eastern and the western Pacific Ocean waters. The strength of the Southern Oscillation is measured by the Southern Oscillation Index (SOI). The SOI is computed from fluctuations in the surface air pressure difference between Tahiti (in the Pacific) and Darwin, Australia (on the Indian Ocean). El Niño episodes have negative SOI, meaning there is lower pressure over Tahiti and higher pressure in Darwin. La Niña episodes on the other hand have positive SOI, meaning there is higher pressure in Tahiti and lower in Darwin. Low atmospheric pressure tends to occur over warm water and high pressure occurs over cold water, in part because of deep convection over the warm water. El Niño episodes are defined as sustained warming of the central and eastern tropical Pacific Ocean, thus resulting in a decrease in the strength of the Pacific trade winds , and a reduction in rainfall over eastern and northern Australia. La Niña episodes are defined as sustained cooling of the central and eastern tropical Pacific Ocean, thus resulting in an increase in the strength of the Pacific trade winds , and the opposite effects in Australia when compared to El Niño. Although the Southern Oscillation Index has a long station record going back to the 1800s, its reliability is limited due to the latitudes of both Darwin and Tahiti being well south of the Equator, so that the surface air pressure at both locations is less directly related to ENSO. To overcome this effect, a new index was created, named the Equatorial Southern Oscillation Index (EQSOI). To generate this index, two new regions, centered on the Equator, were defined. The western region is located over Indonesia and the eastern one over the equatorial Pacific, close to the South American coast. However, data on EQSOI goes back only to 1949. The close relationship between ocean temperatures and the strength of the trade winds was first identified by Jacob Bjerknes in 1969. Bjerknes also hypothesized that ENSO was a positive feedback system where the associated changes in one component of the climate system (the ocean or atmosphere) tend to reinforce changes in the other. : 86 For example, during El Niño, the reduced contrast in ocean temperatures across the Pacific results in weaker trade winds, further reinforcing the El Niño state. This process is known as Bjerknes feedback . Although these associated changes in the ocean and atmosphere often occur together, the state of the atmosphere may resemble a different ENSO phase than the state of the ocean or vice versa. Because their states are closely linked, the variations of ENSO may arise from changes in both the ocean and atmosphere and not necessarily from an initial change of exclusively one or the other. Conceptual models explaining how ENSO operates generally accept the Bjerknes feedback hypothesis. However, ENSO would perpetually remain in one phase if Bjerknes feedback were the only process occurring. : 88 Several theories have been proposed to explain how ENSO can change from one state to the next, despite the positive feedback. These explanations broadly fall under two categories. In one view, the Bjerknes feedback naturally triggers negative feedbacks [ clarification needed ] that end and reverse the abnormal state of the tropical Pacific. This perspective implies that the processes that lead to El Niño and La Niña also eventually bring about their end, making ENSO a self-sustaining [ clarification needed ] process. : 88 Other theories view the state of ENSO as being changed by irregular and external phenomena such as the Madden–Julian oscillation , tropical instability waves , and westerly wind bursts . : 90The three phases of ENSO relate to the Walker circulation, which was named after Gilbert Walker who discovered the Southern Oscillation during the early twentieth century. The Walker circulation is an east-west overturning circulation in the vicinity of the equator in the Pacific. Upward air is associated with high sea temperatures, convection and rainfall, while the downward branch occurs over cooler sea surface temperatures in the east. During El Niño, as the sea surface temperatures change so does the Walker Circulation. Warming in the eastern tropical Pacific weakens or reverses the downward branch, while cooler conditions in the west lead to less rain and downward air, so the Walker Circulation first weakens and may reverse. : 185The Southern Oscillation is the atmospheric component of ENSO. This component is an oscillation in surface air pressure between the tropical eastern and the western Pacific Ocean waters. The strength of the Southern Oscillation is measured by the Southern Oscillation Index (SOI). The SOI is computed from fluctuations in the surface air pressure difference between Tahiti (in the Pacific) and Darwin, Australia (on the Indian Ocean). El Niño episodes have negative SOI, meaning there is lower pressure over Tahiti and higher pressure in Darwin. La Niña episodes on the other hand have positive SOI, meaning there is higher pressure in Tahiti and lower in Darwin. Low atmospheric pressure tends to occur over warm water and high pressure occurs over cold water, in part because of deep convection over the warm water. El Niño episodes are defined as sustained warming of the central and eastern tropical Pacific Ocean, thus resulting in a decrease in the strength of the Pacific trade winds , and a reduction in rainfall over eastern and northern Australia. La Niña episodes are defined as sustained cooling of the central and eastern tropical Pacific Ocean, thus resulting in an increase in the strength of the Pacific trade winds , and the opposite effects in Australia when compared to El Niño. Although the Southern Oscillation Index has a long station record going back to the 1800s, its reliability is limited due to the latitudes of both Darwin and Tahiti being well south of the Equator, so that the surface air pressure at both locations is less directly related to ENSO. To overcome this effect, a new index was created, named the Equatorial Southern Oscillation Index (EQSOI). To generate this index, two new regions, centered on the Equator, were defined. The western region is located over Indonesia and the eastern one over the equatorial Pacific, close to the South American coast. However, data on EQSOI goes back only to 1949. The El Niño–Southern Oscillation is a single climate phenomenon that quasi-periodically fluctuates between three phases: Neutral, La Niña or El Niño. La Niña and El Niño are opposite phases which require certain changes to take place in both the ocean and the atmosphere before an event is declared. The cool phase of ENSO is La Niña, with SST in the eastern Pacific below average, and air pressure high in the eastern Pacific and low in the western Pacific. The ENSO cycle, including both El Niño and La Niña, causes global changes in temperature and rainfall. If the temperature variation from climatology is within 0.5 °C (0.9 °F), ENSO conditions are described as neutral. Neutral conditions are the transition between warm and cold phases of ENSO. Sea surface temperatures (by definition), tropical precipitation, and wind patterns are near average conditions during this phase. Close to half of all years are within neutral periods. During the neutral ENSO phase, other climate anomalies/patterns such as the sign of the North Atlantic Oscillation or the Pacific–North American teleconnection pattern exert more influence. El Niño conditions are established when the Walker circulation weakens or reverses and the Hadley circulation strengthens, [ citation needed ] [ clarification needed ] leading to the development of a band of warm ocean water in the central and east-central equatorial Pacific (approximately between the International Date Line and 120°W), including the area off the west coast of South America , as upwelling of cold water occurs less or not at all offshore. This warming causes a shift in the atmospheric circulation, leading to higher air pressure in the western Pacific and lower in the eastern Pacific, with rainfall reducing over Indonesia, India and northern Australia, while rainfall and tropical cyclone formation increases over the tropical Pacific Ocean. The low-level surface trade winds , which normally blow from east to west along the equator, either weaken or start blowing from the other direction. El Niño phases are known to happen at irregular intervals of two to seven years, and lasts nine months to two years. The average period length is five years. When this warming occurs for seven to nine months, it is classified as El Niño "conditions"; when its duration is longer, it is classified as an El Niño "episode". It is thought that there have been at least 30 El Niño events between 1900 and 2024, with the 1982–83 , 1997–98 and 2014–16 events among the strongest on record. Since 2000, El Niño events have been observed in 2002–03, 2004–05, 2006–07, 2009–10, 2014–16 , 2018–19, and 2023–24 . Major ENSO events were recorded in the years 1790–93, 1828, 1876–78, 1891, 1925–26, 1972–73, 1982–83, 1997–98, 2014–16, and 2023–24. During strong El Niño episodes, a secondary peak in sea surface temperature across the far eastern equatorial Pacific Ocean sometimes follows the initial peak. An especially strong Walker circulation causes La Niña, which is considered to be the cold oceanic and positive atmospheric phase of the broader El Niño–Southern Oscillation (ENSO) weather phenomenon, as well as the opposite of El Niño weather pattern, where sea surface temperature across the eastern equatorial part of the central Pacific Ocean will be lower than normal by 3–5 °C (5.4–9 °F). The phenomenon occurs as strong winds blow warm water at the ocean's surface away from South America, across the Pacific Ocean towards Indonesia. As this warm water moves west, cold water from the deep sea rises to the surface near South America. The movement of so much heat across a quarter of the planet, and particularly in the form of temperature at the ocean surface, can have a significant effect on weather across the entire planet. Tropical instability waves visible on sea surface temperature maps, showing a tongue of colder water, are often present during neutral or La Niña conditions. La Niña is a complex weather pattern that occurs every few years, often persisting for longer than five months. El Niño and La Niña can be indicators of weather changes across the globe. Atlantic and Pacific hurricanes can have different characteristics due to lower or higher wind shear and cooler or warmer sea surface temperatures. La Niña events have been observed for hundreds of years, and occurred on a regular basis during the early parts of both the 17th and 19th centuries. Since the start of the 20th century, La Niña events have occurred during the following years: 1903–04 1906–07 1909–11 1916–18 1924–25 1928–30 1938–39 1942–43 1949–51 1954–57 1964–65 1970–72 1973–76 1983–85 1988–89 1995–96 1998–2001 2005–06 2007–08 2008–09 2010–12 2016 2017–18 2020–23 Transitional phases at the onset or departure of El Niño or La Niña can also be important factors on global weather by affecting teleconnections . Significant episodes, known as Trans-Niño, are measured by the Trans-Niño index (TNI). Examples of affected short-time climate in North America include precipitation in the Northwest US and intense tornado activity in the contiguous US. If the temperature variation from climatology is within 0.5 °C (0.9 °F), ENSO conditions are described as neutral. Neutral conditions are the transition between warm and cold phases of ENSO. Sea surface temperatures (by definition), tropical precipitation, and wind patterns are near average conditions during this phase. Close to half of all years are within neutral periods. During the neutral ENSO phase, other climate anomalies/patterns such as the sign of the North Atlantic Oscillation or the Pacific–North American teleconnection pattern exert more influence. El Niño conditions are established when the Walker circulation weakens or reverses and the Hadley circulation strengthens, [ citation needed ] [ clarification needed ] leading to the development of a band of warm ocean water in the central and east-central equatorial Pacific (approximately between the International Date Line and 120°W), including the area off the west coast of South America , as upwelling of cold water occurs less or not at all offshore. This warming causes a shift in the atmospheric circulation, leading to higher air pressure in the western Pacific and lower in the eastern Pacific, with rainfall reducing over Indonesia, India and northern Australia, while rainfall and tropical cyclone formation increases over the tropical Pacific Ocean. The low-level surface trade winds , which normally blow from east to west along the equator, either weaken or start blowing from the other direction. El Niño phases are known to happen at irregular intervals of two to seven years, and lasts nine months to two years. The average period length is five years. When this warming occurs for seven to nine months, it is classified as El Niño "conditions"; when its duration is longer, it is classified as an El Niño "episode". It is thought that there have been at least 30 El Niño events between 1900 and 2024, with the 1982–83 , 1997–98 and 2014–16 events among the strongest on record. Since 2000, El Niño events have been observed in 2002–03, 2004–05, 2006–07, 2009–10, 2014–16 , 2018–19, and 2023–24 . Major ENSO events were recorded in the years 1790–93, 1828, 1876–78, 1891, 1925–26, 1972–73, 1982–83, 1997–98, 2014–16, and 2023–24. During strong El Niño episodes, a secondary peak in sea surface temperature across the far eastern equatorial Pacific Ocean sometimes follows the initial peak. An especially strong Walker circulation causes La Niña, which is considered to be the cold oceanic and positive atmospheric phase of the broader El Niño–Southern Oscillation (ENSO) weather phenomenon, as well as the opposite of El Niño weather pattern, where sea surface temperature across the eastern equatorial part of the central Pacific Ocean will be lower than normal by 3–5 °C (5.4–9 °F). The phenomenon occurs as strong winds blow warm water at the ocean's surface away from South America, across the Pacific Ocean towards Indonesia. As this warm water moves west, cold water from the deep sea rises to the surface near South America. The movement of so much heat across a quarter of the planet, and particularly in the form of temperature at the ocean surface, can have a significant effect on weather across the entire planet. Tropical instability waves visible on sea surface temperature maps, showing a tongue of colder water, are often present during neutral or La Niña conditions. La Niña is a complex weather pattern that occurs every few years, often persisting for longer than five months. El Niño and La Niña can be indicators of weather changes across the globe. Atlantic and Pacific hurricanes can have different characteristics due to lower or higher wind shear and cooler or warmer sea surface temperatures. La Niña events have been observed for hundreds of years, and occurred on a regular basis during the early parts of both the 17th and 19th centuries. Since the start of the 20th century, La Niña events have occurred during the following years: 1903–04 1906–07 1909–11 1916–18 1924–25 1928–30 1938–39 1942–43 1949–51 1954–57 1964–65 1970–72 1973–76 1983–85 1988–89 1995–96 1998–2001 2005–06 2007–08 2008–09 2010–12 2016 2017–18 2020–23Transitional phases at the onset or departure of El Niño or La Niña can also be important factors on global weather by affecting teleconnections . Significant episodes, known as Trans-Niño, are measured by the Trans-Niño index (TNI). Examples of affected short-time climate in North America include precipitation in the Northwest US and intense tornado activity in the contiguous US. The first ENSO pattern to be recognised, called Eastern Pacific (EP) ENSO, to distinguish if from others, involves temperature anomalies in the eastern Pacific. However, in the 1990s and 2000s, variations of ENSO conditions were observed, in which the usual place of the temperature anomaly (Niño 1 and 2) is not affected, but an anomaly also arises in the central Pacific (Niño 3.4). The phenomenon is called Central Pacific (CP) ENSO, "dateline" ENSO (because the anomaly arises near the dateline ), or ENSO "Modoki" (Modoki is Japanese for "similar, but different"). There are variations of ENSO additional to the EP and CP types, and some scientists argue that ENSO exists as a continuum, often with hybrid types. The effects of the CP ENSO are different from those of the EP ENSO. The El Niño Modoki is associated with more hurricanes more frequently making landfall in the Atlantic. La Niña Modoki leads to a rainfall increase over northwestern Australia and northern Murray–Darling basin , rather than over the eastern portion of the country as in a conventional EP La Niña. Also, La Niña Modoki increases the frequency of cyclonic storms over Bay of Bengal , but decreases the occurrence of severe storms in the Indian Ocean overall. The first recorded El Niño that originated in the central Pacific and moved toward the east was in 1986. Recent Central Pacific El Niños happened in 1986–87, 1991–92, 1994–95, 2002–03, 2004–05 and 2009–10. Furthermore, there were "Modoki" events in 1957–59, 1963–64, 1965–66, 1968–70, 1977–78 and 1979–80. Some sources say that the El Niños of 2006-07 and 2014-16 were also Central Pacific El Niños. Recent years when La Niña Modoki events occurred include 1973–1974, 1975–1976, 1983–1984, 1988–1989, 1998–1999, 2000–2001, 2008–2009, 2010–2011, and 2016–2017. The recent discovery of ENSO Modoki has some scientists believing it to be linked to global warming. However, comprehensive satellite data go back only to 1979. More research must be done to find the correlation and study past El Niño episodes. More generally, there is no scientific consensus on how/if climate change might affect ENSO. There is also a scientific debate on the very existence of this "new" ENSO. A number of studies dispute the reality of this statistical distinction or its increasing occurrence, or both, either arguing the reliable record is too short to detect such a distinction, finding no distinction or trend using other statistical approaches, or that other types should be distinguished, such as standard and extreme ENSO. Likewise, following the asymmetric nature of the warm and cold phases of ENSO, some studies could not identify similar variations for La Niña, both in observations and in the climate models, but some sources could identify variations on La Niña with cooler waters on central Pacific and average or warmer water temperatures on both eastern and western Pacific, also showing eastern Pacific Ocean currents going to the opposite direction compared to the currents in traditional La Niñas. Coined by the Peruvian Comité Multisectorial Encargado del Estudio Nacional del Fenómeno El Niño (ENFEN), ENSO Costero, or ENSO Oriental, is the name given to the phenomenon where the sea-surface temperature anomalies are mostly focused on the South American coastline, especially from Peru and Ecuador. Studies point many factors that can lead to its occurrence, sometimes accompanying, or being accompanied, by a larger EP ENSO occurrence, or even displaying opposite conditions from the observed ones in the other Niño regions when accompanied by Modoki variations. ENSO Costero events usually present more localized effects, with warm phases leading to increased rainfall over the coast of Ecuador, northern Peru and the Amazon rainforest , and increased temperatures over the northern Chilean coast, and cold phases leading to droughts on the peruvian coast, and increased rainfall and decreased temperatures on its mountainous and jungle regions. Because they don't influence the global climate as much as the other types, these events present lesser and weaker correlations to other significant ENSO features, neither always being triggered by Kelvin waves , nor always being accompanied by proportional Southern Oscillation responses. According to the Coastal Niño Index (ICEN), strong El Niño Costero events include 1957, 1982–83, 1997–98 and 2015–16, and La Niña Costera ones include 1950, 1954–56, 1962, 1964, 1966, 1967–68, 1970–71, 1975–76 and 2013. The first ENSO pattern to be recognised, called Eastern Pacific (EP) ENSO, to distinguish if from others, involves temperature anomalies in the eastern Pacific. However, in the 1990s and 2000s, variations of ENSO conditions were observed, in which the usual place of the temperature anomaly (Niño 1 and 2) is not affected, but an anomaly also arises in the central Pacific (Niño 3.4). The phenomenon is called Central Pacific (CP) ENSO, "dateline" ENSO (because the anomaly arises near the dateline ), or ENSO "Modoki" (Modoki is Japanese for "similar, but different"). There are variations of ENSO additional to the EP and CP types, and some scientists argue that ENSO exists as a continuum, often with hybrid types. The effects of the CP ENSO are different from those of the EP ENSO. The El Niño Modoki is associated with more hurricanes more frequently making landfall in the Atlantic. La Niña Modoki leads to a rainfall increase over northwestern Australia and northern Murray–Darling basin , rather than over the eastern portion of the country as in a conventional EP La Niña. Also, La Niña Modoki increases the frequency of cyclonic storms over Bay of Bengal , but decreases the occurrence of severe storms in the Indian Ocean overall. The first recorded El Niño that originated in the central Pacific and moved toward the east was in 1986. Recent Central Pacific El Niños happened in 1986–87, 1991–92, 1994–95, 2002–03, 2004–05 and 2009–10. Furthermore, there were "Modoki" events in 1957–59, 1963–64, 1965–66, 1968–70, 1977–78 and 1979–80. Some sources say that the El Niños of 2006-07 and 2014-16 were also Central Pacific El Niños. Recent years when La Niña Modoki events occurred include 1973–1974, 1975–1976, 1983–1984, 1988–1989, 1998–1999, 2000–2001, 2008–2009, 2010–2011, and 2016–2017. The recent discovery of ENSO Modoki has some scientists believing it to be linked to global warming. However, comprehensive satellite data go back only to 1979. More research must be done to find the correlation and study past El Niño episodes. More generally, there is no scientific consensus on how/if climate change might affect ENSO. There is also a scientific debate on the very existence of this "new" ENSO. A number of studies dispute the reality of this statistical distinction or its increasing occurrence, or both, either arguing the reliable record is too short to detect such a distinction, finding no distinction or trend using other statistical approaches, or that other types should be distinguished, such as standard and extreme ENSO. Likewise, following the asymmetric nature of the warm and cold phases of ENSO, some studies could not identify similar variations for La Niña, both in observations and in the climate models, but some sources could identify variations on La Niña with cooler waters on central Pacific and average or warmer water temperatures on both eastern and western Pacific, also showing eastern Pacific Ocean currents going to the opposite direction compared to the currents in traditional La Niñas. Coined by the Peruvian Comité Multisectorial Encargado del Estudio Nacional del Fenómeno El Niño (ENFEN), ENSO Costero, or ENSO Oriental, is the name given to the phenomenon where the sea-surface temperature anomalies are mostly focused on the South American coastline, especially from Peru and Ecuador. Studies point many factors that can lead to its occurrence, sometimes accompanying, or being accompanied, by a larger EP ENSO occurrence, or even displaying opposite conditions from the observed ones in the other Niño regions when accompanied by Modoki variations. ENSO Costero events usually present more localized effects, with warm phases leading to increased rainfall over the coast of Ecuador, northern Peru and the Amazon rainforest , and increased temperatures over the northern Chilean coast, and cold phases leading to droughts on the peruvian coast, and increased rainfall and decreased temperatures on its mountainous and jungle regions. Because they don't influence the global climate as much as the other types, these events present lesser and weaker correlations to other significant ENSO features, neither always being triggered by Kelvin waves , nor always being accompanied by proportional Southern Oscillation responses. According to the Coastal Niño Index (ICEN), strong El Niño Costero events include 1957, 1982–83, 1997–98 and 2015–16, and La Niña Costera ones include 1950, 1954–56, 1962, 1964, 1966, 1967–68, 1970–71, 1975–76 and 2013. Currently, each country has a different threshold for what constitutes an El Niño event, which is tailored to their specific interests, for example: In climate change science, ENSO is known as one of the internal [ clarification needed ] climate variability phenomena. The other two main ones [ clarification needed ] are Pacific decadal oscillation and Atlantic multidecadal oscillation . : 23 La Niña impacts the global climate and disrupts normal weather patterns, which can lead to intense storms in some places and droughts in others. El Niño events cause short-term (approximately 1 year in length) spikes in global average surface temperature while La Niña events cause short term cooling. Therefore, the relative frequency of El Niño compared to La Niña events can affect global temperature trends on decadal timescales. There is no sign that there are actual changes in the ENSO physical phenomenon due to climate change. Climate models do not simulate ENSO well enough to make reliable predictions. Future trends in ENSO are uncertain as different models make different predictions. It may be that the observed phenomenon of more frequent and stronger El Niño events occurs only in the initial phase of the global warming, and then (e.g., after the lower layers of the ocean get warmer, as well), El Niño will become weaker. It may also be that the stabilizing and destabilizing forces influencing the phenomenon [ clarification needed ] will eventually compensate for each other. The consequences of ENSO in terms of the temperature anomalies and precipitation and weather extremes around the world are clearly increasing and associated with climate change . For example, recent scholarship (since about 2019) has found that climate change is increasing the frequency of extreme El Niño events. Previously there was no consensus on whether climate change will have any influence on the strength or duration of El Niño events, as research alternately supported El Niño events becoming stronger and weaker, longer and shorter. Over the last several decades, the number of El Niño events increased, and the number of La Niña events decreased, although observation of ENSO for much longer is needed to detect robust changes. Studies of historical data show the recent El Niño variation is most likely linked to global warming. For example, some results, even after subtracting the positive influence of decadal variation, are shown to be possibly present in the ENSO trend, the amplitude of the ENSO variability in the observed data still increases, by as much as 60% in the last 50 years. A study published in 2023 by CSIRO researchers found that climate change may have increased by two times the likelihood of strong El Niño events and nine times the likelihood of strong La Niña events. The study stated it found a consensus between different models and experiments. The IPCC Sixth Assessment Report summarized the state of the art of research in 2021 into the future of ENSO as follows: The ENSO is considered to be a potential tipping element in Earth's climate and, under the global warming, can enhance or alternate regional climate extreme events through a strengthened teleconnection. For example, an increase in the frequency and magnitude of El Niño events have triggered warmer than usual temperatures over the Indian Ocean, by modulating the Walker circulation. This has resulted in a rapid warming of the Indian Ocean, and consequently a weakening of the Asian Monsoon . There is no sign that there are actual changes in the ENSO physical phenomenon due to climate change. Climate models do not simulate ENSO well enough to make reliable predictions. Future trends in ENSO are uncertain as different models make different predictions. It may be that the observed phenomenon of more frequent and stronger El Niño events occurs only in the initial phase of the global warming, and then (e.g., after the lower layers of the ocean get warmer, as well), El Niño will become weaker. It may also be that the stabilizing and destabilizing forces influencing the phenomenon [ clarification needed ] will eventually compensate for each other. The consequences of ENSO in terms of the temperature anomalies and precipitation and weather extremes around the world are clearly increasing and associated with climate change . For example, recent scholarship (since about 2019) has found that climate change is increasing the frequency of extreme El Niño events. Previously there was no consensus on whether climate change will have any influence on the strength or duration of El Niño events, as research alternately supported El Niño events becoming stronger and weaker, longer and shorter. Over the last several decades, the number of El Niño events increased, and the number of La Niña events decreased, although observation of ENSO for much longer is needed to detect robust changes. Studies of historical data show the recent El Niño variation is most likely linked to global warming. For example, some results, even after subtracting the positive influence of decadal variation, are shown to be possibly present in the ENSO trend, the amplitude of the ENSO variability in the observed data still increases, by as much as 60% in the last 50 years. A study published in 2023 by CSIRO researchers found that climate change may have increased by two times the likelihood of strong El Niño events and nine times the likelihood of strong La Niña events. The study stated it found a consensus between different models and experiments. The IPCC Sixth Assessment Report summarized the state of the art of research in 2021 into the future of ENSO as follows:The ENSO is considered to be a potential tipping element in Earth's climate and, under the global warming, can enhance or alternate regional climate extreme events through a strengthened teleconnection. For example, an increase in the frequency and magnitude of El Niño events have triggered warmer than usual temperatures over the Indian Ocean, by modulating the Walker circulation. This has resulted in a rapid warming of the Indian Ocean, and consequently a weakening of the Asian Monsoon . El Niño affects the global climate and disrupts normal weather patterns, which can lead to intense storms in some places and droughts in others. Most tropical cyclones form on the side of the subtropical ridge closer to the equator , then move poleward past the ridge axis before recurving into the main belt of the Westerlies . Areas west of Japan and Korea tend to experience many fewer September–November tropical cyclone impacts during El Niño and neutral years. During El Niño years, the break [ clarification needed ] in the subtropical ridge tends to lie near 130°E , which would favor the Japanese archipelago. Based on modeled and observed accumulated cyclone energy (ACE), El Niño years usually result in less active hurricane seasons in the Atlantic Ocean, but instead favor a shift to tropical cyclone activity in the Pacific Ocean, compared to La Niña years favoring above average hurricane development in the Atlantic and less so in the Pacific basin. Over the Atlantic Ocean , vertical wind shear is increased, which inhibits tropical cyclone genesis and intensification, by causing the westerly winds to be stronger. The atmosphere over the Atlantic Ocean can also be drier and more stable during El Niño events, which can inhibit tropical cyclone genesis and intensification. Within the Eastern Pacific basin : El Niño events contribute to decreased easterly vertical wind shear and favor above-normal hurricane activity. However, the impacts of the ENSO state in this region can vary and are strongly influenced by background climate patterns. The Western Pacific basin experiences a change in the location of where tropical cyclones form during El Niño events, with tropical cyclone formation shifting eastward, without a major change in how many develop each year. As a result of this change, Micronesia is more likely, and China less likely, to be affected by tropical cyclones. A change in the location of where tropical cyclones form also occurs within the Southern Pacific Ocean between 135°E and 120°W, with tropical cyclones more likely to occur within the Southern Pacific basin than the Australian region. As a result of this change tropical cyclones are 50% less likely to make landfall on Queensland, while the risk of a tropical cyclone is elevated for island nations like Niue , French Polynesia , Tonga , Tuvalu , and the Cook Islands . A study of climate records has shown that El Niño events in the equatorial Pacific are generally associated with a warm tropical North Atlantic in the following spring and summer. About half of El Niño events persist sufficiently into the spring months for the Western Hemisphere Warm Pool to become unusually large in summer. Occasionally, El Niño's effect on the Atlantic Walker circulation over South America strengthens the easterly trade winds in the western equatorial Atlantic region. As a result, an unusual cooling may occur in the eastern equatorial Atlantic in spring and summer following El Niño peaks in winter. Cases of El Niño-type events in both oceans simultaneously have been linked to severe famines related to the extended failure of monsoon rains. Most tropical cyclones form on the side of the subtropical ridge closer to the equator , then move poleward past the ridge axis before recurving into the main belt of the Westerlies . Areas west of Japan and Korea tend to experience many fewer September–November tropical cyclone impacts during El Niño and neutral years. During El Niño years, the break [ clarification needed ] in the subtropical ridge tends to lie near 130°E , which would favor the Japanese archipelago. Based on modeled and observed accumulated cyclone energy (ACE), El Niño years usually result in less active hurricane seasons in the Atlantic Ocean, but instead favor a shift to tropical cyclone activity in the Pacific Ocean, compared to La Niña years favoring above average hurricane development in the Atlantic and less so in the Pacific basin. Over the Atlantic Ocean , vertical wind shear is increased, which inhibits tropical cyclone genesis and intensification, by causing the westerly winds to be stronger. The atmosphere over the Atlantic Ocean can also be drier and more stable during El Niño events, which can inhibit tropical cyclone genesis and intensification. Within the Eastern Pacific basin : El Niño events contribute to decreased easterly vertical wind shear and favor above-normal hurricane activity. However, the impacts of the ENSO state in this region can vary and are strongly influenced by background climate patterns. The Western Pacific basin experiences a change in the location of where tropical cyclones form during El Niño events, with tropical cyclone formation shifting eastward, without a major change in how many develop each year. As a result of this change, Micronesia is more likely, and China less likely, to be affected by tropical cyclones. A change in the location of where tropical cyclones form also occurs within the Southern Pacific Ocean between 135°E and 120°W, with tropical cyclones more likely to occur within the Southern Pacific basin than the Australian region. As a result of this change tropical cyclones are 50% less likely to make landfall on Queensland, while the risk of a tropical cyclone is elevated for island nations like Niue , French Polynesia , Tonga , Tuvalu , and the Cook Islands . A study of climate records has shown that El Niño events in the equatorial Pacific are generally associated with a warm tropical North Atlantic in the following spring and summer. About half of El Niño events persist sufficiently into the spring months for the Western Hemisphere Warm Pool to become unusually large in summer. Occasionally, El Niño's effect on the Atlantic Walker circulation over South America strengthens the easterly trade winds in the western equatorial Atlantic region. As a result, an unusual cooling may occur in the eastern equatorial Atlantic in spring and summer following El Niño peaks in winter. Cases of El Niño-type events in both oceans simultaneously have been linked to severe famines related to the extended failure of monsoon rains. When El Niño conditions last for many months, extensive ocean warming and the reduction in easterly trade winds limits upwelling of cold nutrient-rich deep water, and its economic effect on local fishing for an international market can be serious. Developing countries that depend on their own agriculture and fishing, particularly those bordering the Pacific Ocean, are usually most affected by El Niño conditions. In this phase of the Oscillation, the pool of warm water in the Pacific near South America is often at its warmest in late December. More generally, El Niño can affect commodity prices and the macroeconomy of different countries. It can constrain the supply of rain-driven agricultural commodities; reduce agricultural output, construction, and services activities; increase food prices; and may trigger social unrest in commodity-dependent poor countries that primarily rely on imported food. A University of Cambridge Working Paper shows that while Australia, Chile, Indonesia, India, Japan, New Zealand and South Africa face a short-lived fall in economic activity in response to an El Niño shock, other countries may actually benefit from an El Niño weather shock (either directly or indirectly through positive spillovers from major trading partners), for instance, Argentina, Canada, Mexico and the United States. Furthermore, most countries experience short-run inflationary pressures following an El Niño shock, while global energy and non-fuel commodity prices increase. The IMF estimates a significant El Niño can boost the GDP of the United States by about 0.5% (due largely to lower heating bills) and reduce the GDP of Indonesia by about 1.0%. Extreme weather conditions related to the El Niño cycle correlate with changes in the incidence of epidemic diseases. For example, the El Niño cycle is associated with increased risks of some of the diseases transmitted by mosquitoes , such as malaria , dengue fever , and Rift Valley fever . Cycles of malaria in India , Venezuela , Brazil , and Colombia have now been linked to El Niño. Outbreaks of another mosquito-transmitted disease, Australian encephalitis ( Murray Valley encephalitis —MVE), occur in temperate south-east Australia after heavy rainfall and flooding, which are associated with La Niña events. A severe outbreak of Rift Valley fever occurred after extreme rainfall in north-eastern Kenya and southern Somalia during the 1997–98 El Niño. ENSO conditions have also been related to Kawasaki disease incidence in Japan and the west coast of the United States, via the linkage to tropospheric winds across the north Pacific Ocean. ENSO may be linked to civil conflicts. Scientists at The Earth Institute of Columbia University , having analyzed data from 1950 to 2004, suggest ENSO may have had a role in 21% of all civil conflicts since 1950, with the risk of annual civil conflict doubling from 3% to 6% in countries affected by ENSO during El Niño years relative to La Niña years. During the 1982–83, 1997–98 and 2015–16 ENSO events, large extensions of tropical forests experienced a prolonged dry period that resulted in widespread fires, and drastic changes in forest structure and tree species composition in Amazonian and Bornean forests. Their impacts do not restrict only vegetation, since declines in insect populations were observed after extreme drought and terrible fires during El Niño 2015–16. Declines in habitat-specialist and disturbance-sensitive bird species and in large-frugivorous mammals were also observed in Amazonian burned forests, while temporary extirpation of more than 100 lowland butterfly species occurred at a burned forest site in Borneo. In seasonally dry tropical forests, which are more drought tolerant, researchers found that El Niño induced drought increased seedling mortality. In a research published in October 2022, researchers studied seasonally dry tropical forests in a national park in Chiang Mai in Thailand for 7 years and observed that El Niño increased seedling mortality even in seasonally dry tropical forests and may impact entire forests in long run. Following the El Nino event in 1997 – 1998, the Pacific Marine Environmental Laboratory attributes the first large-scale coral bleaching event to the warming waters. Most critically, global mass bleaching events were recorded in 1997-98 and 2015–16, when around 75-99% losses of live coral were registered across the world. Considerable attention was also given to the collapse of Peruvian and Chilean anchovy populations that led to a severe fishery crisis following the ENSO events in 1972–73, 1982–83, 1997–98 and, more recently, in 2015–16. In particular, increased surface seawater temperatures in 1982-83 also lead to the probable extinction of two hydrocoral species in Panamá, and to a massive mortality of kelp beds along 600 km of coastline in Chile, from which kelps and associated biodiversity slowly recovered in the most affected areas even after 20 years. All these findings enlarge the role of ENSO events as a strong climatic force driving ecological changes all around the world – particularly in tropical forests and coral reefs. When El Niño conditions last for many months, extensive ocean warming and the reduction in easterly trade winds limits upwelling of cold nutrient-rich deep water, and its economic effect on local fishing for an international market can be serious. Developing countries that depend on their own agriculture and fishing, particularly those bordering the Pacific Ocean, are usually most affected by El Niño conditions. In this phase of the Oscillation, the pool of warm water in the Pacific near South America is often at its warmest in late December. More generally, El Niño can affect commodity prices and the macroeconomy of different countries. It can constrain the supply of rain-driven agricultural commodities; reduce agricultural output, construction, and services activities; increase food prices; and may trigger social unrest in commodity-dependent poor countries that primarily rely on imported food. A University of Cambridge Working Paper shows that while Australia, Chile, Indonesia, India, Japan, New Zealand and South Africa face a short-lived fall in economic activity in response to an El Niño shock, other countries may actually benefit from an El Niño weather shock (either directly or indirectly through positive spillovers from major trading partners), for instance, Argentina, Canada, Mexico and the United States. Furthermore, most countries experience short-run inflationary pressures following an El Niño shock, while global energy and non-fuel commodity prices increase. The IMF estimates a significant El Niño can boost the GDP of the United States by about 0.5% (due largely to lower heating bills) and reduce the GDP of Indonesia by about 1.0%. Extreme weather conditions related to the El Niño cycle correlate with changes in the incidence of epidemic diseases. For example, the El Niño cycle is associated with increased risks of some of the diseases transmitted by mosquitoes , such as malaria , dengue fever , and Rift Valley fever . Cycles of malaria in India , Venezuela , Brazil , and Colombia have now been linked to El Niño. Outbreaks of another mosquito-transmitted disease, Australian encephalitis ( Murray Valley encephalitis —MVE), occur in temperate south-east Australia after heavy rainfall and flooding, which are associated with La Niña events. A severe outbreak of Rift Valley fever occurred after extreme rainfall in north-eastern Kenya and southern Somalia during the 1997–98 El Niño. ENSO conditions have also been related to Kawasaki disease incidence in Japan and the west coast of the United States, via the linkage to tropospheric winds across the north Pacific Ocean. ENSO may be linked to civil conflicts. Scientists at The Earth Institute of Columbia University , having analyzed data from 1950 to 2004, suggest ENSO may have had a role in 21% of all civil conflicts since 1950, with the risk of annual civil conflict doubling from 3% to 6% in countries affected by ENSO during El Niño years relative to La Niña years. During the 1982–83, 1997–98 and 2015–16 ENSO events, large extensions of tropical forests experienced a prolonged dry period that resulted in widespread fires, and drastic changes in forest structure and tree species composition in Amazonian and Bornean forests. Their impacts do not restrict only vegetation, since declines in insect populations were observed after extreme drought and terrible fires during El Niño 2015–16. Declines in habitat-specialist and disturbance-sensitive bird species and in large-frugivorous mammals were also observed in Amazonian burned forests, while temporary extirpation of more than 100 lowland butterfly species occurred at a burned forest site in Borneo. In seasonally dry tropical forests, which are more drought tolerant, researchers found that El Niño induced drought increased seedling mortality. In a research published in October 2022, researchers studied seasonally dry tropical forests in a national park in Chiang Mai in Thailand for 7 years and observed that El Niño increased seedling mortality even in seasonally dry tropical forests and may impact entire forests in long run. Following the El Nino event in 1997 – 1998, the Pacific Marine Environmental Laboratory attributes the first large-scale coral bleaching event to the warming waters. Most critically, global mass bleaching events were recorded in 1997-98 and 2015–16, when around 75-99% losses of live coral were registered across the world. Considerable attention was also given to the collapse of Peruvian and Chilean anchovy populations that led to a severe fishery crisis following the ENSO events in 1972–73, 1982–83, 1997–98 and, more recently, in 2015–16. In particular, increased surface seawater temperatures in 1982-83 also lead to the probable extinction of two hydrocoral species in Panamá, and to a massive mortality of kelp beds along 600 km of coastline in Chile, from which kelps and associated biodiversity slowly recovered in the most affected areas even after 20 years. All these findings enlarge the role of ENSO events as a strong climatic force driving ecological changes all around the world – particularly in tropical forests and coral reefs. Following the El Nino event in 1997 – 1998, the Pacific Marine Environmental Laboratory attributes the first large-scale coral bleaching event to the warming waters. Most critically, global mass bleaching events were recorded in 1997-98 and 2015–16, when around 75-99% losses of live coral were registered across the world. Considerable attention was also given to the collapse of Peruvian and Chilean anchovy populations that led to a severe fishery crisis following the ENSO events in 1972–73, 1982–83, 1997–98 and, more recently, in 2015–16. In particular, increased surface seawater temperatures in 1982-83 also lead to the probable extinction of two hydrocoral species in Panamá, and to a massive mortality of kelp beds along 600 km of coastline in Chile, from which kelps and associated biodiversity slowly recovered in the most affected areas even after 20 years. All these findings enlarge the role of ENSO events as a strong climatic force driving ecological changes all around the world – particularly in tropical forests and coral reefs. Observations of ENSO events since 1950 show that impacts associated with such events depend on the time of year. While certain events and impacts are expected to occur, it is not certain that they will happen. The impacts that generally do occur during most El Niño events include below-average rainfall over Indonesia and northern South America, and above average rainfall in southeastern South America, eastern equatorial Africa, and the southern United States. La Niña results in wetter-than-normal conditions in southern Africa from December to February, and drier-than-normal conditions over equatorial east Africa over the same period. The effects of El Niño on rainfall in southern Africa differ between the summer and winter rainfall areas. Winter rainfall areas tend to get higher rainfall than normal and summer rainfall areas tend to get less rain. The effect on the summer rainfall areas is stronger and has led to severe drought in strong El Niño events. Sea surface temperatures off the west and south coasts of South Africa are affected by ENSO via changes in surface wind strength. During El Niño the south-easterly winds driving upwelling are weaker which results in warmer coastal waters than normal, while during La Niña the same winds are stronger and cause colder coastal waters. These effects on the winds are part of large scale influences on the tropical Atlantic and the South Atlantic High -pressure system, and changes to the pattern of westerly winds further south. There are other influences not known to be related to ENSO of similar importance. Some ENSO events do not lead to the expected changes. Many ENSO linkages exist in the high southern latitudes around Antarctica . Specifically, El Niño conditions result in high-pressure anomalies over the Amundsen and Bellingshausen Seas, causing reduced sea ice and increased poleward heat fluxes in these sectors, as well as the Ross Sea . The Weddell Sea , conversely, tends to become colder with more sea ice during El Niño. The exact opposite heating and atmospheric pressure anomalies occur during La Niña. This pattern of variability is known as the Antarctic dipole mode, although the Antarctic response to ENSO forcing is not ubiquitous. In Western Asia , during the region's November–April rainy season, there is increased precipitation in the El Niño phase and reduced precipitation in the La Niña phase on average. During El Niño years: As warm water spreads from the west Pacific and the Indian Ocean to the east Pacific, it takes the rain with it, causing extensive drought in the western Pacific and rainfall in the normally dry eastern Pacific. Singapore experienced the driest February in 2010 since records began in 1869, with only 6.3 mm of rain falling in the month. The years 1968 and 2005 had the next driest Februaries, when 8.4 mm of rain fell. During La Niña years, the formation of tropical cyclones, along with the subtropical ridge position, shifts westward across the western Pacific Ocean, which increases the landfall threat in China. In March 2008, La Niña caused a drop in sea surface temperatures over Southeast Asia by 2 °C (3.6 °F) . It also caused heavy rains over the Philippines , Indonesia , and Malaysia . Across most of the continent, El Niño and La Niña have more impact on climate variability than any other factor. There is a strong correlation between the strength of La Niña and rainfall: the greater the sea surface temperature and Southern Oscillation difference from normal, the larger the rainfall change. During El Niño events, the shift in rainfall away from the Western Pacific may mean that rainfall across Australia is reduced. Over the southern part of the continent, warmer than average temperatures can be recorded as weather systems are more mobile and fewer blocking areas of high pressure occur. The onset of the Indo-Australian Monsoon in tropical Australia is delayed by two to six weeks, which as a consequence means that rainfall is reduced over the northern tropics. The risk of a significant bushfire season in south-eastern Australia is higher following an El Niño event, especially when it is combined with a positive Indian Ocean Dipole event. Effects of the El Niño–Southern Oscillation in Australia are present across most of Australia , particularly the north and the east , and are one of the main climate drivers of the country. Associated with seasonal abnormality in many areas in the world, Australia is one of the continents most affected and experiences extensive droughts alongside considerable wet periods that cause major floods. There exist three phases — El Niño, La Niña, and Neutral, which help to account for the different states of ENSO. Since 1900, there have been 28 El Niño and 19 La Niña events in Australia including the current 2023 El Niño event, which was declared on 17th of September in 2023. The events usually last for 9 to 12 months, but some can persist for two years, though the ENSO cycle generally operates over a time period from one to eight years. El Niño's effects on Europe are controversial, complex and difficult to analyze, as it is one of several factors that influence the weather over the continent and other factors can overwhelm the signal. La Niña causes mostly the opposite effects of El Niño: above-average precipitation across the northern Midwest , the northern Rockies , Northern California , and the Pacific Northwest 's southern and eastern regions. Meanwhile, precipitation in the southwestern and southeastern states, as well as southern California, is below average. This also allows [ clarification needed ] for the development of many stronger-than-average hurricanes in the Atlantic and fewer in the Pacific. ENSO is linked to rainfall over Puerto Rico. [ clarification needed ] During an El Niño, snowfall is greater than average across the southern Rockies and Sierra Nevada mountain range, and is well-below normal across the Upper Midwest and Great Lakes states. During a La Niña, snowfall is above normal across the Pacific Northwest and western Great Lakes. In Canada, La Niña will, in general, cause a cooler, snowier winter, such as the near-record-breaking amounts of snow recorded in the La Niña winter of 2007–2008 in eastern Canada. In the spring of 2022, La Niña caused above-average precipitation and below-average temperatures in the state of Oregon. April was one of the wettest months on record, and La Niña effects, while less severe, were expected to continue into the summer. Over North America, the main temperature and precipitation impacts of El Niño generally occur in the six months between October and March. In particular, the majority of Canada generally has milder than normal winters and springs, with the exception of eastern Canada where no significant impacts occur. Within the United States, the impacts generally observed during the six-month period include wetter-than-average conditions along the Gulf Coast between Texas and Florida , while drier conditions are observed in Hawaii , the Ohio Valley , Pacific Northwest and the Rocky Mountains . Study of more recent weather events over California and the southwestern United States indicate that there is a variable relationship between El Niño and above-average precipitation, as it strongly depends on the strength of the El Niño event and other factors. Though it has been historically associated with high rainfall in California, the effects of El Niño depend more strongly on the "flavor" [ clarification needed ] of El Niño than its presence or absence, as only "persistent El Niño" events lead to consistently high rainfall. To the north across Alaska , La Niña events lead to drier than normal conditions, while El Niño events do not have a correlation towards dry or wet conditions. During El Niño events, increased precipitation is expected in California due to a more southerly, zonal, storm track . During La Niña, increased precipitation is diverted into the Pacific Northwest due to a more northerly storm track. During La Niña events, the storm track shifts far enough northward to bring wetter than normal winter conditions (in the form of increased snowfall) to the Midwestern states, as well as hot and dry summers. During the El Niño portion of ENSO , increased precipitation falls along the Gulf coast and Southeast due to a stronger than normal, and more southerly, polar jet stream . The synoptic condition for the Tehuantepecer , a violent mountain-gap wind in between the mountains of Mexico and Guatemala , is associated with high-pressure system forming in Sierra Madre of Mexico in the wake of an advancing cold front, which causes winds to accelerate through the Isthmus of Tehuantepec . Tehuantepecers primarily occur during the cold season months for the region in the wake of cold fronts, between October and February, with a summer maximum in July caused by the westward extension of the Azores-Bermuda high pressure system. Wind magnitude is greater during El Niño years than during La Niña years, due to the more frequent cold frontal incursions during El Niño winters. Tehuantepec winds reach 20 knots (40 km/h) to 45 knots (80 km/h) , and on rare occasions 100 knots (190 km/h) . The wind's direction is from the north to north-northeast. It leads to a localized acceleration of the trade winds in the region, and can enhance thunderstorm activity when it interacts with the Intertropical Convergence Zone . The effects can last from a few hours to six days. Between 1942 and 1957, La Niña had an impact that caused isotope changes in the plants of Baja California, and that had helped scientists to study his impact. During an El Niño event, New Zealand tends to experience stronger or more frequent westerly winds during their summer, which leads to an elevated risk of drier than normal conditions along the east coast. There is more rain than usual though on New Zealand's West Coast, because of the barrier effect of the North Island mountain ranges and the Southern Alps. Fiji generally experiences drier than normal conditions during an El Niño, which can lead to drought becoming established over the Islands. However, the main impacts on the island nation is felt about a year after the event becomes established. Within the Samoan Islands, below average rainfall and higher than normal temperatures are recorded during El Niño events, which can lead to droughts and forest fires on the islands. Other impacts include a decrease in the sea level, possibility of coral bleaching in the marine environment and an increased risk of a tropical cyclone affecting Samoa. In the late winter and spring during El Niño events, drier than average conditions can be expected in Hawaii. On Guam during El Niño years, dry season precipitation averages below normal, but the probability of a tropical cyclone is more than triple what is normal, so extreme short duration rainfall events are possible. On American Samoa during El Niño events, precipitation averages about 10 percent above normal, while La Niña events are associated with precipitation averaging about 10 percent below normal. The effects of El Niño in South America are direct and strong. An El Niño is associated with warm and very wet weather months in April–October along the coasts of northern Peru and Ecuador , causing major flooding whenever the event is strong or extreme. Because El Niño's warm pool feeds thunderstorms above, it creates increased rainfall across the east-central and eastern Pacific Ocean, including several portions of the South American west coast. The effects of El Niño in South America are direct and stronger than in North America. An El Niño is associated with warm and very wet weather months in April–October along the coasts of northern Peru and Ecuador , causing major flooding whenever the event is strong or extreme. The effects during the months of February, March, and April may become critical along the west coast of South America , El Niño reduces the upwelling of cold, nutrient-rich water that sustains large fish populations, which in turn sustain abundant sea birds, whose droppings support the fertilizer industry. The reduction in upwelling leads to fish kills off the shore of Peru. The local fishing industry along the affected coastline can suffer during long-lasting El Niño events. Peruvian fisheries collapsed during the 1970s due to overfishing following the 1972 El Niño Peruvian anchoveta reduction. The fisheries were previously the world's largest, however, this collapse led to the decline of these fisheries. During the 1982–83 event, jack mackerel and anchoveta populations were reduced, scallops increased in warmer water, but hake followed cooler water down the continental slope, while shrimp and sardines moved southward, so some catches decreased while others increased. Horse mackerel have increased in the region during warm events. Shifting locations and types of fish due to changing conditions create challenges for the fishing industry. Peruvian sardines have moved during El Niño events to Chilean areas. Other conditions provide further complications, such as the government of Chile in 1991 creating restrictions on the fishing areas for self-employed fishermen and industrial fleets. Southern Brazil and northern Argentina also experience wetter than normal conditions during El Niño years, but mainly during the spring and early summer. Central Chile receives a mild winter with large rainfall, and the Peruvian-Bolivian Altiplano is sometimes exposed to unusual winter snowfall events. Drier and hotter weather occurs in parts of the Amazon River Basin, Colombia , and Central America . During a time of La Niña, drought affects the coastal regions of Peru and Chile. From December to February, northern Brazil is wetter than normal. La Niña causes higher than normal rainfall in the central Andes , which in turn causes catastrophic flooding on the Llanos de Mojos of Beni Department , Bolivia. Such flooding is documented from 1853, 1865, 1872, 1873, 1886, 1895, 1896, 1907, 1921, 1928, 1929 and 1931. The Galápagos Islands are a chain of volcanic islands, nearly 600 miles west of Ecuador, South America. in the Eastern Pacific Ocean. These islands support a wide diversity of terrestrial and marine species. The ecosystem is based on the normal trade winds which influence upwelling of cold, nutrient rich waters to the islands. During an El Niño event the trade winds weaken and sometimes blow from west to east, which causes the Equatorial current to weaken, raising surface water temperatures and decreasing nutrients in waters surrounding the Galápagos. El Niño causes a trophic cascade which impacts entire ecosystems starting with primary producers and ending with critical animals such as sharks, penguins, and seals. The effects of El Niño can become detrimental to populations that often starve and die back during these years. Rapid evolutionary adaptations are displayed amongst animal groups during El Niño years to mitigate El Niño conditions. La Niña results in wetter-than-normal conditions in southern Africa from December to February, and drier-than-normal conditions over equatorial east Africa over the same period. The effects of El Niño on rainfall in southern Africa differ between the summer and winter rainfall areas. Winter rainfall areas tend to get higher rainfall than normal and summer rainfall areas tend to get less rain. The effect on the summer rainfall areas is stronger and has led to severe drought in strong El Niño events. Sea surface temperatures off the west and south coasts of South Africa are affected by ENSO via changes in surface wind strength. During El Niño the south-easterly winds driving upwelling are weaker which results in warmer coastal waters than normal, while during La Niña the same winds are stronger and cause colder coastal waters. These effects on the winds are part of large scale influences on the tropical Atlantic and the South Atlantic High -pressure system, and changes to the pattern of westerly winds further south. There are other influences not known to be related to ENSO of similar importance. Some ENSO events do not lead to the expected changes. Many ENSO linkages exist in the high southern latitudes around Antarctica . Specifically, El Niño conditions result in high-pressure anomalies over the Amundsen and Bellingshausen Seas, causing reduced sea ice and increased poleward heat fluxes in these sectors, as well as the Ross Sea . The Weddell Sea , conversely, tends to become colder with more sea ice during El Niño. The exact opposite heating and atmospheric pressure anomalies occur during La Niña. This pattern of variability is known as the Antarctic dipole mode, although the Antarctic response to ENSO forcing is not ubiquitous. In Western Asia , during the region's November–April rainy season, there is increased precipitation in the El Niño phase and reduced precipitation in the La Niña phase on average. During El Niño years: As warm water spreads from the west Pacific and the Indian Ocean to the east Pacific, it takes the rain with it, causing extensive drought in the western Pacific and rainfall in the normally dry eastern Pacific. Singapore experienced the driest February in 2010 since records began in 1869, with only 6.3 mm of rain falling in the month. The years 1968 and 2005 had the next driest Februaries, when 8.4 mm of rain fell. During La Niña years, the formation of tropical cyclones, along with the subtropical ridge position, shifts westward across the western Pacific Ocean, which increases the landfall threat in China. In March 2008, La Niña caused a drop in sea surface temperatures over Southeast Asia by 2 °C (3.6 °F) . It also caused heavy rains over the Philippines , Indonesia , and Malaysia . Across most of the continent, El Niño and La Niña have more impact on climate variability than any other factor. There is a strong correlation between the strength of La Niña and rainfall: the greater the sea surface temperature and Southern Oscillation difference from normal, the larger the rainfall change. During El Niño events, the shift in rainfall away from the Western Pacific may mean that rainfall across Australia is reduced. Over the southern part of the continent, warmer than average temperatures can be recorded as weather systems are more mobile and fewer blocking areas of high pressure occur. The onset of the Indo-Australian Monsoon in tropical Australia is delayed by two to six weeks, which as a consequence means that rainfall is reduced over the northern tropics. The risk of a significant bushfire season in south-eastern Australia is higher following an El Niño event, especially when it is combined with a positive Indian Ocean Dipole event. Effects of the El Niño–Southern Oscillation in Australia are present across most of Australia , particularly the north and the east , and are one of the main climate drivers of the country. Associated with seasonal abnormality in many areas in the world, Australia is one of the continents most affected and experiences extensive droughts alongside considerable wet periods that cause major floods. There exist three phases — El Niño, La Niña, and Neutral, which help to account for the different states of ENSO. Since 1900, there have been 28 El Niño and 19 La Niña events in Australia including the current 2023 El Niño event, which was declared on 17th of September in 2023. The events usually last for 9 to 12 months, but some can persist for two years, though the ENSO cycle generally operates over a time period from one to eight years. El Niño's effects on Europe are controversial, complex and difficult to analyze, as it is one of several factors that influence the weather over the continent and other factors can overwhelm the signal. La Niña causes mostly the opposite effects of El Niño: above-average precipitation across the northern Midwest , the northern Rockies , Northern California , and the Pacific Northwest 's southern and eastern regions. Meanwhile, precipitation in the southwestern and southeastern states, as well as southern California, is below average. This also allows [ clarification needed ] for the development of many stronger-than-average hurricanes in the Atlantic and fewer in the Pacific. ENSO is linked to rainfall over Puerto Rico. [ clarification needed ] During an El Niño, snowfall is greater than average across the southern Rockies and Sierra Nevada mountain range, and is well-below normal across the Upper Midwest and Great Lakes states. During a La Niña, snowfall is above normal across the Pacific Northwest and western Great Lakes. In Canada, La Niña will, in general, cause a cooler, snowier winter, such as the near-record-breaking amounts of snow recorded in the La Niña winter of 2007–2008 in eastern Canada. In the spring of 2022, La Niña caused above-average precipitation and below-average temperatures in the state of Oregon. April was one of the wettest months on record, and La Niña effects, while less severe, were expected to continue into the summer. Over North America, the main temperature and precipitation impacts of El Niño generally occur in the six months between October and March. In particular, the majority of Canada generally has milder than normal winters and springs, with the exception of eastern Canada where no significant impacts occur. Within the United States, the impacts generally observed during the six-month period include wetter-than-average conditions along the Gulf Coast between Texas and Florida , while drier conditions are observed in Hawaii , the Ohio Valley , Pacific Northwest and the Rocky Mountains . Study of more recent weather events over California and the southwestern United States indicate that there is a variable relationship between El Niño and above-average precipitation, as it strongly depends on the strength of the El Niño event and other factors. Though it has been historically associated with high rainfall in California, the effects of El Niño depend more strongly on the "flavor" [ clarification needed ] of El Niño than its presence or absence, as only "persistent El Niño" events lead to consistently high rainfall. To the north across Alaska , La Niña events lead to drier than normal conditions, while El Niño events do not have a correlation towards dry or wet conditions. During El Niño events, increased precipitation is expected in California due to a more southerly, zonal, storm track . During La Niña, increased precipitation is diverted into the Pacific Northwest due to a more northerly storm track. During La Niña events, the storm track shifts far enough northward to bring wetter than normal winter conditions (in the form of increased snowfall) to the Midwestern states, as well as hot and dry summers. During the El Niño portion of ENSO , increased precipitation falls along the Gulf coast and Southeast due to a stronger than normal, and more southerly, polar jet stream . The synoptic condition for the Tehuantepecer , a violent mountain-gap wind in between the mountains of Mexico and Guatemala , is associated with high-pressure system forming in Sierra Madre of Mexico in the wake of an advancing cold front, which causes winds to accelerate through the Isthmus of Tehuantepec . Tehuantepecers primarily occur during the cold season months for the region in the wake of cold fronts, between October and February, with a summer maximum in July caused by the westward extension of the Azores-Bermuda high pressure system. Wind magnitude is greater during El Niño years than during La Niña years, due to the more frequent cold frontal incursions during El Niño winters. Tehuantepec winds reach 20 knots (40 km/h) to 45 knots (80 km/h) , and on rare occasions 100 knots (190 km/h) . The wind's direction is from the north to north-northeast. It leads to a localized acceleration of the trade winds in the region, and can enhance thunderstorm activity when it interacts with the Intertropical Convergence Zone . The effects can last from a few hours to six days. Between 1942 and 1957, La Niña had an impact that caused isotope changes in the plants of Baja California, and that had helped scientists to study his impact. The synoptic condition for the Tehuantepecer , a violent mountain-gap wind in between the mountains of Mexico and Guatemala , is associated with high-pressure system forming in Sierra Madre of Mexico in the wake of an advancing cold front, which causes winds to accelerate through the Isthmus of Tehuantepec . Tehuantepecers primarily occur during the cold season months for the region in the wake of cold fronts, between October and February, with a summer maximum in July caused by the westward extension of the Azores-Bermuda high pressure system. Wind magnitude is greater during El Niño years than during La Niña years, due to the more frequent cold frontal incursions during El Niño winters. Tehuantepec winds reach 20 knots (40 km/h) to 45 knots (80 km/h) , and on rare occasions 100 knots (190 km/h) . The wind's direction is from the north to north-northeast. It leads to a localized acceleration of the trade winds in the region, and can enhance thunderstorm activity when it interacts with the Intertropical Convergence Zone . The effects can last from a few hours to six days. Between 1942 and 1957, La Niña had an impact that caused isotope changes in the plants of Baja California, and that had helped scientists to study his impact. During an El Niño event, New Zealand tends to experience stronger or more frequent westerly winds during their summer, which leads to an elevated risk of drier than normal conditions along the east coast. There is more rain than usual though on New Zealand's West Coast, because of the barrier effect of the North Island mountain ranges and the Southern Alps. Fiji generally experiences drier than normal conditions during an El Niño, which can lead to drought becoming established over the Islands. However, the main impacts on the island nation is felt about a year after the event becomes established. Within the Samoan Islands, below average rainfall and higher than normal temperatures are recorded during El Niño events, which can lead to droughts and forest fires on the islands. Other impacts include a decrease in the sea level, possibility of coral bleaching in the marine environment and an increased risk of a tropical cyclone affecting Samoa. In the late winter and spring during El Niño events, drier than average conditions can be expected in Hawaii. On Guam during El Niño years, dry season precipitation averages below normal, but the probability of a tropical cyclone is more than triple what is normal, so extreme short duration rainfall events are possible. On American Samoa during El Niño events, precipitation averages about 10 percent above normal, while La Niña events are associated with precipitation averaging about 10 percent below normal. The effects of El Niño in South America are direct and strong. An El Niño is associated with warm and very wet weather months in April–October along the coasts of northern Peru and Ecuador , causing major flooding whenever the event is strong or extreme. Because El Niño's warm pool feeds thunderstorms above, it creates increased rainfall across the east-central and eastern Pacific Ocean, including several portions of the South American west coast. The effects of El Niño in South America are direct and stronger than in North America. An El Niño is associated with warm and very wet weather months in April–October along the coasts of northern Peru and Ecuador , causing major flooding whenever the event is strong or extreme. The effects during the months of February, March, and April may become critical along the west coast of South America , El Niño reduces the upwelling of cold, nutrient-rich water that sustains large fish populations, which in turn sustain abundant sea birds, whose droppings support the fertilizer industry. The reduction in upwelling leads to fish kills off the shore of Peru. The local fishing industry along the affected coastline can suffer during long-lasting El Niño events. Peruvian fisheries collapsed during the 1970s due to overfishing following the 1972 El Niño Peruvian anchoveta reduction. The fisheries were previously the world's largest, however, this collapse led to the decline of these fisheries. During the 1982–83 event, jack mackerel and anchoveta populations were reduced, scallops increased in warmer water, but hake followed cooler water down the continental slope, while shrimp and sardines moved southward, so some catches decreased while others increased. Horse mackerel have increased in the region during warm events. Shifting locations and types of fish due to changing conditions create challenges for the fishing industry. Peruvian sardines have moved during El Niño events to Chilean areas. Other conditions provide further complications, such as the government of Chile in 1991 creating restrictions on the fishing areas for self-employed fishermen and industrial fleets. Southern Brazil and northern Argentina also experience wetter than normal conditions during El Niño years, but mainly during the spring and early summer. Central Chile receives a mild winter with large rainfall, and the Peruvian-Bolivian Altiplano is sometimes exposed to unusual winter snowfall events. Drier and hotter weather occurs in parts of the Amazon River Basin, Colombia , and Central America . During a time of La Niña, drought affects the coastal regions of Peru and Chile. From December to February, northern Brazil is wetter than normal. La Niña causes higher than normal rainfall in the central Andes , which in turn causes catastrophic flooding on the Llanos de Mojos of Beni Department , Bolivia. Such flooding is documented from 1853, 1865, 1872, 1873, 1886, 1895, 1896, 1907, 1921, 1928, 1929 and 1931. The Galápagos Islands are a chain of volcanic islands, nearly 600 miles west of Ecuador, South America. in the Eastern Pacific Ocean. These islands support a wide diversity of terrestrial and marine species. The ecosystem is based on the normal trade winds which influence upwelling of cold, nutrient rich waters to the islands. During an El Niño event the trade winds weaken and sometimes blow from west to east, which causes the Equatorial current to weaken, raising surface water temperatures and decreasing nutrients in waters surrounding the Galápagos. El Niño causes a trophic cascade which impacts entire ecosystems starting with primary producers and ending with critical animals such as sharks, penguins, and seals. The effects of El Niño can become detrimental to populations that often starve and die back during these years. Rapid evolutionary adaptations are displayed amongst animal groups during El Niño years to mitigate El Niño conditions. The Galápagos Islands are a chain of volcanic islands, nearly 600 miles west of Ecuador, South America. in the Eastern Pacific Ocean. These islands support a wide diversity of terrestrial and marine species. The ecosystem is based on the normal trade winds which influence upwelling of cold, nutrient rich waters to the islands. During an El Niño event the trade winds weaken and sometimes blow from west to east, which causes the Equatorial current to weaken, raising surface water temperatures and decreasing nutrients in waters surrounding the Galápagos. El Niño causes a trophic cascade which impacts entire ecosystems starting with primary producers and ending with critical animals such as sharks, penguins, and seals. The effects of El Niño can become detrimental to populations that often starve and die back during these years. Rapid evolutionary adaptations are displayed amongst animal groups during El Niño years to mitigate El Niño conditions. ENSO conditions have occurred at two- to seven-year intervals for at least the past 300 years, but most of them have been weak. El Niño may have led to the demise of the Moche and other pre-Columbian Peruvian cultures . A recent study suggests a strong El Niño effect between 1789 and 1793 caused poor crop yields in Europe, which in turn helped touch off the French Revolution . The extreme weather produced by El Niño in 1876–77 gave rise to the most deadly famines of the 19th century. The 1876 famine alone in northern China killed up to 13 million people. The phenomenon had long been of interest because of its effects on the guano industry and other enterprises that depend on biological productivity of the sea. It is recorded that as early as 1822, cartographer Joseph Lartigue, of the French frigate La Clorinde under Baron Mackau , noted the "counter-current" and its usefulness for traveling southward along the Peruvian coast. Charles Todd , in 1888, suggested droughts in India and Australia tended to occur at the same time; Norman Lockyer noted the same in 1904. An El Niño connection with flooding was reported in 1894 by Victor Eguiguren (1852–1919) and in 1895 by Federico Alfonso Pezet (1859–1929). In 1924, Gilbert Walker (for whom the Walker circulation is named) coined the term "Southern Oscillation". He and others (including Norwegian-American meteorologist Jacob Bjerknes ) are generally credited with identifying the El Niño effect. The major 1982–83 El Niño led to an upsurge of interest from the scientific community. The period 1990–95 was unusual in that El Niños have rarely occurred in such rapid succession. [ unreliable source? ] An especially intense El Niño event in 1998 caused an estimated 16% of the world's reef systems to die. The event temporarily warmed air temperature by 1.5 °C, compared to the usual increase of 0.25 °C associated with El Niño events. Since then, mass coral bleaching has become common worldwide, with all regions having suffered "severe bleaching". Around 1525, when Francisco Pizarro made landfall in Peru, he noted rainfall in the deserts, the first written record of the impacts of El Niño. Evidence is also strong for El Niño events during the early Holocene epoch 10,000 years ago. Different modes of ENSO-like events have been registered in paleoclimatic archives, showing different triggering methods, feedbacks and environmental responses to the geological, atmospheric and oceanographic characteristics of the time. These paleorecords can be used to provide a qualitative basis for conservation practices. Scientists have also found chemical signatures of warmer sea surface temperatures and increased rainfall caused by El Niño in coral specimens that are around 13,000 years old. Pallcacocha Lake, Ecuador / Sediment coreENSO conditions have occurred at two- to seven-year intervals for at least the past 300 years, but most of them have been weak. El Niño may have led to the demise of the Moche and other pre-Columbian Peruvian cultures . A recent study suggests a strong El Niño effect between 1789 and 1793 caused poor crop yields in Europe, which in turn helped touch off the French Revolution . The extreme weather produced by El Niño in 1876–77 gave rise to the most deadly famines of the 19th century. The 1876 famine alone in northern China killed up to 13 million people. The phenomenon had long been of interest because of its effects on the guano industry and other enterprises that depend on biological productivity of the sea. It is recorded that as early as 1822, cartographer Joseph Lartigue, of the French frigate La Clorinde under Baron Mackau , noted the "counter-current" and its usefulness for traveling southward along the Peruvian coast. Charles Todd , in 1888, suggested droughts in India and Australia tended to occur at the same time; Norman Lockyer noted the same in 1904. An El Niño connection with flooding was reported in 1894 by Victor Eguiguren (1852–1919) and in 1895 by Federico Alfonso Pezet (1859–1929). In 1924, Gilbert Walker (for whom the Walker circulation is named) coined the term "Southern Oscillation". He and others (including Norwegian-American meteorologist Jacob Bjerknes ) are generally credited with identifying the El Niño effect. The major 1982–83 El Niño led to an upsurge of interest from the scientific community. The period 1990–95 was unusual in that El Niños have rarely occurred in such rapid succession. [ unreliable source? ] An especially intense El Niño event in 1998 caused an estimated 16% of the world's reef systems to die. The event temporarily warmed air temperature by 1.5 °C, compared to the usual increase of 0.25 °C associated with El Niño events. Since then, mass coral bleaching has become common worldwide, with all regions having suffered "severe bleaching". Around 1525, when Francisco Pizarro made landfall in Peru, he noted rainfall in the deserts, the first written record of the impacts of El Niño. Evidence is also strong for El Niño events during the early Holocene epoch 10,000 years ago. Different modes of ENSO-like events have been registered in paleoclimatic archives, showing different triggering methods, feedbacks and environmental responses to the geological, atmospheric and oceanographic characteristics of the time. These paleorecords can be used to provide a qualitative basis for conservation practices. Scientists have also found chemical signatures of warmer sea surface temperatures and increased rainfall caused by El Niño in coral specimens that are around 13,000 years old. Pallcacocha Lake, Ecuador / Sediment coreThe PMM is not the same thing as the El Niño-Southern Oscillation (ENSO), but there is evidence that PMM events can trigger ENSO events, especially Central Pacific El Niño events. The PMM state can also modulate hurricane activity in the East Pacific and typhoon activity in the West Pacific oceans and alter precipitation on the continents surrounding the Pacific Ocean. The South Pacific Ocean has a PMM-like mode known as the "South Pacific Meridional Mode" (SPMM) that also influences the ENSO cycle. The "South Pacific Meridional Mode" (SPMM) is an analogous climate mode in the south Pacific; Zhang, Clement and Di Nezio proposed its existence in 2014 and it operates in a nearly identical manner to the northern hemisphere PMM albeit according to You and Furtado (2018) with SST anomalies peaking during (austral) summer and wind anomalies during (austral) winter. According to Middlemas et al. (2019), cloud radiative feedbacks counteract the persistence of SPMM. The SPMM has been further related to a different climate mode known as the "South Pacific Quadrupole" and the "South Pacific subtropical dipole mode". The PMM is not the same thing as the El Niño-Southern Oscillation (ENSO), but there is evidence that PMM events can trigger ENSO events, especially Central Pacific El Niño events. The PMM state can also modulate hurricane activity in the East Pacific and typhoon activity in the West Pacific oceans and alter precipitation on the continents surrounding the Pacific Ocean. The South Pacific Ocean has a PMM-like mode known as the "South Pacific Meridional Mode" (SPMM) that also influences the ENSO cycle. The "South Pacific Meridional Mode" (SPMM) is an analogous climate mode in the south Pacific; Zhang, Clement and Di Nezio proposed its existence in 2014 and it operates in a nearly identical manner to the northern hemisphere PMM albeit according to You and Furtado (2018) with SST anomalies peaking during (austral) summer and wind anomalies during (austral) winter. According to Middlemas et al. (2019), cloud radiative feedbacks counteract the persistence of SPMM. The SPMM has been further related to a different climate mode known as the "South Pacific Quadrupole" and the "South Pacific subtropical dipole mode". The "South Pacific Meridional Mode" (SPMM) is an analogous climate mode in the south Pacific; Zhang, Clement and Di Nezio proposed its existence in 2014 and it operates in a nearly identical manner to the northern hemisphere PMM albeit according to You and Furtado (2018) with SST anomalies peaking during (austral) summer and wind anomalies during (austral) winter. According to Middlemas et al. (2019), cloud radiative feedbacks counteract the persistence of SPMM. The SPMM has been further related to a different climate mode known as the "South Pacific Quadrupole" and the "South Pacific subtropical dipole mode".

Wiki

Rift Valley fever

https://api.wikimedia.org/core/v1/wikipedia/en/page/List_of_infectious_sheep_and_goat_diseases/html

List of infectious sheep and goat diseases

Sheep and goats are both small ruminants with cosmopolitan distributions due to their being kept historically and in modern times as grazers both individually and in herds in return for their production of milk , wool , and meat . As such, the diseases of these animals are of great economic importance to humans.Diseases caused by viruses include:Diseases caused by bacteria include:Diseases caused by funguses includeParasites causing disease in sheep and goats include diseases caused by protozoa , helminths , tapeworms and roundworms .

Wiki

Rift Valley fever

https://api.wikimedia.org/core/v1/wikipedia/en/page/Aedes_aegypti/html

Aedes aegypti

Aedes aegypti aegypti Aedes aegypti formosus Aedes aegypti ( /ˈiːdiːz/ from Greek αηδής : "hateful" and /aɪˈdʒɛpti/ from Latin , meaning "of Egypt"), the yellow fever mosquito , is a mosquito that can spread dengue fever , chikungunya , Zika fever , Mayaro and yellow fever viruses, and other disease agents. The mosquito can be recognized by black and white markings on its legs and a marking in the form of a lyre on the upper surface of its thorax . This mosquito originated in Africa, but is now found in tropical , subtropical and temperate regions throughout the world.Aedes aegypti is a 4–7 millimetres ( 5 ⁄ 32 – 35 ⁄ 128 in) long, dark mosquito which can be recognized by white markings on its legs and a marking in the form of a lyre on the upper surface of its thorax . Females are larger than males. Microscopically females possess small palps tipped with silver or white scales, and their antennae have sparse short hairs, whereas those of males are feathery. Aedes aegypti can be confused with Aedes albopictus without a magnifying glass: the latter have a white stripe on the top of the mid thorax. Males live off fruit and only the female bites for blood, which she needs to mature her eggs. To find a host, she is attracted to chemical compounds emitted by mammals, including ammonia , carbon dioxide , lactic acid , and octenol . Scientists at The United States Department of Agriculture (USDA) Agricultural Research Service studied the specific chemical structure of octenol to better understand why this chemical attracts the mosquito to its host and found the mosquito has a preference for "right-handed" ( dextrorotatory ) octenol molecules. The preference for biting humans is dependent on expression of the odorant receptor AaegOr4 . The white eggs are laid separately into water and not together, unlike most other mosquitoes, and soon turn black. The larvae feed on bacteria, growing over a period of weeks until they reach the pupa stage. The lifespan of an adult Ae. aegypti is two to four weeks depending on conditions, but the eggs can be viable for over a year in a dry state, which allows the mosquito to re-emerge after a cold winter or dry spell. Mammalian hosts include domesticated horses , and feral and wild horses and equids more generally. As of 2009 birds were found to be the best food supply for Ae. aegypti among all taxa . Mammalian hosts include domesticated horses , and feral and wild horses and equids more generally. As of 2009 birds were found to be the best food supply for Ae. aegypti among all taxa . Aedes aegypti originated in Africa and was spread to the New World through slave trade, but is now found in tropical , subtropical and temperate regions throughout the world. Ae. aegypti ' s distribution has increased in the past two to three decades worldwide, and it is considered to be among the most widespread mosquito species. In 2016, Zika virus -capable mosquito populations have been found adapting for persistence in warm temperate climates. Such a population has been identified to exist in parts of Washington, DC , and genetic evidence suggests they survived at least the last four winters in the region. One of the study researchers noted, "...some mosquito species are finding ways to survive in normally restrictive environments by taking advantage of underground refugia". As the world's climate becomes warmer, the range of Aedes aegypti and a hardier species originating in Asia, the tiger mosquito Aedes albopictus , which can expand its range to relatively cooler climates, will inexorably spread north and south. Sadie Ryan of the University of Florida was the lead author in a 2019 study that estimated the vulnerability of naïve populations in geographic regions that currently do not harbor vectors i.e., for Zika in the Old World. Ryan's co-author, Georgetown University's Colin Carlson remarked,"Plain and simple, climate change is going to kill a lot of people." As of 2020, the Northern Territory Government Australia and the Darwin City Council have recommended tropical cities initiate rectification programs to rid their cities of potential mosquito breeding stormwater sumps. A 2019 study found that accelerating urbanization and human movement would also contribute to the spread of Aedes mosquitoes. In continental Europe, Aedes aegypti is not established but it has been found in localities close to Europe such as the Asian part of Turkey . However, a single adult female specimen was found in Marseille (Southern France) in 2018. On the basis of a genetic study and an analysis of the movements of commercial ships, the origin of the specimen could be traced as coming from Cameroon , in Central Africa. In 2007, the genome of Aedes aegypti was published, after it had been sequenced and analyzed by a consortium including scientists at The Institute for Genomic Research (now part of the J. Craig Venter Institute ), the European Bioinformatics Institute , the Broad Institute , and the University of Notre Dame . The effort in sequencing its DNA was intended to provide new avenues for research into insecticides and possible genetic modification to prevent the spread of virus. This was the second mosquito species to have its genome sequenced in full (the first was Anopheles gambiae ). The published data included the 1.38 billion base pairs containing the insect's estimated 15,419 protein -encoding genes. The sequence indicates the species diverged from Drosophila melanogaster (the common fruit fly) about 250 million years ago , and Anopheles gambiae and this species diverged about 150 million years ago . Matthews et al. , 2018 finds A. aegypti to carry a large and diverse number of transposable elements . Their analysis suggests this is common to all mosquitoes. Aedes aegypti is a vector for transmitting numerous pathogens . According to the Walter Reed Biosystematics Units as of 2022, it is associated with the following 54 viruses and 2 species of Plasmodium : Aino virus (AINOV), African horse sickness virus (AHSV), Bozo virus (BOZOV), Bussuquara virus (BSQV), Bunyamwera virus (BUNV), Catu virus (CATUV), Chikungunya virus (CHIKV), Chandipura vesiculovirus (CHPV), Cypovirus (unnamed), Cache Valley virus (CVV), Dengue virus (DENV), Eastern Equine Encephalitis virus (EEEV), Epizootic hemorrhagic disease virus (EHDV), Guaroa virus (GROV), Hart Park virus (HPV), Ilheus virus (ILHV), Irituia virus (IRIV), Israel Turkey Meningoencephalitis virus (ITV), Japanaut virus (JAPV), Joinjakaka (JOIV), Japanese encephalitis virus (JBEV), Ketapang virus (KETV), Kunjin virus (KUNV), La Crosse virus (LACV), Mayaro virus (MAYV), Marburg virus (MBGV), Marco virus (MCOV), Melao virus (MELV), Marituba virus (MTBV), Mount Elgon bat virus (MEBV), Mucambo virus (MUCV), Murray Valley Encephalitis virus (MVEV), Navarro virus (NAVV), Nepuyo virus (NEPV), Nola virus (NOLV), Ntaya virus (NTAV), Oriboca virus (ORIV), Orungo virus (ORUV), Restan virus (RESV), Rift Valley fever virus (RVFV), Semliki Forest virus (SFV), Sindbis virus (SINV), Tahyna virus (TAHV), Tsuruse virus (TSUV), Tyuleniy virus (TYUV), Venezuelan equine encephalitis virus (VEEV), Vesicular stomatitis virus (Indiana serotype), Warrego virus (WARV), West Nile virus (WNV), Wesselsbron virus (WSLV), Yaounde virus (YAOV), Yellow fever virus (YFV), Zegla virus (ZEGV), Zika virus , as well as Plasmodium gallinaceum and Plasmodium lophurae . This mosquito also mechanically transmits some veterinary diseases . In 1952 Fenner et al. , found it transmitting the myxoma virus between rabbits and in 2001 Chihota et al. , the lumpy skin disease virus between cattle . The yellow fever mosquito can contribute to the spread of reticular cell sarcoma among Syrian hamsters . The Centers for Disease Control and Prevention traveler's page on preventing dengue fever suggests using mosquito repellents that contain DEET (N, N-diethylmetatoluamide, 20% to 30%). It also suggests: Insect repellents containing DEET (particularly concentrated products) or p -menthane-3,8-diol (from lemon eucalyptus ) were effective in repelling Ae. aegypti mosquitoes, while others were less effective or ineffective in a scientific study. The Centers for Disease Control and Prevention article on "Protection against Mosquitoes, Ticks, & Other Arthropods" notes that "Studies suggest that concentrations of DEET above approximately 50% do not offer a marked increase in protection time against mosquitoes; DEET efficacy tends to plateau at a concentration of approximately 50%". Other insect repellents recommended by the CDC include Picaridin (KBR 3023/ icaridin ), IR3535 , and 2-undecanone . Pyrethroids are commonly used. This widespread use of pyrethroids and DDT has caused Knockdown resistance ( kdr ) mutations. Almost no research has been done on the fitness implications. studies by Kumar et al. , 2009 on deltamethrin in India, Plernsub et al. , 2013 on permethrin in Thailand, by Jaramillo-O et al. , 2014 on λ-cyhalothrin in Colombia, by Alvarez-Gonzalez et al. , 2017 on deltamethrin in Venezuela, are all substantially confounded . As of 2019, understanding of selective pressure under withdrawal of insecticide is hence limited. Ae. aegypti has been genetically modified to suppress its own species in an approach similar to the sterile insect technique , thereby reducing the risk of disease. The mosquitoes, known as OX513A , were developed by Oxitec , a spinout of Oxford University . Field trials in the Cayman Islands , in Juazeiro , Brazil, by Carvalho et al. , 2015, and in Panama by Neira et al. , 2014 have shown that the OX513A mosquitoes reduced the target mosquito populations by more than 90%. This mosquito suppression effect is achieved by a self-limiting gene that prevents the offspring from surviving. Male modified mosquitoes, which do not bite or spread disease, are released to mate with the pest females. Their offspring inherit the self-limiting gene and die before reaching adulthood—before they can reproduce or spread disease. The OX513A mosquitoes and their offspring also carry a fluorescent marker for simple monitoring. To produce more OX513A mosquitoes for control projects, the self-limiting gene is switched off (using the Tet-Off system ) in the mosquito production facility using an antidote (the antibiotic tetracycline ), allowing the mosquitoes to reproduce naturally. In the environment, the antidote is unavailable to rescue mosquito reproduction, so the pest population is suppressed. The mosquito control effect is nontoxic and species-specific, as the OX513A mosquitoes are Ae. aegypti and only breed with Ae. aegypti . The result of the self-limiting approach is that the released insects and their offspring die and do not persist in the environment. In Brazil, the modified mosquitoes were approved by the National Biosecurity Technical Commission for releases throughout the country. Insects were released into the wild populations of Brazil, Malaysia, and the Cayman Islands in 2012. In July 2015, the city of Piracicaba , São Paulo, started releasing the OX513A mosquitoes. In 2015, the UK House of Lords called on the government to support more work on genetically modified insects in the interest of global health. In 2016, the United States Food and Drug Administration granted preliminary approval for the use of modified mosquitoes to prevent the spread of the Zika virus. Another proposed method consists in using radiation to sterilize male larvae so that when they mate, they produce no progeny. Male mosquitoes do not bite or spread disease. Using CRISPR/Cas9 based genome editing to engineer the genome of Aedes aegypti genes like ECFP (enhanced cyan fluorescent protein), Nix (male-determining factor gene), Aaeg-wtrw (Ae. aegypti water witch locus), Kmo (kynurenine 3-monoxygenase), loqs (loquacious), r2d2 (r2d2 protein), ku70 (ku heterodimer protein gene) and lig4 (ligase4) were targeted to modify the genome of Aedes aegypti . The new mutant will become incapable of pathogen transmission or result in population control. In 2016 research into the use of a bacterium called Wolbachia as a method of biocontrol was published showing that invasion of Ae. aegypti by the endosymbiotic bacteria allows mosquitos to be resistant to certain arboviruses such as dengue fever and Zika virus strains currently circulating. In 2017 Alphabet, Inc. started the Debug Project to infect males of this species with Wolbachia bacteria, interrupting the reproductive cycle of these animals. Pyrethroids are commonly used. This widespread use of pyrethroids and DDT has caused Knockdown resistance ( kdr ) mutations. Almost no research has been done on the fitness implications. studies by Kumar et al. , 2009 on deltamethrin in India, Plernsub et al. , 2013 on permethrin in Thailand, by Jaramillo-O et al. , 2014 on λ-cyhalothrin in Colombia, by Alvarez-Gonzalez et al. , 2017 on deltamethrin in Venezuela, are all substantially confounded . As of 2019, understanding of selective pressure under withdrawal of insecticide is hence limited. Ae. aegypti has been genetically modified to suppress its own species in an approach similar to the sterile insect technique , thereby reducing the risk of disease. The mosquitoes, known as OX513A , were developed by Oxitec , a spinout of Oxford University . Field trials in the Cayman Islands , in Juazeiro , Brazil, by Carvalho et al. , 2015, and in Panama by Neira et al. , 2014 have shown that the OX513A mosquitoes reduced the target mosquito populations by more than 90%. This mosquito suppression effect is achieved by a self-limiting gene that prevents the offspring from surviving. Male modified mosquitoes, which do not bite or spread disease, are released to mate with the pest females. Their offspring inherit the self-limiting gene and die before reaching adulthood—before they can reproduce or spread disease. The OX513A mosquitoes and their offspring also carry a fluorescent marker for simple monitoring. To produce more OX513A mosquitoes for control projects, the self-limiting gene is switched off (using the Tet-Off system ) in the mosquito production facility using an antidote (the antibiotic tetracycline ), allowing the mosquitoes to reproduce naturally. In the environment, the antidote is unavailable to rescue mosquito reproduction, so the pest population is suppressed. The mosquito control effect is nontoxic and species-specific, as the OX513A mosquitoes are Ae. aegypti and only breed with Ae. aegypti . The result of the self-limiting approach is that the released insects and their offspring die and do not persist in the environment. In Brazil, the modified mosquitoes were approved by the National Biosecurity Technical Commission for releases throughout the country. Insects were released into the wild populations of Brazil, Malaysia, and the Cayman Islands in 2012. In July 2015, the city of Piracicaba , São Paulo, started releasing the OX513A mosquitoes. In 2015, the UK House of Lords called on the government to support more work on genetically modified insects in the interest of global health. In 2016, the United States Food and Drug Administration granted preliminary approval for the use of modified mosquitoes to prevent the spread of the Zika virus. Another proposed method consists in using radiation to sterilize male larvae so that when they mate, they produce no progeny. Male mosquitoes do not bite or spread disease. Using CRISPR/Cas9 based genome editing to engineer the genome of Aedes aegypti genes like ECFP (enhanced cyan fluorescent protein), Nix (male-determining factor gene), Aaeg-wtrw (Ae. aegypti water witch locus), Kmo (kynurenine 3-monoxygenase), loqs (loquacious), r2d2 (r2d2 protein), ku70 (ku heterodimer protein gene) and lig4 (ligase4) were targeted to modify the genome of Aedes aegypti . The new mutant will become incapable of pathogen transmission or result in population control. In 2016 research into the use of a bacterium called Wolbachia as a method of biocontrol was published showing that invasion of Ae. aegypti by the endosymbiotic bacteria allows mosquitos to be resistant to certain arboviruses such as dengue fever and Zika virus strains currently circulating. In 2017 Alphabet, Inc. started the Debug Project to infect males of this species with Wolbachia bacteria, interrupting the reproductive cycle of these animals. Fungal species Erynia conica (from the family Entomophthoraceae ) infects (and kills) two types of mosquitos: Aedes aegypti and Culex restuans . Studies on the fungus have been carried out on its potiential use as a biological control of the mosquitos. The species was first named (as Culex aegypti ) in 1757 by Fredric Hasselquist in his treatise Iter Palaestinum . Hasselquist was provided with the names and descriptions by his mentor, Carl Linnaeus . This work was later translated into German and published in 1762 as Reise nach Palästina . Since the latter is an uncritical reproduction of the former, they are both considered to antedate the starting point for zoological nomenclature in 1758. Nonetheless, the name Aedes aegypti was frequently used, starting with H. G. Dyar in 1920. [ citation needed ] To stabilise the nomenclature, a petition to the International Commission on Zoological Nomenclature was made by P. F. Mattingly, Alan Stone, and Kenneth L. Knight in 1962. It also transpired that, although the name Aedes aegypti was universally used for the yellow fever mosquito, Linnaeus had actually described a species now known as Aedes ( Ochlerotatus ) caspius . In 1964, the commission ruled in favour of the proposal, validating Linnaeus' name, and transferring it to the species for which it was in general use. The yellow fever mosquito belongs to the tribe Aedini of the dipteran family Culicidae and to the genus Aedes and subgenus Stegomyia . According to one recent analysis, the subgenus Stegomyia of the genus Aedes should be raised to the level of genus. The proposed name change has been ignored by most scientists; at least one scientific journal, the Journal of Medical Entomology , has officially encouraged authors dealing with aedile mosquitoes to continue to use the traditional names, unless they have particular reasons for not doing so. The generic name comes from the Ancient Greek ἀηδής , aēdēs , meaning "unpleasant" or "odious". Two subspecies are commonly recognized: This classification is complicated by the results of Gloria-Soria et al. , 2016. Although confirming the existence of these two major subspecies, Gloria-Sora et al. finds greater worldwide diversity than previously recognized and a large number of distinct populations separated by various geographic factors. Two subspecies are commonly recognized: This classification is complicated by the results of Gloria-Soria et al. , 2016. Although confirming the existence of these two major subspecies, Gloria-Sora et al. finds greater worldwide diversity than previously recognized and a large number of distinct populations separated by various geographic factors.

Wiki

Rift Valley fever

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List of infectious diseases

This is a list of infectious diseases arranged by name, along with the infectious agents that cause them, the vaccines that can prevent or cure them when they exist and their current status. Some on the list are vaccine-preventable diseases .Blood infection: Fever, chills, vomiting, confusion Urinary tract infection: bloody urine, cloudy urine Pneumonia: Fever, chills, coughing high fever that lasts 4–6 days pharyngitis (sore throat) conjunctivitis (inflamed eyes, usually without pus formation like pink eye) enlargement of the lymph nodes of the neck headache, malaise, and weakness Incubation period of 5–9 days Hemolymphatic phase: Fever, lymphadenopathy Neurological phase: Sleep disorders, neurological symptoms, psychiatric symptoms Suramin by injection is used for T. b. rhodesiense Symptoms of vaginal candidiasis are vaginal itching or soreness, pain during sexual intercourse In men, painful or burning sensation when urinating Isolation of C. diphtheriae culture Histopathologic diagnosis Toxin demonstration In vivo tests (guinea pig inoculation) In vitro test: Elek's gel precipitation test, PCR, ELISA, ICA Clinical criteria URT illness with sore throat Low-grade fever An adherent, dense, grey pseudomembrane covering the posterior aspect of the pharynx Pneumonia: fever, lung consolidation, pleural effusion, tachypnea, tachycardia, or hypotension Meningitis: fever, confusion, hypotension, headache, nuchal rigidity, or changing mental status Bacteremia: fever, murmur, evidence of an embolic event, hypotension, phlebitis, tachycardia, tachypnea, splenomegaly, or evidence of heart failure Skin and soft tissue infection, osteomyelitis, septic arthritis, or discitis: fever, cellulitis, arthritis, arthralgia, localized pain, decubitus ulcer, vascular insufficiency of the lower extremity, back pain, wound infection, or neurologic dysfunction Urinary tract infection or pelvic abscess: fever, flank pain, pelvic pain, or abdominal pain fever severe headache muscle aches ( myalgia ) chills and shaking, similar to the symptoms of influenza nausea vomiting loss of appetite unintentional weight loss abdominal pain cough Skin lesion consistent with leprosy and with definite sensory loss. Positive skin smears. Neurological infection Headache, lethargy, confusion, seizures, sudden onset of neurological deficit Cardiac conditions In recorded cases, it has caused damage to heart valves whether natural or prosthetic Lymphocutaneous disease Ocular disease Disseminated nocardiosis Fever, moderate or very high can be seen

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Rift Valley fever

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Pandemic

A pandemic ( / p æ n ˈ d ɛ m ɪ k / pan-DEM-ik ) is an epidemic of an infectious disease that has spread across a large region, for instance multiple continents or worldwide, affecting a substantial number of individuals. Widespread endemic diseases with a stable number of infected individuals such as recurrences of seasonal influenza are generally excluded as they occur simultaneously in large regions of the globe rather than being spread worldwide. Throughout human history , there have been a number of pandemics of diseases such as smallpox . The Black Death , caused by the Plague , wiped out up to half of the population of Europe in the 14th century. The term pandemic had not been used then, but was used for later epidemics, including the 1918 H1N1 influenza A pandemic—more commonly known as the Spanish flu —which is the deadliest pandemic in history . The most recent pandemics include the HIV/AIDS pandemic , [lower-alpha 1] the 2009 swine flu pandemic and the COVID-19 pandemic . Almost all these diseases still circulate among humans though their impact now is often far less. In response to the COVID-19 pandemic, 194 member states of the World Health Organization began negotiations on an International Treaty on Pandemic Prevention, Preparedness and Response , with a requirement to submit a draft of this treaty to the 77th World Health Assembly during its 2024 convention. A medical dictionary definition of pandemic is " an epidemic occurring on a scale that crosses international boundaries, usually affecting people on a worldwide scale ". A disease or condition is not a pandemic merely because it is widespread or kills many people; it must also be infectious. For instance, cancer is responsible for many deaths but is not considered a pandemic because the disease is not contagious —i.e. easily transmissible—and not even simply infectious . This definition differs from colloquial usage in that it encompasses outbreaks of relatively mild diseases. The World Health Organization (WHO) has a category of Public Health Emergency of International Concern , defined as " an extraordinary event which is determined to constitute a public health risk to other States through the international spread of disease and to potentially require a coordinated international response ". There is a rigorous process underlying this categorization and a clearly defined trajectory of responses. A WHO-sponsored international body, tasked with preparing an international agreement on pandemic prevention, preparedness and response has defined a pandemic as " the global spread of a pathogen or variant that infects human populations with limited or no immunity through sustained and high transmissibility from person to person, overwhelming health systems with severe morbidity and high mortality, and causing social and economic disruptions, all of which require effective national and global collaboration and coordination for its control ". The word comes from the Greek παν- pan- meaning "all", or "every" and δῆμος demos "people". A common early characteristic of a pandemic is a rapid, sometimes exponential , growth in the number of infections, coupled with a widening geographical spread. WHO utilises different criteria to declare a Public Health Emergency of International Concern (PHEIC), its nearest equivalent to the term pandemic. The potential consequences of an incident are considered, rather than its current status. For example, polio was declared a PHEIC in 2014 even though only 482 cases were reported globally in the previous year; this was justified by concerns that polio might break out of its endemic areas and again become a significant health threat globally. The PHEIC status of polio is reviewed regularly and is ongoing, despite the small number of cases annually. [lower-alpha 2] The end of a pandemic is more difficult to delineate. Generally, past epidemics & pandemics have faded out as the diseases become accepted into people's daily lives and routines, becoming endemic . The transition from pandemic to endemic may be defined based on: - a high proportion of the global population having immunity (through either natural infection or vaccination) fewer deaths health systems step down from emergency status perceived personal risk is lessened restrictive measures such as travel restrictions removed less coverage in public media. An endemic disease is always present in a population, but at a relatively low and predictable level. There may be periodic spikes of infections or seasonality, (e.g. influenza ) but generally the burden on health systems is manageable. A common early characteristic of a pandemic is a rapid, sometimes exponential , growth in the number of infections, coupled with a widening geographical spread. WHO utilises different criteria to declare a Public Health Emergency of International Concern (PHEIC), its nearest equivalent to the term pandemic. The potential consequences of an incident are considered, rather than its current status. For example, polio was declared a PHEIC in 2014 even though only 482 cases were reported globally in the previous year; this was justified by concerns that polio might break out of its endemic areas and again become a significant health threat globally. The PHEIC status of polio is reviewed regularly and is ongoing, despite the small number of cases annually. [lower-alpha 2] The end of a pandemic is more difficult to delineate. Generally, past epidemics & pandemics have faded out as the diseases become accepted into people's daily lives and routines, becoming endemic . The transition from pandemic to endemic may be defined based on: - a high proportion of the global population having immunity (through either natural infection or vaccination) fewer deaths health systems step down from emergency status perceived personal risk is lessened restrictive measures such as travel restrictions removed less coverage in public media. An endemic disease is always present in a population, but at a relatively low and predictable level. There may be periodic spikes of infections or seasonality, (e.g. influenza ) but generally the burden on health systems is manageable. Pandemic prevention comprises activities such as anticipatory research and development of therapies and vaccines, as well as monitoring for pathogens and disease outbreaks which may have pandemic potential. Routine vaccination programs are a type of prevention strategy, holding back diseases such as influenza and polio which have caused pandemics in the past, and could do so again if not controlled. Prevention overlaps with preparedness which aims to curtail an outbreak and prevent it getting out of control - it involves strategic planning, data collection and modelling to measure the spread, stockpiling of therapies, vaccines, and medical equipment, as well as public health awareness campaigning. By definition, a pandemic involves many countries so international cooperation, data sharing, and collaboration are essential; as is universal access to tests and therapies. Collaboration - In response to the COVID-19 pandemic, WHO established a Pandemic Hub in September 2021 in Berlin, aiming to address weaknesses around the world in how countries detect, monitor and manage public health threats. The Hub's initiatives include using artificial intelligence to analyse more than 35,000 data feeds for indications of emerging health threats, as well as improving facilities and coordination between academic institutions and WHO member countries. Detection - In May 2023, WHO launched the International Pathogen Surveillance Network (IPSN) (hosted by the Pandemic Hub) aiming to detect and respond to disease threats before they become epidemics and pandemics, and to optimize routine disease surveillance. The network provides a platform to connect countries, improving systems for collecting and analysing samples of potentially harmful pathogens . Therapies and Vaccines - The Coalition for Epidemic Preparedness Innovations (CEPI) is developing a program to condense new vaccine development timelines to 100 days, a third of the time it took to develop a COVID-19 vaccine. CEPI aims to reduce global epidemic and pandemic risk by developing vaccines against known pathogens as well as enabling rapid response to Disease X . In the US, the National Institute of Allergy and Infectious Diseases (NIAID) has developed a Pandemic Preparedness Plan which focuses on identifying viruses of concern and developing diagnostics and therapies (including prototype vaccines) to combat them. Modeling is important to inform policy decisions. It helps to predict the burden of disease on healthcare facilities, the effectiveness of control measures, projected geographical spread, and timing and extent of future pandemic waves. Public Awareness involves disseminating reliable information, ensuring consistency on message, transparency, and steps to discredit misinformation . Stockpiling involves maintaining strategic stockpiles of emergency supplies such as personal protective equipment, drugs and vaccines, and equipment such as respirators. Many of these items have limited shelf life , so they require stock rotation even though they may be rarely used. The COVID-19 pandemic highlighted a number of ethical and political issues which must be considered during a pandemic. These included decisions about who should be prioritised for treatment while resources are scarce; whether or not to make vaccination compulsory; the timing and extent of constraints on individual liberty, how to sanction individuals who do not comply with emergency regulations, and the extent of international collaboration and resource sharing. The COVID-19 pandemic highlighted a number of ethical and political issues which must be considered during a pandemic. These included decisions about who should be prioritised for treatment while resources are scarce; whether or not to make vaccination compulsory; the timing and extent of constraints on individual liberty, how to sanction individuals who do not comply with emergency regulations, and the extent of international collaboration and resource sharing. The basic strategies in the control of an outbreak are containment and mitigation . Containment may be undertaken in the early stages of the outbreak, including contact tracing and isolating infected individuals to stop the disease from spreading to the rest of the population, other public health interventions on infection control, and therapeutic countermeasures such as vaccinations which may be effective if available. When it becomes apparent that it is no longer possible to contain the spread of the disease, management will then move on to the mitigation stage, in which measures are taken to slow the spread of the disease and mitigate its effects on society and the healthcare system. In reality, containment and mitigation measures may be undertaken simultaneously. A key part of managing an infectious disease outbreak is trying to decrease the epidemic peak, known as " flattening the curve ". This helps decrease the risk of health services being overwhelmed and provides more time for a vaccine and treatment to be developed. A broad group of non-pharmaceutical interventions may be taken to manage the outbreak. In a flu pandemic, these actions may include personal preventive measures such as hand hygiene, wearing face-masks, and self-quarantine; community measures aimed at social distancing such as closing schools and canceling mass gatherings; community engagement to encourage acceptance and participation in such interventions; and environmental measures such as cleaning of surfaces. Another strategy, suppression , requires more extreme long-term non-pharmaceutical interventions to reverse the pandemic by reducing the basic reproduction number to less than 1. The suppression strategy, which includes stringent population-wide social distancing, home isolation of cases, and household quarantine, was undertaken by China during the COVID-19 pandemic where entire cities were placed under lockdown; such a strategy may carry with it considerable social and economic costs. For a novel influenza virus , WHO previously applied a six-stage classification to delineate the process by which the virus moves from the first few infections in humans through to a pandemic. Starting with phase 1 (infections identified in animals only), it moves through phases of increasing infection and spread to phase 6 (pandemic). In February 2020, a WHO spokesperson clarified that the system is no longer in use. In 2014, the United States Centers for Disease Control and Prevention (CDC) introduced a framework for characterising the progress of an influenza pandemic titled the Pandemic Intervals Framework . The six intervals of the framework are as follows: investigation of cases of novel influenza, recognition of increased potential for ongoing transmission, initiation of a pandemic wave, acceleration of a pandemic wave, deceleration of a pandemic wave, and preparation for future pandemic waves. At the same time, the CDC adopted the Pandemic Severity Assessment Framework (PSAF) to assess the severity of influenza pandemics. The PSAF rates the severity of an influenza outbreak on two dimensions: clinical severity of illness in infected persons; and the transmissibility of the infection in the population. This tool was not applied during the COVID-19 pandemic. For a novel influenza virus , WHO previously applied a six-stage classification to delineate the process by which the virus moves from the first few infections in humans through to a pandemic. Starting with phase 1 (infections identified in animals only), it moves through phases of increasing infection and spread to phase 6 (pandemic). In February 2020, a WHO spokesperson clarified that the system is no longer in use. In 2014, the United States Centers for Disease Control and Prevention (CDC) introduced a framework for characterising the progress of an influenza pandemic titled the Pandemic Intervals Framework . The six intervals of the framework are as follows: investigation of cases of novel influenza, recognition of increased potential for ongoing transmission, initiation of a pandemic wave, acceleration of a pandemic wave, deceleration of a pandemic wave, and preparation for future pandemic waves. At the same time, the CDC adopted the Pandemic Severity Assessment Framework (PSAF) to assess the severity of influenza pandemics. The PSAF rates the severity of an influenza outbreak on two dimensions: clinical severity of illness in infected persons; and the transmissibility of the infection in the population. This tool was not applied during the COVID-19 pandemic. SARS-CoV-2 , a new strain of coronavirus , was first detected in the city of Wuhan, Hubei Province , China, in December 2019. The outbreak was characterized as a Public Health Emergency of International Concern (PHEIC) between January 2020 and May 2023 by WHO. The number of people infected with COVID-19 has reached more than 767 million worldwide, with a death toll of 6.9 million. [lower-alpha 3] It is considered likely that the virus will eventually become endemic and, like the common cold, cause less severe disease for most people. HIV/AIDS was first identified as a disease in 1981, and is an ongoing worldwide public health issue. Since then, HIV/AIDS has killed an estimated 40 million people with a further 630,000 deaths annually; 39 million people are currently living with HIV infection. [lower-alpha 4] HIV has a zoonotic origin, having originated in nonhuman primates in Central Africa and transferred to humans in the early 20th century. The most frequent mode of transmission of HIV is through sexual contact with an infected person. There may be a short period of mild, nonspecific symptoms followed by an asymptomatic (but nevertheless infectious) stage called clinical latency - without treatment, this stage can last between 3 and 20 years. The only way to detect infection is by means of a HIV test. There is no vaccine to prevent HIV infection, but the disease can be held in check by means of antiretroviral therapy . Historical accounts of epidemics are often vague or contradictory in describing how victims were affected. A rash accompanied by a fever might be smallpox, measles, scarlet fever, or varicella , and it is possible that epidemics overlapped, with multiple infections striking the same population at once. It is often impossible to know the exact causes of mortality, although ancient DNA studies can sometimes detect residues of certain pathogens. It is assumed that, prior to the neolithic revolution around 10,000 BC, disease outbreaks were limited to a single family or clan, and did not spread widely before dying out. The domestication of animals increased human-animal contact, increasing the possibility of zoonotic infections. The advent of agriculture, and trade between settled groups, made it possible for pathogens to spread widely. As population increased, contact between groups became more frequent. A history of epidemics maintained by the Chinese Empire from 243 B.C. to 1911 A.C. shows an approximate correlation between the frequency of epidemics and the growth of the population. Here is an incomplete list of known epidemics which spread widely enough to merit the title "pandemic". Beginning from the Middle Ages, encounters between European settlers and native populations in the rest of the world often introduced epidemics of extraordinary virulence. Settlers introduced novel diseases which were endemic in Europe, such as smallpox , measles , pertussis .and influenza , to which the indigenous peoples had no immunity. The Europeans infected with such diseases typically carried them in a dormant state , were actively infected but asymptomatic , or had only mild symptoms. Smallpox was the most destructive disease that was brought by Europeans to the Native Americans, both in terms of morbidity and mortality. The first well-documented smallpox epidemic in the Americas began in Hispaniola in late 1518 and soon spread to Mexico. Estimates of mortality range from one-quarter to one-half of the population of central Mexico. It is estimated that over the 100 years after European arrival in 1492, the indigenous population of the Americas dropped from 60 million to only 6 million, due to a combination of disease, war, and famine. The majority these deaths are attributed to successive waves of introduced diseases such as smallpox, measles, and typhoid fever. In Australia , smallpox was introduced by European settlers in 1789 devastating the Australian Aboriginal population, killing an estimated 50% of those infected with the disease during the first decades of colonisation. In the early 1800s, measles, smallpox and intertribal warfare killed an estimated 20,000 New Zealand Māori . In 1848–49, as many as 40,000 out of 150,000 Hawaiians are estimated to have died of measles , whooping cough and influenza . Measles killed more than 40,000 Fijians , approximately one-third of the population, in 1875, and in the early 19th century devastated the Great Andamanese population. In Hokkaido , an epidemic of smallpox introduced by Japanese settlers is estimated to have killed 34% of the native Ainu population in 1845. SARS-CoV-2 , a new strain of coronavirus , was first detected in the city of Wuhan, Hubei Province , China, in December 2019. The outbreak was characterized as a Public Health Emergency of International Concern (PHEIC) between January 2020 and May 2023 by WHO. The number of people infected with COVID-19 has reached more than 767 million worldwide, with a death toll of 6.9 million. [lower-alpha 3] It is considered likely that the virus will eventually become endemic and, like the common cold, cause less severe disease for most people. HIV/AIDS was first identified as a disease in 1981, and is an ongoing worldwide public health issue. Since then, HIV/AIDS has killed an estimated 40 million people with a further 630,000 deaths annually; 39 million people are currently living with HIV infection. [lower-alpha 4] HIV has a zoonotic origin, having originated in nonhuman primates in Central Africa and transferred to humans in the early 20th century. The most frequent mode of transmission of HIV is through sexual contact with an infected person. There may be a short period of mild, nonspecific symptoms followed by an asymptomatic (but nevertheless infectious) stage called clinical latency - without treatment, this stage can last between 3 and 20 years. The only way to detect infection is by means of a HIV test. There is no vaccine to prevent HIV infection, but the disease can be held in check by means of antiretroviral therapy . SARS-CoV-2 , a new strain of coronavirus , was first detected in the city of Wuhan, Hubei Province , China, in December 2019. The outbreak was characterized as a Public Health Emergency of International Concern (PHEIC) between January 2020 and May 2023 by WHO. The number of people infected with COVID-19 has reached more than 767 million worldwide, with a death toll of 6.9 million. [lower-alpha 3] It is considered likely that the virus will eventually become endemic and, like the common cold, cause less severe disease for most people. HIV/AIDS was first identified as a disease in 1981, and is an ongoing worldwide public health issue. Since then, HIV/AIDS has killed an estimated 40 million people with a further 630,000 deaths annually; 39 million people are currently living with HIV infection. [lower-alpha 4] HIV has a zoonotic origin, having originated in nonhuman primates in Central Africa and transferred to humans in the early 20th century. The most frequent mode of transmission of HIV is through sexual contact with an infected person. There may be a short period of mild, nonspecific symptoms followed by an asymptomatic (but nevertheless infectious) stage called clinical latency - without treatment, this stage can last between 3 and 20 years. The only way to detect infection is by means of a HIV test. There is no vaccine to prevent HIV infection, but the disease can be held in check by means of antiretroviral therapy . Historical accounts of epidemics are often vague or contradictory in describing how victims were affected. A rash accompanied by a fever might be smallpox, measles, scarlet fever, or varicella , and it is possible that epidemics overlapped, with multiple infections striking the same population at once. It is often impossible to know the exact causes of mortality, although ancient DNA studies can sometimes detect residues of certain pathogens. It is assumed that, prior to the neolithic revolution around 10,000 BC, disease outbreaks were limited to a single family or clan, and did not spread widely before dying out. The domestication of animals increased human-animal contact, increasing the possibility of zoonotic infections. The advent of agriculture, and trade between settled groups, made it possible for pathogens to spread widely. As population increased, contact between groups became more frequent. A history of epidemics maintained by the Chinese Empire from 243 B.C. to 1911 A.C. shows an approximate correlation between the frequency of epidemics and the growth of the population. Here is an incomplete list of known epidemics which spread widely enough to merit the title "pandemic".Beginning from the Middle Ages, encounters between European settlers and native populations in the rest of the world often introduced epidemics of extraordinary virulence. Settlers introduced novel diseases which were endemic in Europe, such as smallpox , measles , pertussis .and influenza , to which the indigenous peoples had no immunity. The Europeans infected with such diseases typically carried them in a dormant state , were actively infected but asymptomatic , or had only mild symptoms. Smallpox was the most destructive disease that was brought by Europeans to the Native Americans, both in terms of morbidity and mortality. The first well-documented smallpox epidemic in the Americas began in Hispaniola in late 1518 and soon spread to Mexico. Estimates of mortality range from one-quarter to one-half of the population of central Mexico. It is estimated that over the 100 years after European arrival in 1492, the indigenous population of the Americas dropped from 60 million to only 6 million, due to a combination of disease, war, and famine. The majority these deaths are attributed to successive waves of introduced diseases such as smallpox, measles, and typhoid fever. In Australia , smallpox was introduced by European settlers in 1789 devastating the Australian Aboriginal population, killing an estimated 50% of those infected with the disease during the first decades of colonisation. In the early 1800s, measles, smallpox and intertribal warfare killed an estimated 20,000 New Zealand Māori . In 1848–49, as many as 40,000 out of 150,000 Hawaiians are estimated to have died of measles , whooping cough and influenza . Measles killed more than 40,000 Fijians , approximately one-third of the population, in 1875, and in the early 19th century devastated the Great Andamanese population. In Hokkaido , an epidemic of smallpox introduced by Japanese settlers is estimated to have killed 34% of the native Ainu population in 1845. Prevention of future pandemics requires steps to identify future causes of pandemics and to take preventive measures before the disease moves uncontrollably into the human population. For example, influenza is a rapidly evolving disease which has caused pandemics in the past and has potential to cause future pandemics. WHO collates the findings of 144 national influenza centres worldwide which monitor emerging flu viruses. Virus variants which are assessed as likely to represent a significant risk are identified and can then be incorporated into the next seasonal influenza vaccine program. In a press conference on 28 December 2020, Mike Ryan, head of the WHO Emergencies Program, and other officials said the current COVID-19 pandemic is "not necessarily the big one" and "the next pandemic may be more severe." They called for preparation. WHO and the UN have warned the world must tackle the cause of pandemics and not just the health and economic symptoms. There is always a possibility that a disease which has caused epidemics in the past may return in the future. It is also possible that little known diseases may become more virulent; in order to encourage research, a number of organisations which monitor global health have drawn up lists of diseases which may have pandemic potential; see table below. [lower-alpha 5] Coronavirus diseases are a family of usually mild illnesses in humans, including those such as the common cold , that have resulted in outbreaks and pandemics such as the 1889-1890 pandemic , the 2002–2004 SARS outbreak , Middle East respiratory syndrome–related coronavirus and the COVID-19 pandemic . There is widespread concern that members of the coronavirus family, particularly SARS and MERS have the potential to cause future pandemics. Many human coronaviruses have zoonotic origin, their with natural reservoir in bats or rodents, leading to concerns for future spillover events. Following the end of the COVID-19 pandemic Public Health Emergency of International Concern deceleration by WHO, WHO Director General Tedros Ghebreyesus stated he would not hesitate to re-declare COVID-19 a PHEIC should the global situation worsen in the coming months or years. Influenza was first described by the Greek physician Hippocrates in 412 BC. Since the Middle Ages, influenza pandemics have been recorded every 10 to 30 years as the virus mutates to evade immunity. Influenza is an endemic disease , with a fairly constant number of cases which vary seasonally and can, to a certain extent, be predicted. In a typical year, 5–15% of the population contracts influenza. There are 3–5 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. The 1889–1890 pandemic is estimated to have caused around a million fatalities, and the " Spanish flu " of 1918–1920 eventually infected about one-third of the world's population and caused an estimate 50 million fatalities. The Global Influenza Surveillance and Response System is a global network of laboratories that has for purpose to monitor the spread of influenza with the aim to provide WHO with influenza control information. More than two million respiratory specimens are tested by GISRS annually to monitor the spread and evolution of influenza viruses through a network of about 150 laboratories in 114 countries representing 91% of the world's population. Antibiotic-resistant microorganisms, which sometimes are referred to as " superbugs ", may contribute to the re-emergence of diseases with pandemic potential that are currently well controlled. For example, cases of tuberculosis that are resistant to traditionally effective treatments remain a cause of great concern to health professionals. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. China and India have the highest rate of MDR-TB. WHO reports that approximately 50 million people worldwide are infected with MDR-TB, with 79 percent of those cases resistant to three or more antibiotics. Extensively drug-resistant tuberculosis ( XDR-TB ) was first identified in Africa in 2006 and subsequently discovered to exist in 49 countries. During 2021 there were estimated to be around 25,000 cases XDR-TB worldwide. In the past 20 years, other common bacteria including Staphylococcus aureus , Serratia marcescens and Enterococcus , have developed resistance to a wide range of antibiotics . Antibiotic-resistant organisms have become an important cause of healthcare-associated ( nosocomial ) infections. There are two groups of infectious disease that may be affected by climate change. The first group are vector-borne diseases which are transmitted via insects such as mosquitos or ticks. Some of these diseases, such as malaria , yellow fever , and dengue fever , can have potentially severe health consequences. Climate can affect the distribution of these diseases due to the changing geographic range of their vectors, with the potential to cause serious outbreaks in areas where the disease has not previously been known. The other group comprises water-borne diseases such as cholera, dysentery, and typhoid which may increase in prevalence due to changes in rainfall patterns. The October 2020 'era of pandemics' report by the United Nations ' Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services , written by 22 experts in a variety of fields, said the anthropogenic destruction of biodiversity is paving the way to the pandemic era and could result in as many as 850,000 viruses being transmitted from animals—in particular birds and mammals —to humans. The "exponential rise" in consumption and trade of commodities such as meat , palm oil , and metals, largely facilitated by developed nations, and a growing human population , are the primary drivers of this destruction. According to Peter Daszak , the chair of the group who produced the report, "there is no great mystery about the cause of the Covid-19 pandemic or any modern pandemic. The same human activities that drive climate change and biodiversity loss also drive pandemic risk through their impacts on our environment." Proposed policy options from the report include taxing meat production and consumption, cracking down on the illegal wildlife trade, removing high-risk species from the legal wildlife trade, eliminating subsidies to businesses that are harmful to the natural world, and establishing a global surveillance network. In June 2021, a team of scientists assembled by the Harvard Medical School Center for Health and the Global Environment warned that the primary cause of pandemics so far, the anthropogenic destruction of the natural world through such activities including deforestation and hunting , is being ignored by world leaders. Permafrost covers a fifth of the northern hemisphere and is made up of soil that has been kept at temperatures below freezing for long periods. Viable samples of viruses have been recovered from thawing permafrost, after having been frozen for many years, sometimes for millennia. There is a remote possibility that a thawed pathogen could infect humans or animals. There is always a possibility that a disease which has caused epidemics in the past may return in the future. It is also possible that little known diseases may become more virulent; in order to encourage research, a number of organisations which monitor global health have drawn up lists of diseases which may have pandemic potential; see table below. [lower-alpha 5] Coronavirus diseases are a family of usually mild illnesses in humans, including those such as the common cold , that have resulted in outbreaks and pandemics such as the 1889-1890 pandemic , the 2002–2004 SARS outbreak , Middle East respiratory syndrome–related coronavirus and the COVID-19 pandemic . There is widespread concern that members of the coronavirus family, particularly SARS and MERS have the potential to cause future pandemics. Many human coronaviruses have zoonotic origin, their with natural reservoir in bats or rodents, leading to concerns for future spillover events. Following the end of the COVID-19 pandemic Public Health Emergency of International Concern deceleration by WHO, WHO Director General Tedros Ghebreyesus stated he would not hesitate to re-declare COVID-19 a PHEIC should the global situation worsen in the coming months or years. Influenza was first described by the Greek physician Hippocrates in 412 BC. Since the Middle Ages, influenza pandemics have been recorded every 10 to 30 years as the virus mutates to evade immunity. Influenza is an endemic disease , with a fairly constant number of cases which vary seasonally and can, to a certain extent, be predicted. In a typical year, 5–15% of the population contracts influenza. There are 3–5 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. The 1889–1890 pandemic is estimated to have caused around a million fatalities, and the " Spanish flu " of 1918–1920 eventually infected about one-third of the world's population and caused an estimate 50 million fatalities. The Global Influenza Surveillance and Response System is a global network of laboratories that has for purpose to monitor the spread of influenza with the aim to provide WHO with influenza control information. More than two million respiratory specimens are tested by GISRS annually to monitor the spread and evolution of influenza viruses through a network of about 150 laboratories in 114 countries representing 91% of the world's population. Coronavirus diseases are a family of usually mild illnesses in humans, including those such as the common cold , that have resulted in outbreaks and pandemics such as the 1889-1890 pandemic , the 2002–2004 SARS outbreak , Middle East respiratory syndrome–related coronavirus and the COVID-19 pandemic . There is widespread concern that members of the coronavirus family, particularly SARS and MERS have the potential to cause future pandemics. Many human coronaviruses have zoonotic origin, their with natural reservoir in bats or rodents, leading to concerns for future spillover events. Following the end of the COVID-19 pandemic Public Health Emergency of International Concern deceleration by WHO, WHO Director General Tedros Ghebreyesus stated he would not hesitate to re-declare COVID-19 a PHEIC should the global situation worsen in the coming months or years.Influenza was first described by the Greek physician Hippocrates in 412 BC. Since the Middle Ages, influenza pandemics have been recorded every 10 to 30 years as the virus mutates to evade immunity. Influenza is an endemic disease , with a fairly constant number of cases which vary seasonally and can, to a certain extent, be predicted. In a typical year, 5–15% of the population contracts influenza. There are 3–5 million severe cases annually, with up to 650,000 respiratory-related deaths globally each year. The 1889–1890 pandemic is estimated to have caused around a million fatalities, and the " Spanish flu " of 1918–1920 eventually infected about one-third of the world's population and caused an estimate 50 million fatalities. The Global Influenza Surveillance and Response System is a global network of laboratories that has for purpose to monitor the spread of influenza with the aim to provide WHO with influenza control information. More than two million respiratory specimens are tested by GISRS annually to monitor the spread and evolution of influenza viruses through a network of about 150 laboratories in 114 countries representing 91% of the world's population. Antibiotic-resistant microorganisms, which sometimes are referred to as " superbugs ", may contribute to the re-emergence of diseases with pandemic potential that are currently well controlled. For example, cases of tuberculosis that are resistant to traditionally effective treatments remain a cause of great concern to health professionals. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. China and India have the highest rate of MDR-TB. WHO reports that approximately 50 million people worldwide are infected with MDR-TB, with 79 percent of those cases resistant to three or more antibiotics. Extensively drug-resistant tuberculosis ( XDR-TB ) was first identified in Africa in 2006 and subsequently discovered to exist in 49 countries. During 2021 there were estimated to be around 25,000 cases XDR-TB worldwide. In the past 20 years, other common bacteria including Staphylococcus aureus , Serratia marcescens and Enterococcus , have developed resistance to a wide range of antibiotics . Antibiotic-resistant organisms have become an important cause of healthcare-associated ( nosocomial ) infections. There are two groups of infectious disease that may be affected by climate change. The first group are vector-borne diseases which are transmitted via insects such as mosquitos or ticks. Some of these diseases, such as malaria , yellow fever , and dengue fever , can have potentially severe health consequences. Climate can affect the distribution of these diseases due to the changing geographic range of their vectors, with the potential to cause serious outbreaks in areas where the disease has not previously been known. The other group comprises water-borne diseases such as cholera, dysentery, and typhoid which may increase in prevalence due to changes in rainfall patterns. The October 2020 'era of pandemics' report by the United Nations ' Intergovernmental Science-Policy Platform on Biodiversity and Ecosystem Services , written by 22 experts in a variety of fields, said the anthropogenic destruction of biodiversity is paving the way to the pandemic era and could result in as many as 850,000 viruses being transmitted from animals—in particular birds and mammals —to humans. The "exponential rise" in consumption and trade of commodities such as meat , palm oil , and metals, largely facilitated by developed nations, and a growing human population , are the primary drivers of this destruction. According to Peter Daszak , the chair of the group who produced the report, "there is no great mystery about the cause of the Covid-19 pandemic or any modern pandemic. The same human activities that drive climate change and biodiversity loss also drive pandemic risk through their impacts on our environment." Proposed policy options from the report include taxing meat production and consumption, cracking down on the illegal wildlife trade, removing high-risk species from the legal wildlife trade, eliminating subsidies to businesses that are harmful to the natural world, and establishing a global surveillance network. In June 2021, a team of scientists assembled by the Harvard Medical School Center for Health and the Global Environment warned that the primary cause of pandemics so far, the anthropogenic destruction of the natural world through such activities including deforestation and hunting , is being ignored by world leaders. Permafrost covers a fifth of the northern hemisphere and is made up of soil that has been kept at temperatures below freezing for long periods. Viable samples of viruses have been recovered from thawing permafrost, after having been frozen for many years, sometimes for millennia. There is a remote possibility that a thawed pathogen could infect humans or animals. In 2016, the commission on a Global Health Risk Framework for the Future estimated that pandemic disease events would cost the global economy over $6 trillion in the 21st century—over $60 billion per year. The same report recommended spending $4.5 billion annually on global prevention and response capabilities to reduce the threat posed by pandemic events, a figure that the World Bank Group raised to $13 billion in a 2019 report. It has been suggested that such costs be paid from a tax on aviation rather than from, e.g., income taxes, given the crucial role of air traffic in transforming local epidemics into pandemics (being the only factor considered in state-of-the-art models of long-range disease transmission ). The COVID-19 pandemic is expected to have a profound negative effect on the global economy , potentially for years to come, with substantial drops in GDP accompanied by increases in unemployment noted around the world. The slowdown of economic activity early in the COVID-19 pandemic had a profound effect on emissions of pollutants and greenhouse gases. Analysis of ice cores taken from the Swiss Alps have revealed a reduction in atmospheric lead pollution over a four-year period corresponding to the years 1349 to 1353 (when the Black Death was ravaging Europe), indicating a reduction in mining and economic activity generally.

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Rift Valley fever

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Lassa fever

Lassa fever , also known as Lassa hemorrhagic fever , is a type of viral hemorrhagic fever caused by the Lassa virus . Many of those infected by the virus do not develop symptoms . When symptoms occur they typically include fever , weakness, headaches, vomiting , and muscle pains . Less commonly there may be bleeding from the mouth or gastrointestinal tract . The risk of death once infected is about one percent and frequently occurs within two weeks of the onset of symptoms. Of those who survive, about a quarter have hearing loss , which improves within three months in about half of these cases. The disease is usually initially spread to people via contact with the urine or feces of an infected multimammate mouse . Spread can then occur via direct contact between people. Diagnosis based on symptoms is difficult. Confirmation is by laboratory testing to detect the virus's RNA , antibodies for the virus, or the virus itself in cell culture . Other conditions that may present similarly include Ebola , malaria , typhoid fever , and yellow fever . The Lassa virus is a member of the Arenaviridae family of viruses . There is no vaccine . Prevention requires isolating those who are infected and decreasing contact with the mice. Other efforts to control the spread of disease include having a cat to hunt vermin , and storing food in sealed containers. Treatment is directed at addressing dehydration and improving symptoms. The antiviral medication ribavirin has been recommended, but evidence to support its use is weak. Descriptions of the disease date from the 1950s. The virus was first described in 1969 from a case in the town of Lassa, in Borno State , Nigeria . Lassa fever is relatively common in West Africa including the countries of Nigeria , Liberia , Sierra Leone , Guinea , and Ghana . There are about 300,000 to 500,000 cases which result in 5,000 deaths a year. Onset of symptoms is typically 7 to 21 days after exposure. In 80% of those who are infected few or no symptoms occur. These mild symptoms may include fever, tiredness, weakness, and headache. In 20% of people more severe symptoms such as bleeding gums, breathing problems, vomiting, chest pain, or dangerously low blood pressure may occur. Long term complications may include hearing loss . In those who are pregnant , miscarriage may occur in 95% of child-bearing females . Lassa fever can be difficult to distinguish clinically from other viral hemorrhagic fevers, such as Ebola virus disease . A combination of pharyngitis , pain behind the sternum , presence of excess protein in the urine and fever can indicate Lassa fever with higher specificity. In cases in which death occurs, this typically occurs within 14 days of onset. About 1% of all Lassa virus infections result in death. Approximately 15%-20% of those who have required hospitalization for Lassa fever die. The risk of death is greater in those who are pregnant. A "Swollen baby syndrome" may occur in newborns, infants and toddlers with pitting edema , abdominal distension and bleeding. Lassa virus is a member of the Arenaviridae , a family of negative-sense, single-stranded RNA viruses . Specifically it is an old world arenavirus, which is enveloped, single-stranded, and bi-segmented RNA. Lassa virus contains both a large and a small genome section, with seven lineages identified to date: Lineages I, II, and III from Nigeria ; Lineage IV from Sierra Leone , Guinea , and Liberia ; Lineage V from Cote D'Ivoire and Mali Lineage VI from Togo ; and Lineage VII from Benin . Lassa virus commonly spreads to humans from other animals, specifically the Natal multimammate mouse or African rat, also called the Natal multimammate rat ( Mastomys natalensis ). This is probably the most common mouse in equatorial Africa, common in human households and eaten as a delicacy in some areas. The multimammate mouse can quickly produce a large number of offspring, tends to colonize human settlements, increasing the risk of rodent-human contact, and is found throughout the west, central and eastern parts of the African continent. Once the mouse has become a carrier, it will excrete the virus throughout the rest of its lifetime through feces and urine creating ample opportunity for exposure. The virus is probably transmitted by contact with the feces or urine of animals accessing grain stores in residences. No study has proven presence in breast milk, but the high level of viremia suggests it may be possible. Individuals who are at a higher risk of contracting the infection are those who live in rural areas where Mastomys are discovered, and where sanitation is not prevalent. Infection typically occurs by direct or indirect exposure to animal excrement through the respiratory or gastrointestinal tracts. Inhalation of tiny particles of infectious material (aerosol) is believed to be the most significant means of exposure. It is possible to acquire the infection through broken skin or mucous membranes that are directly exposed to infectious material. Transmission from person to person has been established, presenting a disease risk for healthcare workers. The virus is present in urine for between three and nine weeks after infection, and it can be transmitted in semen for up to three months after becoming infected. Lassa virus is a member of the Arenaviridae , a family of negative-sense, single-stranded RNA viruses . Specifically it is an old world arenavirus, which is enveloped, single-stranded, and bi-segmented RNA. Lassa virus contains both a large and a small genome section, with seven lineages identified to date: Lineages I, II, and III from Nigeria ; Lineage IV from Sierra Leone , Guinea , and Liberia ; Lineage V from Cote D'Ivoire and Mali Lineage VI from Togo ; and Lineage VII from Benin . Lassa virus commonly spreads to humans from other animals, specifically the Natal multimammate mouse or African rat, also called the Natal multimammate rat ( Mastomys natalensis ). This is probably the most common mouse in equatorial Africa, common in human households and eaten as a delicacy in some areas. The multimammate mouse can quickly produce a large number of offspring, tends to colonize human settlements, increasing the risk of rodent-human contact, and is found throughout the west, central and eastern parts of the African continent. Once the mouse has become a carrier, it will excrete the virus throughout the rest of its lifetime through feces and urine creating ample opportunity for exposure. The virus is probably transmitted by contact with the feces or urine of animals accessing grain stores in residences. No study has proven presence in breast milk, but the high level of viremia suggests it may be possible. Individuals who are at a higher risk of contracting the infection are those who live in rural areas where Mastomys are discovered, and where sanitation is not prevalent. Infection typically occurs by direct or indirect exposure to animal excrement through the respiratory or gastrointestinal tracts. Inhalation of tiny particles of infectious material (aerosol) is believed to be the most significant means of exposure. It is possible to acquire the infection through broken skin or mucous membranes that are directly exposed to infectious material. Transmission from person to person has been established, presenting a disease risk for healthcare workers. The virus is present in urine for between three and nine weeks after infection, and it can be transmitted in semen for up to three months after becoming infected. A range of laboratory investigations are performed, where possible, to diagnose the disease and assess its course and complications. The confidence of a diagnosis can be compromised if laboratory tests are not available. One comprising factor is the number of febrile illnesses present in Africa, such as malaria or typhoid fever that could potentially exhibit similar symptoms, particularly for non-specific manifestations of Lassa fever. In cases with abdominal pain , in countries where Lassa is common, Lassa fever is often misdiagnosed as appendicitis and intussusception which delays treatment with the antiviral ribavirin . In West Africa, where Lassa is most common, it is difficult to diagnose due to the absence of proper equipment to perform testing. The FDA has yet to approve a widely validated laboratory test for Lassa, but there are tests that have been able to provide definitive proof of the presence of the LASV virus. These tests include cell cultures, PCR, ELISA antigen assays, plaque neutralization assays, and immunofluorescence essays. However, immunofluorescence essays provide less definitive proof of Lassa infection. An ELISA test for antigen and Immunoglobulin M antibodies give 88% sensitivity and 90% specificity for the presence of the infection. Other laboratory findings in Lassa fever include lymphocytopenia (low white blood cell count), thrombocytopenia (low platelets), and elevated aspartate transaminase levels in the blood. Lassa fever virus can also be found in cerebrospinal fluid . Control of the Mastomys rodent population is impractical, so measures focus on keeping rodents out of homes and food supplies, encouraging effective personal hygiene, storing grain and other foodstuffs in rodent-proof containers, and disposing of garbage far from the home to help sustain clean households. Gloves, masks, laboratory coats, and goggles are advised while in contact with an infected person, to avoid contact with blood and body fluids. These issues in many countries are monitored by a department of public health . In less developed countries, these types of organizations may not have the necessary means to effectively control outbreaks. There is no vaccine for humans as of 2023. Researchers at the United States Army Medical Research Institute of Infectious Diseases facility had a promising vaccine candidate in 2002. They have developed a replication -competent vaccine against Lassa virus based on recombinant vesicular stomatitis virus vectors expressing the Lassa virus glycoprotein. After a single intramuscular injection , test primates have survived lethal challenge, while showing no clinical symptoms. There is no vaccine for humans as of 2023. Researchers at the United States Army Medical Research Institute of Infectious Diseases facility had a promising vaccine candidate in 2002. They have developed a replication -competent vaccine against Lassa virus based on recombinant vesicular stomatitis virus vectors expressing the Lassa virus glycoprotein. After a single intramuscular injection , test primates have survived lethal challenge, while showing no clinical symptoms. Treatment is directed at addressing dehydration and improving symptoms. All persons suspected of Lassa fever infection should be admitted to isolation facilities and their body fluids and excreta properly disposed of. [ citation needed ] The antiviral medication ribavirin has been recommended, but evidence to support its use is weak. Some evidence has found that it may worsen outcomes in certain cases. Fluid replacement, blood transfusions, and medication for low blood pressure may be required. Intravenous interferon therapy has also been used. When Lassa fever infects pregnant women late in their third trimester, inducing delivery is necessary for the mother to have a good chance of survival. This is because the virus has an affinity for the placenta and other highly vascular tissues. The fetus has only a one in ten chance of survival no matter what course of action is taken; hence, the focus is always on saving the life of the mother. Following delivery, women should receive the same treatment as other people with Lassa fever. [ citation needed ]The antiviral medication ribavirin has been recommended, but evidence to support its use is weak. Some evidence has found that it may worsen outcomes in certain cases. Fluid replacement, blood transfusions, and medication for low blood pressure may be required. Intravenous interferon therapy has also been used. When Lassa fever infects pregnant women late in their third trimester, inducing delivery is necessary for the mother to have a good chance of survival. This is because the virus has an affinity for the placenta and other highly vascular tissues. The fetus has only a one in ten chance of survival no matter what course of action is taken; hence, the focus is always on saving the life of the mother. Following delivery, women should receive the same treatment as other people with Lassa fever. [ citation needed ]About 15–20% of hospitalized people with Lassa fever will die from the illness. The overall case fatality rate is estimated to be 1%, but during epidemics , mortality can climb as high as 50%. The mortality rate is greater than 80% when it occurs in pregnant women during their third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of death to the mother. Some survivors experience lasting effects of the disease, and can include partial or complete deafness. Because of treatment with ribavirin , fatality rates have declined. There are about 300,000 to 500,000 cases which result in 5,000 deaths a year. One estimate places the number as high as 3 million cases per year. Estimates of Lassa fever are complicated by the lack of easy-available diagnosis, limited public health surveillance infrastructure, and high clustering of incidence near high intensity sampling. The infection affects females 1.2 times more than males. The age group predominantly infected is 21–30 years. Lassa high risk areas are near the western and eastern extremes of West Africa. As of 2018, the Lassa belt includes Guinea, Nigeria, Sierra Leone and Liberia. As of 2003, 10-16% of people in Sierra Leone and Liberia admitted to hospital had the virus. The case fatality rate for those who are hospitalized for the disease is about 15-20%. Research showed a twofold increase risk of infection for those living in close proximity to someone with infection symptoms within the last year. [ citation needed ] The high risk areas cannot be well defined by any known biogeographical or environmental breaks except for the multimammate rat, particularly Guinea ( Kindia , Faranah and Nzérékoré regions), Liberia (mostly in Lofa , Bong , and Nimba counties), Nigeria (in about 10 of 36 states) and Sierra Leone (typically from Kenema and Kailahun districts). It is less common in the Central African Republic, Mali, Senegal and other nearby countries, and less common yet in Ghana and the Democratic Republic of the Congo. Benin had its first confirmed cases in 2014, and Togo had its first confirmed cases in 2016. As of 2013, the spread of Lassa outside of West Africa had been very limited. Twenty to thirty cases had been described in Europe, as being caused by importation through infected individuals. These cases found outside of West Africa were found to have a high fatality risk because of the delay of diagnosis and treatment due to being unaware of the risk associated with the symptoms. Imported cases have not manifested in larger epidemics outside of Africa due to a lack of human to human transmission in hospital settings. An exception had occurred in 2003 when a healthcare worker became infected before the person showed clear symptoms. An outbreak of Lassa fever occurred in Nigeria during 2018 and spread to 18 of the country's states; it was the largest outbreak of Lassa recorded. On 25 February 2018, there were 1081 suspected cases and 90 reported deaths; 317 of the cases and 72 deaths were confirmed as Lassa which increased to a total of 431 reported cases in 2018. The total cases in Nigeria in 2019 was 810 with 167 deaths, the largest case fatality rate (23.3%) until then. The epidemic started from the second week of the January. By the tenth week the total number of cases has risen to 855 and deaths to 144, the case fatality rate of 16.8%. On the 8th of December 2021, the Nigeria Centre for Disease Control (NCDC) was notified of the death of two persons from Lassa fever. The epidemic took a new form, from 3 to 30 January 2022, 211 laboratory confirmed Lassa fever cases including 40 deaths (case fatality ratio: 19%) have been cumulatively reported in 14 of the 36 Nigerian states and the Federal Capital Territory across the country. In total from January until March, 132 deaths have been reported with a case fatality rate (CFR) of 19.1% which is lower than the CFR for the same period in 2021 (21.0%). Lassa high risk areas are near the western and eastern extremes of West Africa. As of 2018, the Lassa belt includes Guinea, Nigeria, Sierra Leone and Liberia. As of 2003, 10-16% of people in Sierra Leone and Liberia admitted to hospital had the virus. The case fatality rate for those who are hospitalized for the disease is about 15-20%. Research showed a twofold increase risk of infection for those living in close proximity to someone with infection symptoms within the last year. [ citation needed ] The high risk areas cannot be well defined by any known biogeographical or environmental breaks except for the multimammate rat, particularly Guinea ( Kindia , Faranah and Nzérékoré regions), Liberia (mostly in Lofa , Bong , and Nimba counties), Nigeria (in about 10 of 36 states) and Sierra Leone (typically from Kenema and Kailahun districts). It is less common in the Central African Republic, Mali, Senegal and other nearby countries, and less common yet in Ghana and the Democratic Republic of the Congo. Benin had its first confirmed cases in 2014, and Togo had its first confirmed cases in 2016. As of 2013, the spread of Lassa outside of West Africa had been very limited. Twenty to thirty cases had been described in Europe, as being caused by importation through infected individuals. These cases found outside of West Africa were found to have a high fatality risk because of the delay of diagnosis and treatment due to being unaware of the risk associated with the symptoms. Imported cases have not manifested in larger epidemics outside of Africa due to a lack of human to human transmission in hospital settings. An exception had occurred in 2003 when a healthcare worker became infected before the person showed clear symptoms. An outbreak of Lassa fever occurred in Nigeria during 2018 and spread to 18 of the country's states; it was the largest outbreak of Lassa recorded. On 25 February 2018, there were 1081 suspected cases and 90 reported deaths; 317 of the cases and 72 deaths were confirmed as Lassa which increased to a total of 431 reported cases in 2018. The total cases in Nigeria in 2019 was 810 with 167 deaths, the largest case fatality rate (23.3%) until then. The epidemic started from the second week of the January. By the tenth week the total number of cases has risen to 855 and deaths to 144, the case fatality rate of 16.8%. On the 8th of December 2021, the Nigeria Centre for Disease Control (NCDC) was notified of the death of two persons from Lassa fever. The epidemic took a new form, from 3 to 30 January 2022, 211 laboratory confirmed Lassa fever cases including 40 deaths (case fatality ratio: 19%) have been cumulatively reported in 14 of the 36 Nigerian states and the Federal Capital Territory across the country. In total from January until March, 132 deaths have been reported with a case fatality rate (CFR) of 19.1% which is lower than the CFR for the same period in 2021 (21.0%). An outbreak of Lassa fever occurred in Nigeria during 2018 and spread to 18 of the country's states; it was the largest outbreak of Lassa recorded. On 25 February 2018, there were 1081 suspected cases and 90 reported deaths; 317 of the cases and 72 deaths were confirmed as Lassa which increased to a total of 431 reported cases in 2018. The total cases in Nigeria in 2019 was 810 with 167 deaths, the largest case fatality rate (23.3%) until then. The epidemic started from the second week of the January. By the tenth week the total number of cases has risen to 855 and deaths to 144, the case fatality rate of 16.8%. On the 8th of December 2021, the Nigeria Centre for Disease Control (NCDC) was notified of the death of two persons from Lassa fever. The epidemic took a new form, from 3 to 30 January 2022, 211 laboratory confirmed Lassa fever cases including 40 deaths (case fatality ratio: 19%) have been cumulatively reported in 14 of the 36 Nigerian states and the Federal Capital Territory across the country. In total from January until March, 132 deaths have been reported with a case fatality rate (CFR) of 19.1% which is lower than the CFR for the same period in 2021 (21.0%). Lassa fever is endemic in Liberia. From 1 January 2017 through 23 January 2018, 91 suspected cases were reported from six counties: Bong, Grand Bassa, Grand Kru, Lofa, Margibi, and Nimba. Thirty-three of these cases were laboratory confirmed, including 15 deaths (case fatality rate for confirmed cases = 45.4%). In February 2020, a total of 24 confirmed cases with nine associated deaths has been reported from nine health districts in six counties. Grand Bossa and Bong counties account for 20 of the confirmed cases. The disease was identified in Nigeria in 1969. It is named after the town of Lassa, where it was discovered. A prominent expert in the disease, Aniru Conteh , died from the disease. The Lassa virus is one of several viruses identified by WHO as a likely cause of a future epidemic. They therefore list it for urgent research and development to develop new diagnostic tests, vaccines, and medicines. In 2007, SIGA Technologies , studied a medication in guinea pig with Lassa fever. Work on a vaccine is continuing, with multiple approaches showing positive results in animal trials.

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Rift Valley fever

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Flaviviridae

Flaviviridae is a family of enveloped positive-strand RNA viruses which mainly infect mammals and birds . They are primarily spread through arthropod vectors (mainly ticks and mosquitoes ). The family gets its name from the yellow fever virus; flavus is Latin for "yellow", and yellow fever in turn was named because of its propensity to cause jaundice in victims. There are 89 species in the family divided among four genera. Diseases associated with the group include: hepatitis ( hepaciviruses ), hemorrhagic syndromes , fatal mucosal disease ( pestiviruses ), hemorrhagic fever , encephalitis , and the birth defect microcephaly ( flaviviruses ). Virus particles are enveloped and spherical with icosahedral-like geometries that have pseudo T=3 symmetry. They are about 40–60 nm in diameter. Members of the family Flaviviridae have monopartite, linear, single-stranded RNA genomes of positive polarity, and 9.6 to 12.3 kilobase in total length. The 5'-termini of flaviviruses carry a methylated nucleotide cap, while other members of this family are uncapped and encode an internal ribosome entry site. The genome encodes a single polyprotein with multiple transmembrane domains that is cleaved, by both host and viral proteases, into structural and non-structural proteins. Among the non-structural protein products (NS), the locations and sequences of NS3 and NS5, which contain motifs essential for polyprotein processing and RNA replication respectively, are relatively well conserved across the family and may be useful for phylogenetic analysis.Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the viral envelope protein E to host receptors, which mediates clathrin -mediated endocytosis. Replication follows the positive-stranded RNA virus replication model. Positive-stranded RNA virus transcription is the method of transcription. Translation takes place by viral initiation. The virus exits the host cell by budding. Humans and mammals serve as the natural hosts. The virus is transmitted via vectors (ticks and mosquitoes). The family has four genera: Other Orthoflaviviruses are known that have yet to be classified. These include Wenling shark virus. Jingmenvirus is a group of unclassified viruses in the family which includes Alongshan virus , Guaico Culex virus, Jingmen tick virus and Mogiana tick virus. These viruses have a segmented genome of 4 or 5 pieces. Two of these segments are derived from flaviviruses. A number of viruses may be related to the flaviviruses, but have features that are atypical of the flaviviruses. These include citrus Jingmen-like virus, soybean cyst nematode virus 5, Toxocara canis larva agent, Wuhan cricket virus, and possibly Gentian Kobu-sho-associated virus.Major diseases caused by members of the family Flaviviridae include:

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Rift Valley fever

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West Nile virus

West Nile virus ( WNV ) is a single-stranded RNA virus that causes West Nile fever . It is a member of the family Flaviviridae , from the genus Flavivirus , which also contains the Zika virus , dengue virus , and yellow fever virus. The virus is primarily transmitted by mosquitoes , mostly species of Culex . The primary hosts of WNV are birds, so that the virus remains within a "bird–mosquito–bird" transmission cycle. The virus is genetically related to the Japanese encephalitis family of viruses. Humans and horses both exhibit disease symptoms from the virus, and symptoms rarely occur in other animals.Contrary to popular belief, West Nile virus was not named after the Nile River , rather, the West Nile district of Uganda where the virus was first isolated in 1937. After its original discovery in this region, it was found in many other parts of the world. Most likely, it spread from the original West Nile district.Like most other flaviviruses, WNV is an enveloped virus with icosahedral symmetry . Electron microscope studies reveal a 45–50 nm virion covered with a relatively smooth protein shell; this structure is similar to the dengue fever virus, another Flavivirus . The protein shell is made of two structural proteins: the glycoprotein E and the small membrane protein M. Protein E has numerous functions including receptor binding, viral attachment, and entry into the cell through membrane fusion . The outer protein shell is covered by a host-derived lipid membrane , the viral envelope . The flavivirus lipid membrane has been found to contain cholesterol and phosphatidylserine , but other elements of the membrane have yet to be identified. The lipid membrane has many roles in viral infection , including acting as signaling molecules and enhancing entry into the cell. Cholesterol, in particular, plays an integral part in WNV entering a host cell. The two viral envelope proteins, E and M, are inserted into the membrane. The RNA genome is bound to capsid (C) proteins, which are 105 amino-acid residues long, to form the nucleocapsid . The capsid proteins are one of the first proteins created in an infected cell; the capsid protein is a structural protein whose main purpose is to package RNA into the developing viruses. The capsid has been found to prevent apoptosis by affecting the Akt pathway. WNV is a positive-sense, single-stranded RNA virus . Its genome is approximately 11,000 nucleotides long and is flanked by 5′ and 3′ non-coding stem loop structures. The coding region of the genome codes for three structural proteins and seven nonstructural (NS) proteins , proteins that are not incorporated into the structure of new viruses. The WNV genome is first translated into a polyprotein and later cleaved by virus and host proteases into separate proteins (i.e. NS1, C, E). Structural proteins (C, prM/M, E) are capsid, precursor membrane proteins, and envelope proteins, respectively. The structural proteins are located at the 5′ end of the genome and are cleaved into mature proteins by both host and viral proteases. [ citation needed ] Nonstructural proteins consist of NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5. These proteins mainly assist with viral replication or act as proteases. The nonstructural proteins are located near the 3′ end of the genome.WNV is a positive-sense, single-stranded RNA virus . Its genome is approximately 11,000 nucleotides long and is flanked by 5′ and 3′ non-coding stem loop structures. The coding region of the genome codes for three structural proteins and seven nonstructural (NS) proteins , proteins that are not incorporated into the structure of new viruses. The WNV genome is first translated into a polyprotein and later cleaved by virus and host proteases into separate proteins (i.e. NS1, C, E). Structural proteins (C, prM/M, E) are capsid, precursor membrane proteins, and envelope proteins, respectively. The structural proteins are located at the 5′ end of the genome and are cleaved into mature proteins by both host and viral proteases. [ citation needed ]Nonstructural proteins consist of NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5. These proteins mainly assist with viral replication or act as proteases. The nonstructural proteins are located near the 3′ end of the genome.Once WNV has successfully entered the bloodstream of a host animal, the envelope protein, E, binds to attachment factors called glycosaminoglycans on the host cell. These attachment factors aid entry into the cell, however, binding to primary receptors is also necessary. Primary receptors include DC-SIGN , DC-SIGN-R, and the integrin α v β 3 . By binding to these primary receptors, WNV enters the cell through clathrin-mediated endocytosis . As a result of endocytosis, WNV enters the cell within an endosome . [ citation needed ] The acidity of the endosome catalyzes the fusion of the endosomal and viral membranes, allowing the genome to be released into the cytoplasm. Translation of the positive-sense single-stranded RNA occurs at the endoplasmic reticulum ; the RNA is translated into a polyprotein which is then cleaved by both host and viral proteases NS2B-NS3 to produce mature proteins. In order to replicate its genome, NS5, a RNA polymerase , forms a replication complex with other nonstructural proteins to produce an intermediary negative-sense single-stranded RNA ; the negative-sense strand serves as a template for synthesis of the final positive-sense RNA. Once the positive-sense RNA has been synthesized, the capsid protein, C, encloses the RNA strands into immature virions. The rest of the virus is assembled along the endoplasmic reticulum and through the Golgi apparatus , and results in non-infectious immature virions. The E protein is then glycosylated and prM is cleaved by furin , a host cell protease, into the M protein, thereby producing an infectious mature virion. The mature viruses are then secreted out of the cell. [ citation needed ]WNV is one of the Japanese encephalitis antigenic serocomplex of viruses, together with Japanese encephalitis virus, Murray Valley encephalitis virus , Saint Louis encephalitis virus and some other flaviviruses. Studies of phylogenetic lineages have determined that WNV emerged as a distinct virus around 1000 years ago. This initial virus developed into two distinct lineages. Lineage 1 and its multiple profiles is the source of the epidemic transmission in Africa and throughout the world. Lineage 2 was considered an African zoonosis . However, in 2008, lineage 2, previously only seen in horses in sub-Saharan Africa and Madagascar, began to appear in horses in Europe, where the first known outbreak affected 18 animals in Hungary. Lineage 1 West Nile virus was detected in South Africa in 2010 in a mare and her aborted fetus ; previously, only lineage 2 West Nile virus had been detected in horses and humans in South Africa. Kunjin virus is a subtype of West Nile virus endemic to Oceania . A 2007 fatal case in a killer whale in Texas broadened the known host range of West Nile virus to include cetaceans . Since the first North American cases in 1999, the virus has been reported throughout the United States, Canada, Mexico, the Caribbean, and Central America. There have been human cases and equine cases, and many birds are infected. The Barbary macaque , Macaca sylvanus , was the first nonhuman primate to contract WNV. Both the American and Israeli strains are marked by high mortality rates in infected avian populations; the presence of dead birds—especially Corvidae —can be an early indicator of the arrival of the virus. [ citation needed ]The natural hosts for WNV are birds and mosquitoes. Over 300 different species of bird have been shown to be infected with the virus. Some birds, including the American crow ( Corvus brachyrhynchos ), blue jay ( Cyanocitta cristata ) and greater sage-grouse ( Centrocercus urophasianus ), are killed by the infection, but others survive. The American robin ( Turdus migratorius ) and house sparrow ( Passer domesticus ) are thought to be among the most important reservoir species in N. American and European cities. Brown thrashers ( Toxostoma rufum ), gray catbirds ( Dumetella carolinensis ), northern cardinals ( Cardinalis cardinalis ), northern mockingbirds ( Mimus polyglottos ), wood thrushes ( Hylocichla mustelina ) and the dove family are among the other common N. American birds in which high levels of antibodies against WNV have been found. WNV has been demonstrated in a large number of mosquito species, but the most significant for viral transmission are Culex species that feed on birds, including Culex pipiens , C. restuans , C. salinarius , C. quinquefasciatus , C. nigripalpus , C. erraticus and C. tarsalis . Experimental infection has also been demonstrated with soft tick vectors, but is unlikely to be important in natural transmission. WNV has a broad host range, and is also known to be able to infect at least 30 mammalian species, including humans, some non-human primates, horses, dogs and cats. Some infected humans and horses experience disease but dogs and cats rarely show symptoms. Reptiles and amphibians can also be infected, including some species of crocodiles, alligators, snakes, lizards and frogs. Mammals are considered incidental or dead-end hosts for the virus: they do not usually develop a high enough level of virus in the blood ( viremia ) to infect another mosquito feeding on them and carry on the transmission cycle; some birds are also dead-end hosts. In the normal rural or enzootic transmission cycle, the virus alternates between the bird reservoir and the mosquito vector. It can also be transmitted between birds via direct contact, by eating an infected bird carcass or by drinking infected water. Vertical transmission between female and offspring is possible in mosquitoes, and might potentially be important in overwintering. In the urban or spillover cycle, infected mosquitoes that have fed on infected birds transmit the virus to humans. This requires mosquito species that bite both birds and humans, which are termed bridge vectors. The virus can also rarely be spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding. Unlike in birds, it does not otherwise spread directly between people. West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes . In about 80% of infections people have few or no symptoms . About 20% of people develop a fever , headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent. West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease . Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, but it otherwise does not spread directly between people. Risks for severe disease include being over 60 years old and having other health problems. Diagnosis is typically based on symptoms and blood tests. There is no human vaccine . The best way to reduce the risk of infection is to avoid mosquito bites. Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. When mosquitoes cannot be avoided, mosquito repellent , window screens , and mosquito nets reduce the likelihood of being bitten. There is no specific treatment for the disease; pain medications may reduce symptoms. Severe disease may also occur in horses. Several vaccines for these animals are now available. Before the availability of veterinary vaccines, around 40% of horses infected in North America died. West Nile fever is an infection by the West Nile virus, which is typically spread by mosquitoes . In about 80% of infections people have few or no symptoms . About 20% of people develop a fever , headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent. West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease . Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, but it otherwise does not spread directly between people. Risks for severe disease include being over 60 years old and having other health problems. Diagnosis is typically based on symptoms and blood tests. There is no human vaccine . The best way to reduce the risk of infection is to avoid mosquito bites. Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. When mosquitoes cannot be avoided, mosquito repellent , window screens , and mosquito nets reduce the likelihood of being bitten. There is no specific treatment for the disease; pain medications may reduce symptoms. Severe disease may also occur in horses. Several vaccines for these animals are now available. Before the availability of veterinary vaccines, around 40% of horses infected in North America died. According to the Center for Disease Control , infection with West Nile Virus is seasonal in temperate zones. Climates that are temperate, such as those in the United States and Europe, see peak season from July to October. Peak season changes depending on geographic region and warmer and humid climates can see longer peak seasons. All ages are equally likely to be infected but there is a higher amount of death and neuroinvasive West Nile Virus in people 60–89 years old. People of older age are more likely to have adverse effects. [ citation needed ] There are several modes of transmission, but the most common cause of infection in humans is by being bitten by an infected mosquito. Other modes of transmission include blood transfusion, organ transplantation, breast-feeding, transplacental transmission, and laboratory acquisition. These alternative modes of transmission are extremely rare. Prevention efforts against WNV mainly focus on preventing human contact with and being bitten by infected mosquitoes. This is twofold, first by personal protective actions and second by mosquito-control actions. When a person is in an area that has WNV, it is important to avoid outdoor activity, and if they go outside they should use a mosquito repellent with DEET. A person can also wear clothing that covers more skin, such as long sleeves and pants. Mosquito control can be done at the community level and include surveillance programs and control programs including pesticides and reducing mosquito habitats. This includes draining standing water. Surveillance systems in birds is particularly useful. If dead birds are found in a neighborhood, the event should be reported to local authorities. This may help health departments do surveillance and determine if the birds are infected with West Nile Virus. Despite the commercial availability of four veterinary vaccines for horses, no human vaccine has progressed beyond phase II clinical trials . Efforts have been made to produce a vaccine for human use and several candidates have been produced but none are licensed to use. The best method to reduce the risk of infections is avoiding mosquito bites. This may be done by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. Mosquito repellent , window screens , mosquito nets , and avoiding areas where mosquitoes occur may also be useful. Like other tropical diseases which are expected to have increased spread due to climate change, there is concern that changing weather conditions will increase West Nile Virus spread. Climate change will affect disease rates, ranges, and seasonality and affects the distribution of West Nile Virus. Projected changes in flood frequency and severity can bring new challenges in flood risk management , allowing for increased mosquito populations in urban areas. Weather conditions affected by climate change including temperature, precipitation and wind may affect the survival and reproduction rates of mosquitoes, suitable habitats, distribution, and abundance. Ambient temperatures drive mosquito replication rates and transmission of WNV by affecting the peak season of mosquitoes and geographic variations. For example, increased temperatures can affect the rate of virus replication, speed up the virus evolution rate, and viral transmission efficiency. Furthermore, higher winter temperatures and warmer spring may lead to larger summer mosquito populations, increasing the risk for WNV. Similarly, rainfall may also drive mosquito replication rates and affect the seasonality and geographic variations of the virus. Studies show an association between heavy precipitation and higher incidence of reported WNV. Likewise, wind is another environmental factor that serves as a dispersal mechanism for mosquitoes. Mosquitoes have extremely wide environmental tolerances and a nearly ubiquitous geographical distribution, being present on all major land masses except Antarctica and Iceland. Nevertheless, changes in climate and land use on ecological timescales can variously expand or fragment their distribution patterns, raising consequent concerns for human health.

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Rift Valley fever

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Oropouche orthobunyavirus

Oropouche orthobunyavirus ( OROV ) is one of the most common orthobunyaviruses . When OROV infects humans, it causes a rapid fever illness called Oropouche fever . OROV was originally reported in Trinidad and Tobago in 1955 from the blood sample of a fever patient and from a pool of Coquillettidia venezuelensis mosquitoes. In 1960, OROV was isolated from a sloth ( Bradypus tridactylus ) and a pool of Ochlerotatus serratus mosquitoes in Brazil. The virus is considered a public health threat in tropical and subtropical areas of Central and South America, with over half a million infected people as of 2005. OROV is considered to be an arbovirus due to the method of transmission by the mosquitoes Aedes serratus and Culex quinquefasciatus among sloths, marsupials, primates, and birds. Between 1961 and 1980, OROV was reported in the northern state of Pará, Brazil, and from 1980 to 2004, OROV had spread to the Amazonas, Amapá, Acre, Rondônia, Tocantins, and Maranhão. The virus causes Oropouche fever, an urban arboviral disease that has since resulted in >30 epidemics during 1960–2009. Currently, based on the small segment (SRNA) genetic information, there are 4 major genotypes (I–IV) of OROV. Genotype I was isolated from strains in Acre, Amazonas, Maranhão, Tocantins, Pará, Trinidad, and Tobago. Genotype II was obtained during the spread in Amapá, Pará, Rondônia, and Peru. Genotype III was isolated from samples in Acre, Minas Gerais, Panama, and Rondônia. The final genotype IV was isolated from Amazonas. A possible dispersal could be predicted for the four genotypes based on time-scaled analysis and epidemiologic data association. Genotype I possibly dispersed towards western Pará, Trinidad, and Tobago. After, genotype I progressed towards Amazonas, Acre, Maranhao, and Tocantins. Genotype II possibly emerged in Amapá, Pará, Rondônia, and Peru at the same time. Genotype III emerged in Rondônia, moved towards Panama, Acre, and Maranhão. From Maranhão, the genotype progressed towards Minas Gerais. Finally, genotype IV emerged from the city of Manaus and Amazonas. OROV has been used extensively in testing with HeLa cells to study the mechanisms of apoptosis induced by the virus. It was found that OROV causes apoptosis by DNA fragmentation. In UV-inactivated OROV, virus-receptor binding was not enough and that viral uncoating and replication were needed to induce apoptosis.

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Rift Valley fever

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West Nile fever

West Nile fever is an infection by the West Nile virus , which is typically spread by mosquitoes . In about 80% of infections people have few or no symptoms . About 20% of people develop a fever , headache, vomiting, or a rash. In less than 1% of people, encephalitis or meningitis occurs, with associated neck stiffness, confusion, or seizures. Recovery may take weeks to months. The risk of death among those in whom the nervous system is affected is about 10 percent. West Nile virus (WNV) is usually spread by mosquitoes that become infected when they feed on infected birds, which often carry the disease . Rarely the virus is spread through blood transfusions, organ transplants, or from mother to baby during pregnancy, delivery, or breastfeeding, but it otherwise does not spread directly between people. Risks for severe disease include being over 60 years old and having other health problems. Diagnosis is typically based on symptoms and blood tests. There is no human vaccine . The best way to reduce the risk of infection is to avoid mosquito bites. Mosquito populations may be reduced by eliminating standing pools of water, such as in old tires, buckets, gutters, and swimming pools. When mosquitoes cannot be avoided, mosquito repellent , window screens , and mosquito nets reduce the likelihood of being bitten. There is no specific treatment for the disease; pain medications may reduce symptoms. The virus was discovered in Uganda in 1937, and was first detected in North America in 1999. WNV has occurred in Europe, Africa, Asia, Australia, and North America. In the United States thousands of cases are reported a year, with most occurring in August and September. It can occur in outbreaks of disease. Severe disease may also occur in horses, for which a vaccine is available. A surveillance system in birds is useful for early detection of a potential human outbreak. About 80% of those infected with West Nile virus (WNV) show no symptoms and go unreported. About 20% of infected people develop symptoms. These vary in severity, and begin 3 to 14 days after being bitten. Most people with mild symptoms of WNV recover completely, though fatigue and weakness may last for weeks or months. Symptoms may range from mild, such as fever , to severe, such as paralysis and meningitis . A severe infection can last weeks and can, rarely, cause permanent brain damage . Death may ensue if the central nervous system is affected. Medical conditions such as cancer and diabetes , and age over 60 years, increase the risk of developing severe symptoms. Headache can be a prominent symptom of WNV fever, meningitis, encephalitis, meningoencephalitis, and it may or may not be present in poliomyelitis-like syndrome. Thus, headache is not a useful indicator of neuroinvasive disease.WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae . The genetic material of WNV is a positive-sense , single strand of RNA , which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12- kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral membrane proteins. West Nile virus has been seen to replicate faster and spread more easily to birds at higher temperatures; one of several ways climate change could affect the epidemiology of this disease. The prime method of spread of the West Nile virus (WNV) is the female mosquito. In Europe, cats were identified as being hosts for West Nile virus . The important mosquito vectors vary according to area; in the United States, Culex pipiens (Eastern United States, and urban and residential areas of the United States north of 36–39°N), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main vector species. The mosquito species that are most frequently infected with WNV feed primarily on birds. Different species of mosquitos take a blood meal from different types of vertebrate hosts , Mosquitoes show further selectivity, exhibiting preference for different species of birds. In the United States, WNV mosquito vectors feed preferentially on members of the Corvidae and thrush family . Among the preferred species within these families are the American crow , a corvid, and the American robin ( Turdus migratorius ). Some species of birds develop sufficient viral levels (>~10 4.2 log PFU/ml; ) after being infected to transmit the infection to biting mosquitoes that in turn go on to infect other birds. In birds that die from WNV, death usually occurs after 4 to 6 days. In mammals and several species of birds, the virus does not multiply as readily and so does not develop high viremia during infection. Mosquitoes biting such hosts are not believed to ingest sufficient virus to become infected, making them so-called dead-end hosts . As a result of the differential infectiousness of hosts, the feeding patterns of mosquitoes play an important role in WNV transmission, and they are partly genetically controlled, even within a species. Direct human-to-human transmission initially was believed to be caused only by occupational exposure, such as in a laboratory setting, or conjunctival exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion, organ transplant, intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UK's National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada, or the northeastern provinces of Italy, and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating. There also have been reports of possible transmission of the virus from mother to child during pregnancy or breastfeeding or exposure to the virus in a lab, but these are rare cases and not conclusively confirmed. Recently, the potential for mosquito saliva to affect the course of WNV disease was demonstrated. Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation , platelet aggregation , inflammation , and immunity . It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease. Vertical transmission , the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature. Mosquito progeny infected vertically in autumn may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall. Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension , and diabetes mellitus . A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5 made up 4.0 to 4.5% of a sample of people with West Nile disease, while the incidence of the gene in the general population is only 1.0%. The most at risk occupations in the U.S. are outdoor workers, for example farmers, loggers, landscapers/groundskeepers, construction workers, painters, summer camp workers and pavers. Two reports of accidental exposure by laboratory personnel working with infected fluids or tissues have been received. While this appears to be a rare occurrence, it highlights the need for proper handling of infected materials. The World Health Organization states that there are no known cases of health care workers acquiring the virus from infected patients when the appropriate infection control precautions are observed. WNV is one of the Japanese encephalitis antigenic serocomplex of viruses. Image reconstructions and cryoelectron microscopy reveal a 45–50 nm virion covered with a relatively smooth protein surface. This structure is similar to the dengue fever virus; both belong to the genus Flavivirus within the family Flaviviridae . The genetic material of WNV is a positive-sense , single strand of RNA , which is between 11,000 and 12,000 nucleotides long; these genes encode seven nonstructural proteins and three structural proteins. The RNA strand is held within a nucleocapsid formed from 12- kDa protein blocks; the capsid is contained within a host-derived membrane altered by two viral membrane proteins. West Nile virus has been seen to replicate faster and spread more easily to birds at higher temperatures; one of several ways climate change could affect the epidemiology of this disease. The prime method of spread of the West Nile virus (WNV) is the female mosquito. In Europe, cats were identified as being hosts for West Nile virus . The important mosquito vectors vary according to area; in the United States, Culex pipiens (Eastern United States, and urban and residential areas of the United States north of 36–39°N), Culex tarsalis (Midwest and West), and Culex quinquefasciatus (Southeast) are the main vector species. The mosquito species that are most frequently infected with WNV feed primarily on birds. Different species of mosquitos take a blood meal from different types of vertebrate hosts , Mosquitoes show further selectivity, exhibiting preference for different species of birds. In the United States, WNV mosquito vectors feed preferentially on members of the Corvidae and thrush family . Among the preferred species within these families are the American crow , a corvid, and the American robin ( Turdus migratorius ). Some species of birds develop sufficient viral levels (>~10 4.2 log PFU/ml; ) after being infected to transmit the infection to biting mosquitoes that in turn go on to infect other birds. In birds that die from WNV, death usually occurs after 4 to 6 days. In mammals and several species of birds, the virus does not multiply as readily and so does not develop high viremia during infection. Mosquitoes biting such hosts are not believed to ingest sufficient virus to become infected, making them so-called dead-end hosts . As a result of the differential infectiousness of hosts, the feeding patterns of mosquitoes play an important role in WNV transmission, and they are partly genetically controlled, even within a species. Direct human-to-human transmission initially was believed to be caused only by occupational exposure, such as in a laboratory setting, or conjunctival exposure to infected blood. The US outbreak identified additional transmission methods through blood transfusion, organ transplant, intrauterine exposure, and breast feeding. Since 2003, blood banks in the United States routinely screen for the virus among their donors. As a precautionary measure, the UK's National Blood Service initially ran a test for this disease in donors who donate within 28 days of a visit to the United States, Canada, or the northeastern provinces of Italy, and the Scottish National Blood Transfusion Service asks prospective donors to wait 28 days after returning from North America or the northeastern provinces of Italy before donating. There also have been reports of possible transmission of the virus from mother to child during pregnancy or breastfeeding or exposure to the virus in a lab, but these are rare cases and not conclusively confirmed. Recently, the potential for mosquito saliva to affect the course of WNV disease was demonstrated. Mosquitoes inoculate their saliva into the skin while obtaining blood. Mosquito saliva is a pharmacological cocktail of secreted molecules, principally proteins, that can affect vascular constriction, blood coagulation , platelet aggregation , inflammation , and immunity . It clearly alters the immune response in a manner that may be advantageous to a virus. Studies have shown it can specifically modulate the immune response during early virus infection, and mosquito feeding can exacerbate WNV infection, leading to higher viremia and more severe forms of disease. Vertical transmission , the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature. Mosquito progeny infected vertically in autumn may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall. Vertical transmission , the transmission of a viral or bacterial disease from the female of the species to her offspring, has been observed in various West Nile virus studies, amongst different species of mosquitoes in both the laboratory and in nature. Mosquito progeny infected vertically in autumn may potentially serve as a mechanism for WNV to overwinter and initiate enzootic horizontal transmission the following spring, although it likely plays little role in transmission in the summer and fall. Risk factors independently associated with developing a clinical infection with WNV include a suppressed immune system and a patient history of organ transplantation. For neuroinvasive disease the additional risk factors include older age (>50+), male sex, hypertension , and diabetes mellitus . A genetic factor also appears to increase susceptibility to West Nile disease. A mutation of the gene CCR5 gives some protection against HIV but leads to more serious complications of WNV infection. Carriers of two mutated copies of CCR5 made up 4.0 to 4.5% of a sample of people with West Nile disease, while the incidence of the gene in the general population is only 1.0%. The most at risk occupations in the U.S. are outdoor workers, for example farmers, loggers, landscapers/groundskeepers, construction workers, painters, summer camp workers and pavers. Two reports of accidental exposure by laboratory personnel working with infected fluids or tissues have been received. While this appears to be a rare occurrence, it highlights the need for proper handling of infected materials. The World Health Organization states that there are no known cases of health care workers acquiring the virus from infected patients when the appropriate infection control precautions are observed. Preliminary diagnosis is often based on the patient's clinical symptoms, places and dates of travel (if patient is from a non endemic country or area), activities, and epidemiologic history of the location where infection occurred. A recent history of mosquito bites and an acute febrile illness associated with neurologic signs and symptoms should cause clinical suspicion of WNV. Diagnosis of West Nile virus infections is generally accomplished by serologic testing of blood serum or cerebrospinal fluid (CSF), which is obtained via a lumbar puncture . Initial screening could be done using the ELISA technique detecting immunoglobulins in the sera of the tested individuals. Typical findings of WNV infection include lymphocytic pleocytosis , elevated protein level, reference glucose and lactic acid levels, and no erythrocytes . Definitive diagnosis of WNV is obtained through detection of virus-specific antibody IgM and neutralizing antibodies . Cases of West Nile virus meningitis and encephalitis that have been serologically confirmed produce similar degrees of CSF pleocytosis and are often associated with substantial CSF neutrophilia . Specimens collected within eight days following onset of illness may not test positive for West Nile IgM, and testing should be repeated. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavivirus infection and is not by itself evidence of an acute West Nile virus infection. If cases of suspected West Nile virus infection, sera should be collected on both the acute and convalescent phases of the illness. Convalescent specimens should be collected 2–3 weeks after acute specimens. It is common in serologic testing for cross-reactions to occur among flaviviruses such as dengue virus (DENV) and tick-borne encephalitis virus ; this necessitates caution when evaluating serologic results of flaviviral infections. Four FDA -cleared WNV IgM ELISA kits are commercially available from different manufacturers in the U.S., each of these kits is indicated for use on serum to aid in the presumptive laboratory diagnosis of WNV infection in patients with clinical symptoms of meningitis or encephalitis. Positive WNV test results obtained via use of these kits should be confirmed by additional testing at a state health department laboratory or CDC. In fatal cases, nucleic acid amplification, histopathology with immunohistochemistry , and virus culture of autopsy tissues can also be useful. Only a few state laboratories or other specialized laboratories, including those at CDC, are capable of doing this specialized testing. A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis. A number of various diseases may present with symptoms similar to those caused by a clinical West Nile virus infection. Those causing neuroinvasive disease symptoms include the enterovirus infection and bacterial meningitis. Accounting for differential diagnoses is a crucial step in the definitive diagnosis of WNV infection. Consideration of a differential diagnosis is required when a patient presents with unexplained febrile illness, extreme headache, encephalitis or meningitis. Diagnostic and serologic laboratory testing using polymerase chain reaction (PCR) testing and viral culture of CSF to identify the specific pathogen causing the symptoms, is the only currently available means of differentiating between causes of encephalitis and meningitis. Many of the guidelines for preventing occupational West Nile virus exposure are common to all mosquito-borne diseases . Public health measures include taking steps to reduce mosquito populations. Personal recommendations are to reduce the likelihood of being bitten. General measures to avoid bites include: West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps , carbon dioxide -baited light traps, and gravid traps, testing blood samples drawn from wild birds, dogs, and sentinel monkeys, and testing brains of dead birds found by various animal control agencies and the public. [ citation needed ] Testing of the mosquito samples requires the use of reverse-transcriptase PCR ( RT-PCR ) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC) or enzyme-linked immunosorbent assay (ELISA). Dead birds, after necropsy , or their oral swab samples collected on specific RNA-preserving filter paper card, can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate- enzyme reaction. West Nile control is achieved through mosquito control , by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides . [ citation needed ] Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, Culex pipiens , is a canopy feeder. [ citation needed ]West Nile virus can be sampled from the environment by the pooling of trapped mosquitoes via ovitraps , carbon dioxide -baited light traps, and gravid traps, testing blood samples drawn from wild birds, dogs, and sentinel monkeys, and testing brains of dead birds found by various animal control agencies and the public. [ citation needed ] Testing of the mosquito samples requires the use of reverse-transcriptase PCR ( RT-PCR ) to directly amplify and show the presence of virus in the submitted samples. When using the blood sera of wild birds and sentinel chickens, samples must be tested for the presence of WNV antibodies by use of immunohistochemistry (IHC) or enzyme-linked immunosorbent assay (ELISA). Dead birds, after necropsy , or their oral swab samples collected on specific RNA-preserving filter paper card, can have their virus presence tested by either RT-PCR or IHC, where virus shows up as brown-stained tissue because of a substrate- enzyme reaction. West Nile control is achieved through mosquito control , by elimination of mosquito breeding sites such as abandoned pools, applying larvacide to active breeding areas, and targeting the adult population via lethal ovitraps and aerial spraying of pesticides . [ citation needed ] Environmentalists have condemned attempts to control the transmitting mosquitoes by spraying pesticide, saying the detrimental health effects of spraying outweigh the relatively few lives that may be saved, and more environmentally friendly ways of controlling mosquitoes are available. They also question the effectiveness of insecticide spraying, as they believe mosquitoes that are resting or flying above the level of spraying will not be killed; the most common vector in the northeastern United States, Culex pipiens , is a canopy feeder. [ citation needed ]No specific treatment is available for WNV infection. Most people recover without treatment. In mild cases, over-the-counter pain relievers can help ease mild headaches and muscle aches in adults. In severe cases supportive care is provided, often in hospital, with intravenous fluids , pain medication, respiratory support, and prevention of secondary infections. While the general prognosis is favorable, current studies indicate that West Nile Fever can often be more severe than previously recognized, with studies of various recent outbreaks indicating that it may take as long as 60 to 90 days to recover. Patients with milder WNF are just as likely as those with more severe manifestations of neuroinvasive disease to experience multiple somatic complaints such as tremor, and dysfunction in motor skills and executive functions for over a year. People with milder symptoms are just as likely as people with more severe symptoms to experience adverse outcomes. Recovery is marked by a long convalescence with fatigue . One study found that neuroinvasive WNV infection was associated with an increased risk for subsequent kidney disease. WNV was first isolated from a feverish 37-year-old woman at Omogo in the West Nile District of Uganda in 1937 during research on yellow fever virus . A series of serosurveys in 1939 in central Africa found anti-WNV positive results ranging from 1.4% (Congo) to 46.4% (White Nile region, Sudan). It was subsequently identified in Egypt (1942) and India (1953), a 1950 serosurvey in Egypt found 90% of those over 40 years in age had WNV antibodies. The ecology was characterized in 1953 with studies in Egypt and Israel . The virus became recognized as a cause of severe human meningoencephalitis in elderly patients during an outbreak in Israel in 1957. The disease was first noted in horses in Egypt and France in the early 1960s and found to be widespread in southern Europe, southwest Asia and Australia. [ citation needed ] The first appearance of WNV in the Western Hemisphere was in 1999 with encephalitis reported in humans, dogs, cats, and horses, and the subsequent spread in the United States may be an important milestone in the evolving history of this virus. The American outbreak began in College Point, Queens in New York City and was later spread to the neighboring states of New Jersey and Connecticut . The virus is believed to have entered in an infected bird or mosquito, although there is no clear evidence. West Nile virus is now endemic in Africa, Europe, the Middle East, west and central Asia, Oceania (subtype Kunjin ), and most recently, North America and is spreading into Central and South America. Outbreaks of West Nile virus encephalitis in humans have occurred in Algeria (1994), Romania (1996 to 1997), the Czech Republic (1997), Congo (1998), Russia (1999), the United States (1999 to 2009), Canada (1999–2007), Israel (2000) and Greece (2010). Epizootics of disease in horses occurred in Morocco (1996), Italy (1998), the United States (1999 to 2001), and France (2000), Mexico (2003) and Sardinia (2011). [ citation needed ] Outdoor workers (including biological fieldworkers, construction workers, farmers, landscapers, and painters), healthcare personnel, and laboratory personnel who perform necropsies on animals are at risk of contracting WNV. In 2012, the US experienced one of its worst epidemics in which 286 people died, with the state of Texas being hard hit by this virus. Drought has been associated with a higher number of West Nile virus cases in the following year. As drought can decrease fish and other populations that eat mosquito eggs, higher numbers of mosquitoes can result. Higher temperatures are linked to decreased time for replication and increased viral load in birds and mosquitoes. Drought has been associated with a higher number of West Nile virus cases in the following year. As drought can decrease fish and other populations that eat mosquito eggs, higher numbers of mosquitoes can result. Higher temperatures are linked to decreased time for replication and increased viral load in birds and mosquitoes. A vaccine for horses ( ATCvet code: QI05AA10 ( WHO ) ) based on killed viruses exists; some zoos have given this vaccine to their birds, although its effectiveness is unknown. Dogs and cats show few if any signs of infection. There have been no known cases of direct canine-human or feline-human transmission; although these pets can become infected, it is unlikely they are, in turn, capable of infecting native mosquitoes and thus continuing the disease cycle. AMD3100 , which had been proposed as an antiretroviral drug for HIV, has shown promise against West Nile encephalitis. Morpholino antisense oligos conjugated to cell penetrating peptides have been shown to partially protect mice from WNV disease. There have also been attempts to treat infections using ribavirin , intravenous immunoglobulin , or alpha interferon . GenoMed, a U.S. biotech company, has found that blocking angiotensin II can treat the " cytokine storm " of West Nile virus encephalitis as well as other viruses. As of 2019, six vaccines had progressed to human trials but none had been licensed in the United States. Only the two live attenuated vaccines produced strong immunity after a single dose.

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Rift Valley fever

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Notifiable diseases in the United Kingdom

A notifiable disease is one which the law requires to be reported to government authorities. In England and Wales, notification of infectious diseases is a statutory duty for registered medical practitioners and laboratories, under the Public Health (Control of Disease) Act 1984 and (in England) the Health Protection (Notification) Regulations 2010. Similar provision, albeit with a different list of diseases, is made for Wales in the Health Protection (Notification) (Wales) Regulations 2010. Medical practitioners are required to notify their local authority of diseases on the list in writing within three days, or if the situation is urgent, by telephone within 24 hours. For Scotland, similar provision is made by the Public Health etc. (Scotland) Act 2008 . The diseases notifiable in England to local authorities under the Health Protection (Notification) Regulations 2010 are: The causative organisms which the laboratories shall notify to the proper authority under the Health Protection (Notification) Regulations 2010 are: [ citation needed ]

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Rift Valley fever

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Murray Valley encephalitis virus

Murray Valley encephalitis virus (MVEV) is a zoonotic flavivirus endemic to northern Australia and Papua New Guinea . It is the causal agent of Murray Valley encephalitis (MVE; previously known as Australian encephalitis or Australian X disease). In humans, it can cause permanent neurological disease or death. MVEV is related to Kunjin virus , which has a similar ecology, but a lower morbidity rate. Although the arbovirus is endemic to Northern Australia, it has occasionally spread to the southern states during times of heavy rainfall during the summer monsoon season via seasonal flooding of the Murray-Darling River system. These outbreaks can be "...decades apart, with no or very few cases identified in between". MVEV is a mosquito-borne virus that is maintained in a bird-mosquito-bird cycle. Water birds from the order Ciconiiformes , including herons and cormorants , provide the natural reservoir for MVEV. The major mosquito vector is Culex annulirostris . Human infection occurs only through bites from infected mosquitoes ; the virus cannot be transmitted from person to person. The first epidemics of MVE occurred in 1917 and 1918 in Southeastern Australia following years of high rainfall. The virus was isolated from human samples in 1951 during an epidemic in the Murray Valley , Australia. Epidemics usually occur due to either infected birds or mosquitoes migrating from endemic areas to non-endemic areas. The New South Wales government has placed 'sentinel flocks' of chickens near known bird breeding sites as an early warning system. These flocks are tested for MVE during the mosquito breeding season. The majority of MVEV infections are sub-clinical, i.e. do not produce disease symptoms, although some people may experience a mild form of the disease with symptoms such as fever, headaches, nausea and vomiting and only a very small number of these cases go on to develop MVE. In fact, serological surveys which measure the level of anti-MVEV antibodies within the population estimate that only one in 800–1000 of all infections result in clinical disease. The incubation period following exposure to the virus is around 1 to 4 weeks. Following infection, a person has lifelong immunity to the virus. When a patient appears to show MVE symptoms and has been in an MVE-endemic area during the wet season, when outbreaks usually occur, MVE infection must be confirmed by laboratory diagnosis, usually by detection of a significant rise of MVE-specific antibodies in the patient's serum . Of those who contract MVE, one-quarter die from the disease. The scientific study of the genetics of MVEV has been facilitated by the construction and manipulation of an infectious cDNA clone of the virus. Mutations in the envelope gene have been linked to the attenuation of disease in mouse models of infection.

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Rift Valley fever

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Orthornavirae

Positive-strand RNA viruses Negative-strand RNA viruses Double-stranded RNA viruses Orthornavirae is a kingdom of viruses that have genomes made of ribonucleic acid (RNA), including genes which encode an RNA-dependent RNA polymerase (RdRp). The RdRp is used to transcribe the viral RNA genome into messenger RNA (mRNA) and to replicate the genome. Viruses in this kingdom share a number of characteristics which promote rapid evolution , including high rates of genetic mutation , recombination , and reassortment . Viruses in Orthornavirae belong to the realm Riboviria . They are descended from a common ancestor that may have been a non-viral molecule that encoded a reverse transcriptase instead of an RdRp for replication. The kingdom is subdivided into five phyla that separate member viruses based on their genome type, host range, and genetic similarity. Viruses with three genome types are included: positive-strand RNA viruses , negative-strand RNA viruses , and double-stranded RNA viruses . Many of the most widely known viral diseases are caused by members of this kingdom, including coronaviruses , the Ebola virus , influenza viruses , the measles virus , and the rabies virus , as well as the first virus ever discovered, tobacco mosaic virus . In modern history, RdRp-encoding RNA viruses have caused numerous disease outbreaks, and they infect many economically important crops. Most eukaryotic viruses, including most human, animal, and plant viruses, are RdRp-encoding RNA viruses. In contrast, there are relatively few prokaryotic viruses in the kingdom.The first part of Orthornavirae comes from Greek ὀρθός [orthós], meaning straight, the middle part, rna , refers to RNA, and - virae is the suffix used for virus kingdoms. RNA viruses in Orthornavirae typically do not encode many proteins, but most positive-sense, single-stranded (+ssRNA) viruses and some double-stranded RNA (dsRNA) viruses encode a major capsid protein that has a single jelly roll fold , so named because the folded structure of the protein contains a structure that resembles a jelly roll . Many also possess an envelope , a type of lipid membrane that typically surrounds the capsid. In particular, the viral envelope is near-universal among negative-sense, single-stranded (-ssRNA) viruses. Viruses in Orthornavirae have three different types of genomes: dsRNA, +ssRNA, and -ssRNA. Single-stranded RNA viruses have either a positive or negative sense strand , and dsRNA viruses have both. This structure of the genome is important in terms of transcription to synthesize viral mRNA as well as replication of the genome, both of which are carried out by the viral enzyme RNA-dependent RNA polymerase (RdRp), also called RNA replicase. Positive-strand RNA viruses have genomes that can function as mRNA, so transcription is not necessary. However, +ssRNA will produce dsRNA forms as part of the process of replicating their genomes. From the dsRNA, additional positive strands are synthesized, which may be used as mRNA or for genomes for progeny. Because +ssRNA viruses create intermediate dsRNA forms, they have to avoid the host's immune system in order to replicate. +ssRNA viruses accomplish this by replicating in membrane-associated vesicles that are used as replication factories. For many +ssRNA viruses, subgenomic portions of the genome will be transcribed to translate specific proteins, whereas others will transcribe a polyprotein that is cleaved to produce separate proteins. Negative-strand RNA viruses have genomes that function as templates from which mRNA can be synthesized directly by RdRp. Replication is the same process but executed on the positive sense antigenome, during which RdRp ignores all transcription signals so that a complete -ssRNA genome can be synthesized. -ssRNA viruses vary between those that initiate transcription by the RdRp creating a cap on the 5'-end (usually pronounced "five prime end") of the genome or by snatching a cap from host mRNA and attaching it to the viral RNA. For many -ssRNA viruses, at the end of transcription, RdRp stutters on a uracil in the genome, synthesizing hundreds of adenines in a row as part of creating a polyadenylated tail for the mRNA. Some -ssRNA viruses are essentially ambisense, and have proteins encoded by both the positive and negative strand, so mRNA is synthesized directly from the genome and from a complementary strand. For dsRNA viruses, RdRp transcribes mRNA by using the negative strand as a template. Positive strands may also be used as templates to synthesize negative strands for the construction of genomic dsRNA. dsRNA is not a molecule produced by cells, so cellular life has evolved mechanisms to detect and inactivate viral dsRNA. To counter this, dsRNA viruses typically retain their genomes inside of viral capsid in order to evade the host's immune system. RNA viruses in Orthornavirae experience a high rate of genetic mutations because RdRp is prone to making errors in replication since it typically lacks proofreading mechanisms to repair errors. [note 1] Mutations in RNA viruses are often influenced by host factors such as dsRNA-dependent adenosine deaminases , which edit viral genomes by changing adenosines to inosines . Mutations in genes that are essential for replication lead to a reduced number of progeny, so viral genomes typically contain sequences that are highly conserved over time with relatively few mutations. Many RdRp-encoding RNA viruses also experience a high rate of genetic recombination , though rates of recombination vary significantly, with lower rates in -ssRNA viruses and higher rates in dsRNA and +ssRNA viruses. There are two types of recombination: copy choice recombination and reassortment. Copy choice recombination occurs when the RdRp switches templates during synthesis without releasing the prior, newly created RNA strand, which generates a genome of mixed ancestry. Reassortment , which is restricted to viruses with segmented genomes, has segments from different genomes packaged into a single virion, or virus particle, which also produces hybrid progeny. For reassortment, some segmented viruses package their genomes into multiple virions, which produces genomes that are random mixtures of parents, whereas for those that are packaged into a single virion, typically individual segments are swapped. Both forms of recombination can only occur if more than one virus is present in a cell, and the more alleles are present, the more likely recombination is to occur. A key difference between copy choice recombination and reassortment is that copy choice recombination can occur anywhere in a genome, whereas reassortment swaps fully-replicated segments. Therefore, copy choice recombination can produce non-functional viral proteins whereas reassortment cannot. The mutation rate of a virus is associated with the rate of genetic recombinations. Higher mutation rates increase both the number of advantageous and disadvantageous mutations, whereas higher rates of recombination allows for beneficial mutations to be separated from deleterious ones. [ vague ] Therefore, higher rates of mutations and recombinations, up to a certain point, improve viruses' ability to adapt. Notable examples of this include reassortments that enable cross-species transmission of influenza viruses, which have led to numerous pandemics, as well as the emergence of drug-resistance influenza strains via mutations that were reassorted. RNA viruses in Orthornavirae typically do not encode many proteins, but most positive-sense, single-stranded (+ssRNA) viruses and some double-stranded RNA (dsRNA) viruses encode a major capsid protein that has a single jelly roll fold , so named because the folded structure of the protein contains a structure that resembles a jelly roll . Many also possess an envelope , a type of lipid membrane that typically surrounds the capsid. In particular, the viral envelope is near-universal among negative-sense, single-stranded (-ssRNA) viruses. Viruses in Orthornavirae have three different types of genomes: dsRNA, +ssRNA, and -ssRNA. Single-stranded RNA viruses have either a positive or negative sense strand , and dsRNA viruses have both. This structure of the genome is important in terms of transcription to synthesize viral mRNA as well as replication of the genome, both of which are carried out by the viral enzyme RNA-dependent RNA polymerase (RdRp), also called RNA replicase. Positive-strand RNA viruses have genomes that can function as mRNA, so transcription is not necessary. However, +ssRNA will produce dsRNA forms as part of the process of replicating their genomes. From the dsRNA, additional positive strands are synthesized, which may be used as mRNA or for genomes for progeny. Because +ssRNA viruses create intermediate dsRNA forms, they have to avoid the host's immune system in order to replicate. +ssRNA viruses accomplish this by replicating in membrane-associated vesicles that are used as replication factories. For many +ssRNA viruses, subgenomic portions of the genome will be transcribed to translate specific proteins, whereas others will transcribe a polyprotein that is cleaved to produce separate proteins. Negative-strand RNA viruses have genomes that function as templates from which mRNA can be synthesized directly by RdRp. Replication is the same process but executed on the positive sense antigenome, during which RdRp ignores all transcription signals so that a complete -ssRNA genome can be synthesized. -ssRNA viruses vary between those that initiate transcription by the RdRp creating a cap on the 5'-end (usually pronounced "five prime end") of the genome or by snatching a cap from host mRNA and attaching it to the viral RNA. For many -ssRNA viruses, at the end of transcription, RdRp stutters on a uracil in the genome, synthesizing hundreds of adenines in a row as part of creating a polyadenylated tail for the mRNA. Some -ssRNA viruses are essentially ambisense, and have proteins encoded by both the positive and negative strand, so mRNA is synthesized directly from the genome and from a complementary strand. For dsRNA viruses, RdRp transcribes mRNA by using the negative strand as a template. Positive strands may also be used as templates to synthesize negative strands for the construction of genomic dsRNA. dsRNA is not a molecule produced by cells, so cellular life has evolved mechanisms to detect and inactivate viral dsRNA. To counter this, dsRNA viruses typically retain their genomes inside of viral capsid in order to evade the host's immune system. Positive-strand RNA viruses have genomes that can function as mRNA, so transcription is not necessary. However, +ssRNA will produce dsRNA forms as part of the process of replicating their genomes. From the dsRNA, additional positive strands are synthesized, which may be used as mRNA or for genomes for progeny. Because +ssRNA viruses create intermediate dsRNA forms, they have to avoid the host's immune system in order to replicate. +ssRNA viruses accomplish this by replicating in membrane-associated vesicles that are used as replication factories. For many +ssRNA viruses, subgenomic portions of the genome will be transcribed to translate specific proteins, whereas others will transcribe a polyprotein that is cleaved to produce separate proteins. Negative-strand RNA viruses have genomes that function as templates from which mRNA can be synthesized directly by RdRp. Replication is the same process but executed on the positive sense antigenome, during which RdRp ignores all transcription signals so that a complete -ssRNA genome can be synthesized. -ssRNA viruses vary between those that initiate transcription by the RdRp creating a cap on the 5'-end (usually pronounced "five prime end") of the genome or by snatching a cap from host mRNA and attaching it to the viral RNA. For many -ssRNA viruses, at the end of transcription, RdRp stutters on a uracil in the genome, synthesizing hundreds of adenines in a row as part of creating a polyadenylated tail for the mRNA. Some -ssRNA viruses are essentially ambisense, and have proteins encoded by both the positive and negative strand, so mRNA is synthesized directly from the genome and from a complementary strand. For dsRNA viruses, RdRp transcribes mRNA by using the negative strand as a template. Positive strands may also be used as templates to synthesize negative strands for the construction of genomic dsRNA. dsRNA is not a molecule produced by cells, so cellular life has evolved mechanisms to detect and inactivate viral dsRNA. To counter this, dsRNA viruses typically retain their genomes inside of viral capsid in order to evade the host's immune system. RNA viruses in Orthornavirae experience a high rate of genetic mutations because RdRp is prone to making errors in replication since it typically lacks proofreading mechanisms to repair errors. [note 1] Mutations in RNA viruses are often influenced by host factors such as dsRNA-dependent adenosine deaminases , which edit viral genomes by changing adenosines to inosines . Mutations in genes that are essential for replication lead to a reduced number of progeny, so viral genomes typically contain sequences that are highly conserved over time with relatively few mutations. Many RdRp-encoding RNA viruses also experience a high rate of genetic recombination , though rates of recombination vary significantly, with lower rates in -ssRNA viruses and higher rates in dsRNA and +ssRNA viruses. There are two types of recombination: copy choice recombination and reassortment. Copy choice recombination occurs when the RdRp switches templates during synthesis without releasing the prior, newly created RNA strand, which generates a genome of mixed ancestry. Reassortment , which is restricted to viruses with segmented genomes, has segments from different genomes packaged into a single virion, or virus particle, which also produces hybrid progeny. For reassortment, some segmented viruses package their genomes into multiple virions, which produces genomes that are random mixtures of parents, whereas for those that are packaged into a single virion, typically individual segments are swapped. Both forms of recombination can only occur if more than one virus is present in a cell, and the more alleles are present, the more likely recombination is to occur. A key difference between copy choice recombination and reassortment is that copy choice recombination can occur anywhere in a genome, whereas reassortment swaps fully-replicated segments. Therefore, copy choice recombination can produce non-functional viral proteins whereas reassortment cannot. The mutation rate of a virus is associated with the rate of genetic recombinations. Higher mutation rates increase both the number of advantageous and disadvantageous mutations, whereas higher rates of recombination allows for beneficial mutations to be separated from deleterious ones. [ vague ] Therefore, higher rates of mutations and recombinations, up to a certain point, improve viruses' ability to adapt. Notable examples of this include reassortments that enable cross-species transmission of influenza viruses, which have led to numerous pandemics, as well as the emergence of drug-resistance influenza strains via mutations that were reassorted. The exact origin of Orthornavirae is not well established, but the viral RdRp shows a relation to the reverse transcriptase (RT) enzymes of group II introns that encode RTs and retrotransposons , the latter of which are self-replicating DNA sequences that integrate themselves into other parts of the same DNA molecule. A larger study (2022) where new lieneages (phyla) were described, has suggested that RNA viruses descend from the RNA world , suggesting that retroelements (retrotransposons and group II introns) originated from an ancestor related to the phylum Lenarviricota and that members of a newly discovered Taraviricota lineage (phylum) would be the ancestors of all RNA viruses. According to this study the genomes of both dsRNA, +ssRNA and -ssRNA evolved independently and were altered several times in evolution. RNA viruses that encode RdRp are assigned to the kingdom Orthornavirae , which contains five official phyla, six unofficial phyla and several taxa that are unassigned to a phylum due to lack of information. The five phyla are separated based on the genome types, host ranges, and genetic similarity of member viruses. The unassigned taxa are listed hereafter (- viridae denotes family and - virus denotes genus). The kingdom contains three groups in the Baltimore classification system, which groups viruses together based on their manner of mRNA synthesis, and which is often used alongside standard virus taxonomy, which is based on evolutionary history. Those three groups are Group III: dsRNA viruses, Group IV: +ssRNA viruses, and Group V: -ssRNA viruses. RNA viruses are associated with a wide range of disease, including many of the most widely known viral diseases. Notable disease-causing viruses in Orthornavirae include: Animal viruses in Orthornavirae include orbiviruses , which cause various diseases in ruminants and horses, including Bluetongue virus , African horse sickness virus , Equine encephalosis virus , and epizootic hemorrhagic disease virus . The vesicular stomatitis virus causes disease in cattle, horses, and pigs. Bats harbor many viruses including ebolaviruses and henipaviruses , which also can cause disease in humans. Similarly, arthropod viruses in the Flavivirus and Phlebovirus genera are numerous and often transmitted to humans. Coronaviruses and influenza viruses cause disease in various vertebrates, including bats, birds, and pigs. Plant viruses in the kingdom are numerous and infect many economically important crops. Tomato spotted wilt virus is estimated to cause more than 1 billion USD in damages annually, affecting more than 800 plant species including chrysanthemum, lettuce, peanut, pepper, and tomato. Cucumber mosaic virus infects more than 1,200 plant species and likewise causes significant crop losses. Potato virus Y causes significant reductions in yield and quality for pepper, potato, tobacco, and tomato, and Plum pox virus is the most important virus among stone fruit crops. Brome mosaic virus , while not causing significant economic losses, is found throughout much of the world and primarily infects grasses, including cereals. Diseases caused by RNA viruses in Orthornavirae have been known throughout much of history, but their cause was only discovered in modern times. As a whole, RNA viruses were discovered during a time period of major advancements in molecular biology, including the discovery of mRNA as the immediate carrier of genetic information for protein synthesis. Tobacco mosaic virus was discovered in 1898 and was the first virus to be discovered. Viruses in the kingdom that are transmitted by arthropods have been a key target in the development of vector control , which often aims to prevent viral infections. In modern history, numerous disease outbreaks have been caused by RdRp-encoding RNA viruses, including outbreaks caused by coronaviruses, ebola, and influenza. Orthornavirae was established in 2019 as a kingdom within the realm Riboviria , intended to accommodate all RdRp-encoding RNA viruses. Prior to 2019, Riboviria was established in 2018 and included only RdRp-encoding RNA viruses. In 2019, Riboviria was expanded to also include reverse transcribing viruses, placed under the kingdom Pararnavirae , so Orthornavirae was established to separate RdRp-encoding RNA viruses from reversing transcribing viruses.

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Rift Valley fever

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Nova virus

Nova virus is a single-stranded, negative-sense, enveloped RNA virus with a trisegmented genome. It belongs to one of the most divergent lineages of the hantavirus group, which consists of zoonotic viruses belonging to the family Bunyaviridae. As of now, no human cases of infection have been reported. It was previously believed that hantaviruses were primarily rodent-borne. However, over the last two decades, multiple species have also been detected in shrews, moles and bats. In 2009, Nova virus was first isolated from the archival liver tissue of the European mole ( Talpa europaea ) captured in Hungary in 1999. The first complete genome characterization was published in 2015 and it was obtained from a European mole originating from Belgium. It has been concluded that the virus shows a close phylogenetic relationship with bat- and shrew-borne hantaviruses. Furthermore, there is a chance that the early or original hosts of primordial hantaviruses may have been ancestral soricomorphs, rather than rodents. Studies have been conducted to explore the prevalence of Nova virus infection in European moles – in a region of France, almost 65% of captured moles were positive, and a similarly high prevalence has been found in Poland. Those results suggest an efficient enzootic transmission, a well-established host-pathogen relationship, and also that the fact that the Nova virus might be widespread throughout the distribution range of the European mole, which extends from Great Britain and Spain to the Asian part of Russia, through most of continental Europe. Not all hantaviruses are pathogenic but several species are able to cause rapidly progressive and often fatal zoonotic diseases, such as hemorrhagic fever with renal syndrome (HFRS) carried by murine and arvicoline rodents in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) harbored by neotomine and sigmodontine rodents in the Americas. Not a lot is known about the pathogenicity of the insectivore-borne hantaviruses, even though the number of identified species is constantly increasing. Neither one of them, including the Nova virus, has yet been connected to a disease in humans. Considering the fact that the viral sequences have been detected in kidney tissue, it is possible that viruses could be present in urine, and that the mode of transmission could be through virus shedding in secretions and excretions. Certain professions or individuals might be at risk of infection – those who might be exposed to shrews, moles and their presumably infectious excretions or secretions, for example mammalogists, field biologists, forestry workers and outdoor cat owners.

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Rift Valley fever

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RVF

RVF may refer to:

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Rift Valley fever

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Zika virus

Zika virus ( ZIKV ; pronounced / ˈ z iː k ə / or / ˈ z ɪ k ə / ) is a member of the virus family Flaviviridae . It is spread by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus . Its name comes from the Ziika Forest of Uganda , where the virus was first isolated in 1947. Zika virus shares a genus with the dengue , yellow fever , Japanese encephalitis , and West Nile viruses. Since the 1950s, it has been known to occur within a narrow equatorial belt from Africa to Asia. From 2007 to 2016 [ update ] , the virus spread eastward, across the Pacific Ocean to the Americas, leading to the 2015–2016 Zika virus epidemic . The infection, known as Zika fever or Zika virus disease, often causes no or only mild symptoms, similar to a very mild form of dengue fever . While there is no specific treatment, paracetamol (acetaminophen) and rest may help with the symptoms. As of April 2019, no vaccines have been approved for clinical use, however a number of vaccines are currently in clinical trials. Zika can spread from a pregnant woman to her baby. This can result in microcephaly , severe brain malformations , and other birth defects. Zika infections in adults may result rarely in Guillain–Barré syndrome . In January 2016, the United States Centers for Disease Control and Prevention (CDC) issued travel guidance on affected countries, including the use of enhanced precautions, and guidelines for pregnant women including considering postponing travel. Other governments or health agencies also issued similar travel warnings, while Colombia , the Dominican Republic , Puerto Rico , Ecuador , El Salvador , and Jamaica advised women to postpone getting pregnant until more is known about the risks. Zika virus belongs to the family Flaviviridae and the genus Flavivirus , thus is related to the dengue , yellow fever , Japanese encephalitis , and West Nile viruses. Like other flaviviruses, Zika virus is enveloped and icosahedral and has a nonsegmented, single-stranded, 10 kilobase , positive-sense RNA genome . It is most closely related to the Spondweni virus and is one of the two known viruses in the Spondweni virus clade . A positive-sense RNA genome can be directly translated into viral proteins. As in other flaviviruses, such as the similarly sized West Nile virus, the RNA genome encodes seven nonstructural proteins and three structural proteins in the form of a single polyprotein ( Q32ZE1 ). One of the structural proteins encapsulates the virus. This protein is the flavivirus envelope glycoprotein, that binds to the endosomal membrane of the host cell to initiate endocytosis. The RNA genome forms a nucleocapsid along with copies of the 12-kDa capsid protein. The nucleocapsid, in turn, is enveloped within a host-derived membrane modified with two viral glycoproteins . Viral genome replication depends on the making of double-stranded RNA from the single-stranded, positive-sense RNA (ssRNA(+)) genome followed by transcription and replication to provide viral mRNAs and new ssRNA(+) genomes. A longitudinal study shows that 6 hours after cells are infected with Zika virus , the vacuoles and mitochondria in the cells begin to swell. This swelling becomes so severe, it results in cell death, also known as paraptosis. This form of programmed cell death requires gene expression. IFITM3 is a trans-membrane protein in a cell that is able to protect it from viral infection by blocking virus attachment. Cells are most susceptible to Zika infection when levels of IFITM3 are low. Once the cell has been infected, the virus restructures the endoplasmic reticulum, forming the large vacuoles, resulting in cell death. There are two Zika lineages: the African lineage and the Asian lineage. Phylogenetic studies indicate that the virus spreading in the Americas is 89% identical to African genotypes, but is most closely related to the Asian strain that circulated in French Polynesia during the 2013 – 2014 outbreak . The Asian strain appears to have first evolved around 1928. The vertebrate hosts of the virus were primarily monkeys in a so-called enzootic mosquito-monkey-mosquito cycle, with only occasional transmission to humans. Before 2007, Zika "rarely caused recognized 'spillover' infections in humans, even in highly enzootic areas". Infrequently, however, other arboviruses have become established as a human disease and spread in a mosquito–human–mosquito cycle, like the yellow fever virus and the dengue fever virus (both flaviviruses), and the chikungunya virus (a togavirus ). Though the reason for the pandemic is unknown, dengue, a related arbovirus that infects the same species of mosquito vectors , is known in particular to be intensified by urbanization and globalization . Zika is primarily spread by Aedes aegypti mosquitoes, and can also be transmitted through sexual contact or blood transfusions . The basic reproduction number ( R 0 , a measure of transmissibility) of Zika virus has been estimated to be between 1.4 and 6.6 . In 2015, news reports drew attention to the rapid spread of Zika in Latin America and the Caribbean. At that time, the Pan American Health Organization published a list of countries and territories that experienced "local Zika virus transmission" comprising Barbados, Bolivia, Brazil, Colombia, the Dominican Republic, Ecuador, El Salvador, French Guiana, Guadeloupe, Guatemala, Guyana, Haiti, Honduras, Martinique, Mexico, Panama, Paraguay, Puerto Rico, Saint Martin, Suriname, and Venezuela. By August 2016, more than 50 countries had experienced active (local) transmission of Zika virus . Zika is primarily spread by the female Aedes aegypti mosquito, which is active mostly in the daytime. The mosquitos must feed on blood to lay eggs. : 2 The virus has also been isolated from a number of arboreal mosquito species in the genus Aedes , such as A. africanus , A. apicoargenteus , A. furcifer , A. hensilli , A. luteocephalus , and A. vittatus , with an extrinsic incubation period in mosquitoes around 10 days. The true extent of the vectors is still unknown. Zika has been detected in many more species of Aedes , along with Anopheles coustani, Mansonia uniformis , and Culex perfuscus , although this alone does not incriminate them as vectors. To detect the presence of the virus usually requires genetic material to be analysed in a lab using the technique RT-PCR . A much cheaper and faster method involves shining a light at the head and thorax of the mosquito, and detecting chemical compounds characteristic of the virus using near-infrared spectroscopy . Transmission by A. albopictus , the tiger mosquito, was reported from a 2007 urban outbreak in Gabon, where it had newly invaded the country and become the primary vector for the concomitant chikungunya and dengue virus outbreaks. New outbreaks can occur if a person carrying the virus travels to another region where A. albopictus is common. The potential societal risk of Zika can be delimited by the distribution of the mosquito species that transmit it. The global distribution of the most cited carrier of Zika, A. aegypti , is expanding due to global trade and travel. A. aegypti distribution is now the most extensive ever recorded – on parts of all continents except Antarctica, including North America and even the European periphery ( Madeira , the Netherlands, and the northeastern Black Sea coast). A mosquito population capable of carrying Zika has been found in a Capitol Hill neighborhood of Washington, DC, and genetic evidence suggests they survived at least four consecutive winters in the region. The study authors conclude that mosquitos are adapting for persistence in a northern climate. Zika virus appears to be contagious via mosquitoes for around a week after infection. The virus is thought to be infectious for a longer period of time after infection (at least 2 weeks) when transmitted via semen . Research into its ecological niche suggests that Zika may be influenced to a greater degree by changes in precipitation and temperature than dengue, making it more likely to be confined to tropical areas. However, rising global temperatures would allow for the disease vector to expand its range further north, allowing Zika to follow. Zika can be transmitted from men and women to their sexual partners; most known cases involve transmission from symptomatic men to women. As of April 2016, sexual transmission of Zika has been documented in six countries – Argentina, Australia, France, Italy, New Zealand, and the United States – during the 2015 outbreak. ZIKV can persist in semen for several months, with viral RNA detected up to one year. The virus replicates in the human testis, where it infects several cell types including testicular macrophages, peritubular cells and germ cells, the spermatozoa precursors. Semen parameters can be altered in patients for several weeks post-symptoms onset, and spermatozoa can be infectious. Since October 2016, the CDC has advised men who have traveled to an area with Zika should use condoms or not have sex for at least six months after their return as the virus is still transmissible even if symptoms never develop. Zika virus can spread by vertical (or "mother-to-child") transmission , during pregnancy or at delivery. An infection during pregnancy has been linked to changes in neuronal development of the unborn child. Severe progressions of infection have been linked to the development of microcephaly in the unborn child, while mild infections potentially can lead to neurocognitive disorders later in life. Congenital brain abnormalities other than microcephaly have also been reported after a Zika outbreak. Studies in mice have suggested that maternal immunity to dengue virus may enhance fetal infection with Zika, worsen the microcephaly phenotype and/or enhance damage during pregnancy, but it is unknown whether this occurs in humans. As of April 2016 [ update ] , two cases of Zika transmission through blood transfusions have been reported globally, both from Brazil, after which the US Food and Drug Administration (FDA) recommended screening blood donors and deferring high-risk donors for 4 weeks. A potential risk had been suspected based on a blood-donor screening study during the French Polynesian Zika outbreak, in which 2.8% (42) of donors from November 2013 and February 2014 tested positive for Zika RNA and were all asymptomatic at the time of blood donation. Eleven of the positive donors reported symptoms of Zika fever after their donation, but only three of 34 samples grew in culture. Zika is primarily spread by the female Aedes aegypti mosquito, which is active mostly in the daytime. The mosquitos must feed on blood to lay eggs. : 2 The virus has also been isolated from a number of arboreal mosquito species in the genus Aedes , such as A. africanus , A. apicoargenteus , A. furcifer , A. hensilli , A. luteocephalus , and A. vittatus , with an extrinsic incubation period in mosquitoes around 10 days. The true extent of the vectors is still unknown. Zika has been detected in many more species of Aedes , along with Anopheles coustani, Mansonia uniformis , and Culex perfuscus , although this alone does not incriminate them as vectors. To detect the presence of the virus usually requires genetic material to be analysed in a lab using the technique RT-PCR . A much cheaper and faster method involves shining a light at the head and thorax of the mosquito, and detecting chemical compounds characteristic of the virus using near-infrared spectroscopy . Transmission by A. albopictus , the tiger mosquito, was reported from a 2007 urban outbreak in Gabon, where it had newly invaded the country and become the primary vector for the concomitant chikungunya and dengue virus outbreaks. New outbreaks can occur if a person carrying the virus travels to another region where A. albopictus is common. The potential societal risk of Zika can be delimited by the distribution of the mosquito species that transmit it. The global distribution of the most cited carrier of Zika, A. aegypti , is expanding due to global trade and travel. A. aegypti distribution is now the most extensive ever recorded – on parts of all continents except Antarctica, including North America and even the European periphery ( Madeira , the Netherlands, and the northeastern Black Sea coast). A mosquito population capable of carrying Zika has been found in a Capitol Hill neighborhood of Washington, DC, and genetic evidence suggests they survived at least four consecutive winters in the region. The study authors conclude that mosquitos are adapting for persistence in a northern climate. Zika virus appears to be contagious via mosquitoes for around a week after infection. The virus is thought to be infectious for a longer period of time after infection (at least 2 weeks) when transmitted via semen . Research into its ecological niche suggests that Zika may be influenced to a greater degree by changes in precipitation and temperature than dengue, making it more likely to be confined to tropical areas. However, rising global temperatures would allow for the disease vector to expand its range further north, allowing Zika to follow. Zika can be transmitted from men and women to their sexual partners; most known cases involve transmission from symptomatic men to women. As of April 2016, sexual transmission of Zika has been documented in six countries – Argentina, Australia, France, Italy, New Zealand, and the United States – during the 2015 outbreak. ZIKV can persist in semen for several months, with viral RNA detected up to one year. The virus replicates in the human testis, where it infects several cell types including testicular macrophages, peritubular cells and germ cells, the spermatozoa precursors. Semen parameters can be altered in patients for several weeks post-symptoms onset, and spermatozoa can be infectious. Since October 2016, the CDC has advised men who have traveled to an area with Zika should use condoms or not have sex for at least six months after their return as the virus is still transmissible even if symptoms never develop. Zika virus can spread by vertical (or "mother-to-child") transmission , during pregnancy or at delivery. An infection during pregnancy has been linked to changes in neuronal development of the unborn child. Severe progressions of infection have been linked to the development of microcephaly in the unborn child, while mild infections potentially can lead to neurocognitive disorders later in life. Congenital brain abnormalities other than microcephaly have also been reported after a Zika outbreak. Studies in mice have suggested that maternal immunity to dengue virus may enhance fetal infection with Zika, worsen the microcephaly phenotype and/or enhance damage during pregnancy, but it is unknown whether this occurs in humans. As of April 2016 [ update ] , two cases of Zika transmission through blood transfusions have been reported globally, both from Brazil, after which the US Food and Drug Administration (FDA) recommended screening blood donors and deferring high-risk donors for 4 weeks. A potential risk had been suspected based on a blood-donor screening study during the French Polynesian Zika outbreak, in which 2.8% (42) of donors from November 2013 and February 2014 tested positive for Zika RNA and were all asymptomatic at the time of blood donation. Eleven of the positive donors reported symptoms of Zika fever after their donation, but only three of 34 samples grew in culture. Zika virus replicates in the mosquito's midgut epithelial cells and then its salivary gland cells. After 5–10 days, the virus can be found in the mosquito's saliva. If the mosquito's saliva is inoculated into human skin, the virus can infect epidermal keratinocytes, skin fibroblasts in the skin and the Langerhans cells . The pathogenesis of the virus is hypothesized to continue with a spread to lymph nodes and the bloodstream. Flaviviruses replicate in the cytoplasm , but Zika antigens have been found in infected cell nuclei. The viral protein numbered NS4A can lead to small head size ( microcephaly ) because it disrupts brain growth by hijacking a pathway which regulates growth of new neurons. In fruit flies, both NS4A and the neighboring NS4B restrict eye growth. Zika fever (also known as Zika virus disease) is an illness caused by Zika virus . Around 80% of cases are estimated to be asymptomatic, though the accuracy of this figure is hindered by the wide variance in data quality, and figures from different outbreaks can vary significantly. Symptomatic cases are usually mild and can resemble dengue fever . Symptoms may include fever , red eyes , joint pain , headache, and a maculopapular rash . Symptoms generally last less than seven days. It has not caused any reported deaths during the initial infection. Infection during pregnancy causes microcephaly and other brain malformations in some babies. Infection in adults has been linked to Guillain–Barré syndrome (GBS) and Zika virus has been shown to infect human Schwann cells . Diagnosis is by testing the blood, urine, or saliva for the presence of Zika virus RNA when the person is sick. In 2019, an improved diagnostic test, based on research from Washington University in St. Louis , that detects Zika infection in serum was granted market authorization by the FDA . Prevention involves decreasing mosquito bites in areas where the disease occurs, and proper use of condoms. Efforts to prevent bites include the use of DEET or picaridin - based insect repellent , covering much of the body with clothing, mosquito nets , and getting rid of standing water where mosquitoes reproduce. There is no vaccine . Health officials recommended that women in areas affected by the 2015–2016 Zika outbreak consider putting off pregnancy and that pregnant women not travel to these areas. While no specific treatment exists, paracetamol (acetaminophen) and rest may help with the symptoms. Admission to a hospital is rarely necessary. It is advised, for an affected person with the zika virus, to drink a lot of water to stay hydrated, to lie down, and to treat the fever and agony with liquid solutions; taking drugs like acetaminophen or paracetamol helps to relieve fever and pain. [ according to whom? ] Referring to the US CDC it is not recommended to take anti-inflammatory and non-steroid drugs like aspirin for example. If the patient affected is already taking treatment for another medical condition it is advisable to inform your attending physician before taking any other drug or additional treatment; The World Health Organization has suggested that priority should be to develop inactivated vaccines and other nonlive vaccines, which are safe to use in pregnant women. As of March 2016 [ update ] , 18 companies and institutions were developing vaccines against Zika, but they state a vaccine is unlikely to be widely available for about 10 years. In June 2016, the FDA granted the first approval for a human clinical trial for a Zika vaccine. In March 2017, a DNA vaccine was approved for phase-2 clinical trials. This vaccine consists of a small, circular piece of DNA, known as a plasmid, that expresses the genes for the Zika virus envelope proteins. As the vaccine does not contain the full sequence of the virus, it cannot cause infection. As of April 2017, both subunit and inactivated vaccines have entered clinical trials. It is advised, for an affected person with the zika virus, to drink a lot of water to stay hydrated, to lie down, and to treat the fever and agony with liquid solutions; taking drugs like acetaminophen or paracetamol helps to relieve fever and pain. [ according to whom? ] Referring to the US CDC it is not recommended to take anti-inflammatory and non-steroid drugs like aspirin for example. If the patient affected is already taking treatment for another medical condition it is advisable to inform your attending physician before taking any other drug or additional treatment; The World Health Organization has suggested that priority should be to develop inactivated vaccines and other nonlive vaccines, which are safe to use in pregnant women. As of March 2016 [ update ] , 18 companies and institutions were developing vaccines against Zika, but they state a vaccine is unlikely to be widely available for about 10 years. In June 2016, the FDA granted the first approval for a human clinical trial for a Zika vaccine. In March 2017, a DNA vaccine was approved for phase-2 clinical trials. This vaccine consists of a small, circular piece of DNA, known as a plasmid, that expresses the genes for the Zika virus envelope proteins. As the vaccine does not contain the full sequence of the virus, it cannot cause infection. As of April 2017, both subunit and inactivated vaccines have entered clinical trials. The virus was first isolated in April 1947 from a rhesus macaque monkey placed in a cage in the Ziika Forest of Uganda , near Lake Victoria , by the scientists of the Yellow Fever Research Institute . A second isolation from the mosquito A. africanus followed at the same site in January 1948. When the monkey developed a fever, researchers isolated from its serum a "filterable transmissible agent" which was named Zika in 1948. Zika was first known to infect humans from the results of a serological survey in Uganda, published in 1952. Of 99 human blood samples tested, 6.1% had neutralizing antibodies. As part of a 1954 outbreak investigation of jaundice suspected to be yellow fever, researchers reported isolation of the virus from a patient, but the pathogen was later shown to be the closely related Spondweni virus . Spondweni was also determined to be the cause of a self-inflicted infection in a researcher reported in 1956. Subsequent serological studies in several African and Asian countries indicated the virus had been widespread within human populations in these regions. The first true case of human infection was identified by Simpson in 1964, who was himself infected while isolating the virus from mosquitoes. From then until 2007, there were only 13 further confirmed human cases of Zika infection from Africa and Southeast Asia. A study published in 2017 showed that the Zika virus, despite only a few cases were reported, has been silently circulated in West Africa for the last two decades when blood samples collected between 1992 and 2016 were tested for the ZIKV IgM antibodies. In 2017, Angola reported two cases of Zika fever. Zika was also occurring in Tanzania as of 2016. In April 2007, the first outbreak outside of Africa and Asia occurred on the island of Yap in the Federated States of Micronesia, characterized by rash, conjunctivitis, and arthralgia, which was initially thought to be dengue, chikungunya , or Ross River disease . Serum samples from patients in the acute phase of illness contained RNA of Zika. There were 49 confirmed cases, 59 unconfirmed cases, no hospitalizations, and no deaths. After October 2013 Oceania's first outbreak showed an estimated 11% population infected for French Polynesia that also presented with Guillain–Barre syndrome (GBS). The spread of ZIKV continued to New Caledonia, Easter Island, and the Cook Islands and where 1385 cases were confirmed by January 2014. During the same year, Easter Island acknowledged 51 cases. Australia began seeing cases in 2012. Research showed it was brought by travelers returning from Indonesia and other infected countries. New Zealand also experienced infections rate increases through returning foreign travelers. Oceania countries experiencing Zika today are New Caledonia, Vanuatu, Solomon Islands, Marshall Islands, American Samoa, Samoa, and Tonga. Between 2013 and 2014, further epidemics occurred in French Polynesia , Easter Island , the Cook Islands , and New Caledonia . There was an epidemic in 2015 and 2016 in the Americas . The outbreak began in April 2015 in Brazil , and spread to other countries in South America , Central America , North America , and the Caribbean . In January 2016, the WHO said the virus was likely to spread throughout most of the Americas by the end of the year; and in February 2016, the WHO declared the cluster of microcephaly and Guillain–Barré syndrome cases reported in Brazil – strongly suspected to be associated with the Zika outbreak – a Public Health Emergency of International Concern . It was estimated that 1.5 million people were infected by Zika in Brazil, with over 3,500 cases of microcephaly reported between October 2015 and January 2016. A number of countries issued travel warnings , and the outbreak was expected to significantly impact the tourism industry. Several countries have taken the unusual step of advising their citizens to delay pregnancy until more is known about the virus and its impact on fetal development. With the 2016 Summer Olympics hosted in Rio de Janeiro , health officials worldwide voiced concerns over a potential crisis, both in Brazil and when international athletes and tourists returned home and possibly would spread the virus. Some researchers speculated that only one or two tourists might be infected during the three-week period, or approximately 3.2 infections per 100,000 tourists. In November 2016, the World Health Organization declared that Zika virus was no longer a global emergency while noting that the virus still represents "a highly significant and a long-term problem". As of August 2017 the number of new Zika virus cases in the Americas had fallen dramatically. On May 15, 2017, three cases of Zika virus infection in India were reported in the state of Gujarat . By late 2018, there had been at least 159 cases in Rajasthan and 127 in Madhya Pradesh . In July 2021, the first case of Zika virus infection in the Indian state of Kerala was reported. After the first confirmed case, 19 other people who had previously presented symptoms were tested, and 13 of those had positive results, showing that Zika had been circulating in Kerala since at least May 2021. By August 6th 2021, there had been 65 reported cases in Kerala. On October 22, 2021, an officer in the Indian Air Force in Kanpur tested positive for Zika virus, making it the first reported case in the Indian state of Uttar Pradesh . On 22 March 2016, Reuters reported that Zika was isolated from a 2014 blood sample of an elderly man in Chittagong in Bangladesh as part of a retrospective study . Between August and November 2016, 455 cases of Zika virus infection were confirmed in Singapore . In 2023, 722 Zika virus cases were reported in Thailand. From 2019-2022 the Robert Koch-Institut reported 29 imported Zikavirus cases imported into Germany. Of the altogether 16 imported Zika virus cases in 2023, 10 were diagnosed after a trip to Thailand with 62% of all Zika virus cases a significant relative and absolute increase. The virus was first isolated in April 1947 from a rhesus macaque monkey placed in a cage in the Ziika Forest of Uganda , near Lake Victoria , by the scientists of the Yellow Fever Research Institute . A second isolation from the mosquito A. africanus followed at the same site in January 1948. When the monkey developed a fever, researchers isolated from its serum a "filterable transmissible agent" which was named Zika in 1948. Zika was first known to infect humans from the results of a serological survey in Uganda, published in 1952. Of 99 human blood samples tested, 6.1% had neutralizing antibodies. As part of a 1954 outbreak investigation of jaundice suspected to be yellow fever, researchers reported isolation of the virus from a patient, but the pathogen was later shown to be the closely related Spondweni virus . Spondweni was also determined to be the cause of a self-inflicted infection in a researcher reported in 1956. Subsequent serological studies in several African and Asian countries indicated the virus had been widespread within human populations in these regions. The first true case of human infection was identified by Simpson in 1964, who was himself infected while isolating the virus from mosquitoes. From then until 2007, there were only 13 further confirmed human cases of Zika infection from Africa and Southeast Asia. A study published in 2017 showed that the Zika virus, despite only a few cases were reported, has been silently circulated in West Africa for the last two decades when blood samples collected between 1992 and 2016 were tested for the ZIKV IgM antibodies. In 2017, Angola reported two cases of Zika fever. Zika was also occurring in Tanzania as of 2016. In April 2007, the first outbreak outside of Africa and Asia occurred on the island of Yap in the Federated States of Micronesia, characterized by rash, conjunctivitis, and arthralgia, which was initially thought to be dengue, chikungunya , or Ross River disease . Serum samples from patients in the acute phase of illness contained RNA of Zika. There were 49 confirmed cases, 59 unconfirmed cases, no hospitalizations, and no deaths. After October 2013 Oceania's first outbreak showed an estimated 11% population infected for French Polynesia that also presented with Guillain–Barre syndrome (GBS). The spread of ZIKV continued to New Caledonia, Easter Island, and the Cook Islands and where 1385 cases were confirmed by January 2014. During the same year, Easter Island acknowledged 51 cases. Australia began seeing cases in 2012. Research showed it was brought by travelers returning from Indonesia and other infected countries. New Zealand also experienced infections rate increases through returning foreign travelers. Oceania countries experiencing Zika today are New Caledonia, Vanuatu, Solomon Islands, Marshall Islands, American Samoa, Samoa, and Tonga. Between 2013 and 2014, further epidemics occurred in French Polynesia , Easter Island , the Cook Islands , and New Caledonia . There was an epidemic in 2015 and 2016 in the Americas . The outbreak began in April 2015 in Brazil , and spread to other countries in South America , Central America , North America , and the Caribbean . In January 2016, the WHO said the virus was likely to spread throughout most of the Americas by the end of the year; and in February 2016, the WHO declared the cluster of microcephaly and Guillain–Barré syndrome cases reported in Brazil – strongly suspected to be associated with the Zika outbreak – a Public Health Emergency of International Concern . It was estimated that 1.5 million people were infected by Zika in Brazil, with over 3,500 cases of microcephaly reported between October 2015 and January 2016. A number of countries issued travel warnings , and the outbreak was expected to significantly impact the tourism industry. Several countries have taken the unusual step of advising their citizens to delay pregnancy until more is known about the virus and its impact on fetal development. With the 2016 Summer Olympics hosted in Rio de Janeiro , health officials worldwide voiced concerns over a potential crisis, both in Brazil and when international athletes and tourists returned home and possibly would spread the virus. Some researchers speculated that only one or two tourists might be infected during the three-week period, or approximately 3.2 infections per 100,000 tourists. In November 2016, the World Health Organization declared that Zika virus was no longer a global emergency while noting that the virus still represents "a highly significant and a long-term problem". As of August 2017 the number of new Zika virus cases in the Americas had fallen dramatically. On May 15, 2017, three cases of Zika virus infection in India were reported in the state of Gujarat . By late 2018, there had been at least 159 cases in Rajasthan and 127 in Madhya Pradesh . In July 2021, the first case of Zika virus infection in the Indian state of Kerala was reported. After the first confirmed case, 19 other people who had previously presented symptoms were tested, and 13 of those had positive results, showing that Zika had been circulating in Kerala since at least May 2021. By August 6th 2021, there had been 65 reported cases in Kerala. On October 22, 2021, an officer in the Indian Air Force in Kanpur tested positive for Zika virus, making it the first reported case in the Indian state of Uttar Pradesh . On 22 March 2016, Reuters reported that Zika was isolated from a 2014 blood sample of an elderly man in Chittagong in Bangladesh as part of a retrospective study . Between August and November 2016, 455 cases of Zika virus infection were confirmed in Singapore . In 2023, 722 Zika virus cases were reported in Thailand. From 2019-2022 the Robert Koch-Institut reported 29 imported Zikavirus cases imported into Germany. Of the altogether 16 imported Zika virus cases in 2023, 10 were diagnosed after a trip to Thailand with 62% of all Zika virus cases a significant relative and absolute increase.

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Rift Valley fever

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Hantavirus hemorrhagic fever with renal syndrome

Hantavirus hemorrhagic fever with renal syndrome ( HFRS ) is a group of clinically similar illnesses caused by species of hantaviruses . It is also known as Korean hemorrhagic fever and epidemic hemorrhagic fever . It is found in Europe, Asia, and Africa. The species that cause HFRS include Hantaan orthohantavirus , Dobrava-Belgrade orthohantavirus , Saaremaa virus , Seoul orthohantavirus , Puumala orthohantavirus and other orthohantaviruses. Of these species, Hantaan River virus and Dobrava-Belgrade virus cause the most severe form of the syndrome and have the highest morbidity rates. When caused by the Puumala virus, it is also called nephropathia epidemica . This infection is known as sorkfeber (vole fever) in Swedish, myyräkuume (vole fever) in Finnish, and musepest (mouse plague) in Norwegian. Both HFRS and hantavirus pulmonary syndrome (HPS) are caused by hantaviruses, specifically when humans inhale aerosolized excrements of infected rodents. Both diseases appear to be immunopathologic , and inflammatory mediators are important in causing the clinical manifestations. Symptoms of HFRS usually develop within one to two weeks after exposure to infectious material, but in rare cases, they may take up to eight weeks to develop. In Nephropathia epidemica, the incubation period is three weeks. Initial symptoms begin suddenly and include intense headaches, back and abdominal pain, fever, chills, nausea, and blurred vision. Individuals may have flushing of the face, inflammation or redness of the eyes, or a rash. Later symptoms can include low blood pressure, acute shock, vascular leakage, and acute kidney failure, which can cause severe fluid overload. The severity of the disease varies depending upon the virus causing the infection. Hantaan and Dobrava virus infections usually cause severe symptoms, while Seoul, Saaremaa, and Puumala virus infections are usually more moderate. Complete recovery can take weeks or months. The course of the illness can be split into five phases: This syndrome can also be fatal. In some cases, it has been known to cause permanent renal failure. Hantaviruses infect various rodents, generally without causing disease. Transmission by aerosolized rodent excreta still remains the only known way the virus is transmitted to humans. In general, droplet and/or fomite transfer has not been shown in the hantaviruses in either the pulmonary or hemorrhagic forms. For Nephropathia epidemica, the bank vole is the reservoir for the virus, which humans contract through inhalation of aerosolised vole droppings. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a one-week interval and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. HFRS should be suspected in patients with acute febrile flu-like illness, kidney failure of unknown origin and sometimes liver dysfunction. Rodent control in and around the home remains the primary prevention strategy, as well as eliminating contact with rodents in the workplace and campsite. Closed storage sheds and cabins are often ideal sites for rodent infestations. Airing out of such spaces prior to use is recommended. Avoid direct contact with rodent droppings and wear a mask to avoid inhalation of aerosolized rodent secretions. There is no cure for HFRS. Treatment involves supportive therapy including renal dialysis. Treatment with ribavirin in China and Korea, administered within seven days of onset of fever, resulted in a reduced mortality as well as shortened course of illness. HFRS is primarily a Eurasian disease, whereas HPS appears to be confined to the Americas. The geography is directly related to the indigenous rodent hosts and the viruses that coevolved with them. Although fatal in a small percentage of cases, nephropathia epidemica is generally milder than the HFRS that is caused by hantaviruses in other parts of the world. HFRS was the subject of an episode of the television series M*A*S*H. In season 8, episode 9 the 4077th dealt with a condition, with similar symptoms to HFRS, called "Korean Hemorrhagic Fever".

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Rift Valley fever

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Lassa mammarenavirus

Lassa virus Lassa mammarenavirus ( LASV ) is an arenavirus that causes Lassa hemorrhagic fever , a type of viral hemorrhagic fever (VHF), in humans and other primates . Lassa mammarenavirus is an emerging virus and a select agent , requiring Biosafety Level 4-equivalent containment . It is endemic in West African countries, especially Sierra Leone , the Republic of Guinea , Nigeria , and Liberia , where the annual incidence of infection is between 300,000 and 500,000 cases, resulting in 5,000 deaths per year. As of 2012 discoveries within the Mano River region of west Africa have expanded the endemic zone between the two known Lassa endemic regions, indicating that LASV is more widely distributed throughout the tropical wooded savannah ecozone in west Africa. There are no approved vaccines against Lassa fever for use in humans. In 1969, missionary nurse Laura Wine fell ill with a mysterious disease she contracted from an obstetrical patient in Lassa, a village in Borno State , Nigeria. She was then transported to Jos , where she died. Subsequently, two others became infected, one of whom was fifty-two-year-old nurse Lily Pinneo who had cared for Laura Wine. Samples from Pinneo were sent to Yale University in New Haven where a new virus, that would later be known as Lassa mammarenavirus , was isolated for the first time by Jordi Casals-Ariet , Sonja Buckley , and others. Casals contracted the fever, and nearly lost his life; one technician died from it. By 1972, the multimammate rat, Mastomys natalensis , was found to be the main reservoir of the virus in West Africa, able to shed virus in its urine and feces without exhibiting visible symptoms. Lassa viruses are enveloped, single-stranded, bisegmented, ambisense RNA viruses . Their genome is contained in two RNA segments that code for two proteins each, one in each sense, for a total of four viral proteins. The large segment encodes a small zinc finger protein (Z) that regulates transcription and replication, and the RNA polymerase (L). The small segment encodes the nucleoprotein (NP) and the surface glycoprotein precursor (GP, also known as the viral spike ), which is proteolytically cleaved into the envelope glycoproteins GP1 and GP2 that bind to the alpha-dystroglycan receptor and mediate host cell entry. Lassa fever causes hemorrhagic fever frequently shown by immunosuppression. Lassa mammarenavirus replicates very rapidly, and demonstrates temporal control in replication. The first replication step is transcription of mRNA copies of the negative- or minus-sense genome. This ensures an adequate supply of viral proteins for subsequent steps of replication, as the NP and L proteins are translated from the mRNA. The positive- or plus-sense genome, then makes viral complementary RNA (vcRNA) copies of itself. The RNA copies are a template for producing negative-sense progeny, but mRNA is also synthesized from it. The mRNA synthesized from vcRNA are translated to make the GP and Z proteins. This temporal control allows the spike proteins to be produced last, and therefore, delay recognition by the host immune system. [ citation needed ] Nucleotide studies of the genome have shown that Lassa has four lineages: three found in Nigeria and the fourth in Guinea, Liberia, and Sierra Leone. The Nigerian strains seem likely to have been ancestral to the others but additional work is required to confirm this. Lassa mammarenavirus gains entry into the host cell by means of the cell-surface receptor the alpha-dystroglycan (alpha-DG), a versatile receptor for proteins of the extracellular matrix . It shares this receptor with the prototypic Old World arenavirus lymphocytic choriomeningitis virus . Receptor recognition depends on a specific sugar modification of alpha-dystroglycan by a group of glycosyltransferases known as the LARGE proteins. Specific variants of the genes encoding these proteins appear to be under positive selection in West Africa where Lassa is endemic. Alpha-dystroglycan is also used as a receptor by viruses of the New World clade C arenaviruses (Oliveros and Latino viruses). In contrast, the New World arenaviruses of clades A and B, which include the important viruses Machupo , Guanarito , Junin , and Sabia in addition to the non pathogenic Amapari virus, use the transferrin receptor 1 . A small aliphatic amino acid at the GP1 glycoprotein amino acid position 260 is required for high-affinity binding to alpha-DG. In addition, GP1 amino acid position 259 also appears to be important, since all arenaviruses showing high-affinity alpha-DG binding possess a bulky aromatic amino acid (tyrosine or phenylalanine) at this position. [ citation needed ] Unlike most enveloped viruses which use clathrin coated pits for cellular entry and bind to their receptors in a pH dependent fashion, Lassa and lymphocytic choriomeningitis virus instead use an endocytotic pathway independent of clathrin, caveolin , dynamin and actin . Once within the cell the viruses are rapidly delivered to endosomes via vesicular trafficking albeit one that is largely independent of the small GTPases Rab5 and Rab7 . On contact with the endosome pH-dependent membrane fusion occurs mediated by the envelope glycoprotein, which at the lower pH of the endosome binds the lysosome protein LAMP1 which results in membrane fusion and escape from the endosome. [ citation needed ] The life cycle of Lassa mammarenavirus is similar to the Old World arenaviruses. Lassa mammarenavirus enters the cell by the receptor-mediated endocytosis . Which endocytotic pathway is used is not known yet, but at least the cellular entry is sensitive to cholesterol depletion. It was reported that virus internalization is limited upon cholesterol depletion. The receptor used for cell entry is alpha- dystroglycan , a highly conserved and ubiquitously expressed cell surface receptor for extracellular matrix proteins. Dystroglycan, which is later cleaved into alpha-dystroglycan and beta-dystroglycan is originally expressed in most cells to mature tissues, and it provides molecular link between the ECM and the actin-based cytoskeleton. After the virus enters the cell by alpha-dystroglycan mediated endocytosis, the low-pH environment triggers pH-dependent membrane fusion and releases RNP (viral ribonucleoprotein) complex into the cytoplasm. Viral RNA is unpacked, and replication and transcription initiate in the cytoplasm. As replication starts, both S and L RNA genomes synthesize the antigenomic S and L RNAs, and from the antigenomic RNAs, genomic S and L RNA are synthesized. Both genomic and antigenomic RNAs are needed for transcription and translation . The S RNA encodes GP and NP (viral nucleocapsid protein) proteins, while L RNA encodes Z and L proteins. The L protein most likely represents the viral RNA-dependent RNA polymerase. When the cell is infected by the virus, L polymerase is associated with the viral RNP and initiates the transcription of the genomic RNA. The 5' and 3' terminal 19 nt viral promoter regions of both RNA segments are necessary for recognition and binding of the viral polymerase . The primary transcription first transcribes mRNAs from the genomic S and L RNAs, which code NP and L proteins, respectively. Transcription terminates at the stem-loop (SL) structure within the intergenomic region. Arenaviruses use a cap snatching strategy to gain the cap structures from the cellular mRNAs, and it is mediated by the endonuclease activity of the L polymerase and the cap binding activity of NP. Antigenomic RNA transcribes viral genes GPC and Z, encoded in genomic orientation, from S and L segments respectively. The antigenomic RNA also serves as the template for the replication. After translation of GPC, it is posttranslationally modified in the endoplasmic reticulum . GPC is cleaved into GP1 and GP2 at the later stage of the secretory pathway. It has been reported that the cellular protease SKI-1/S1P is responsible for this cleavage. The cleaved glycoproteins are incorporated into the virion envelope when the virus buds and release from the cell membrane. Lassa viruses are enveloped, single-stranded, bisegmented, ambisense RNA viruses . Their genome is contained in two RNA segments that code for two proteins each, one in each sense, for a total of four viral proteins. The large segment encodes a small zinc finger protein (Z) that regulates transcription and replication, and the RNA polymerase (L). The small segment encodes the nucleoprotein (NP) and the surface glycoprotein precursor (GP, also known as the viral spike ), which is proteolytically cleaved into the envelope glycoproteins GP1 and GP2 that bind to the alpha-dystroglycan receptor and mediate host cell entry. Lassa fever causes hemorrhagic fever frequently shown by immunosuppression. Lassa mammarenavirus replicates very rapidly, and demonstrates temporal control in replication. The first replication step is transcription of mRNA copies of the negative- or minus-sense genome. This ensures an adequate supply of viral proteins for subsequent steps of replication, as the NP and L proteins are translated from the mRNA. The positive- or plus-sense genome, then makes viral complementary RNA (vcRNA) copies of itself. The RNA copies are a template for producing negative-sense progeny, but mRNA is also synthesized from it. The mRNA synthesized from vcRNA are translated to make the GP and Z proteins. This temporal control allows the spike proteins to be produced last, and therefore, delay recognition by the host immune system. [ citation needed ] Nucleotide studies of the genome have shown that Lassa has four lineages: three found in Nigeria and the fourth in Guinea, Liberia, and Sierra Leone. The Nigerian strains seem likely to have been ancestral to the others but additional work is required to confirm this. Lassa mammarenavirus gains entry into the host cell by means of the cell-surface receptor the alpha-dystroglycan (alpha-DG), a versatile receptor for proteins of the extracellular matrix . It shares this receptor with the prototypic Old World arenavirus lymphocytic choriomeningitis virus . Receptor recognition depends on a specific sugar modification of alpha-dystroglycan by a group of glycosyltransferases known as the LARGE proteins. Specific variants of the genes encoding these proteins appear to be under positive selection in West Africa where Lassa is endemic. Alpha-dystroglycan is also used as a receptor by viruses of the New World clade C arenaviruses (Oliveros and Latino viruses). In contrast, the New World arenaviruses of clades A and B, which include the important viruses Machupo , Guanarito , Junin , and Sabia in addition to the non pathogenic Amapari virus, use the transferrin receptor 1 . A small aliphatic amino acid at the GP1 glycoprotein amino acid position 260 is required for high-affinity binding to alpha-DG. In addition, GP1 amino acid position 259 also appears to be important, since all arenaviruses showing high-affinity alpha-DG binding possess a bulky aromatic amino acid (tyrosine or phenylalanine) at this position. [ citation needed ] Unlike most enveloped viruses which use clathrin coated pits for cellular entry and bind to their receptors in a pH dependent fashion, Lassa and lymphocytic choriomeningitis virus instead use an endocytotic pathway independent of clathrin, caveolin , dynamin and actin . Once within the cell the viruses are rapidly delivered to endosomes via vesicular trafficking albeit one that is largely independent of the small GTPases Rab5 and Rab7 . On contact with the endosome pH-dependent membrane fusion occurs mediated by the envelope glycoprotein, which at the lower pH of the endosome binds the lysosome protein LAMP1 which results in membrane fusion and escape from the endosome. [ citation needed ]The life cycle of Lassa mammarenavirus is similar to the Old World arenaviruses. Lassa mammarenavirus enters the cell by the receptor-mediated endocytosis . Which endocytotic pathway is used is not known yet, but at least the cellular entry is sensitive to cholesterol depletion. It was reported that virus internalization is limited upon cholesterol depletion. The receptor used for cell entry is alpha- dystroglycan , a highly conserved and ubiquitously expressed cell surface receptor for extracellular matrix proteins. Dystroglycan, which is later cleaved into alpha-dystroglycan and beta-dystroglycan is originally expressed in most cells to mature tissues, and it provides molecular link between the ECM and the actin-based cytoskeleton. After the virus enters the cell by alpha-dystroglycan mediated endocytosis, the low-pH environment triggers pH-dependent membrane fusion and releases RNP (viral ribonucleoprotein) complex into the cytoplasm. Viral RNA is unpacked, and replication and transcription initiate in the cytoplasm. As replication starts, both S and L RNA genomes synthesize the antigenomic S and L RNAs, and from the antigenomic RNAs, genomic S and L RNA are synthesized. Both genomic and antigenomic RNAs are needed for transcription and translation . The S RNA encodes GP and NP (viral nucleocapsid protein) proteins, while L RNA encodes Z and L proteins. The L protein most likely represents the viral RNA-dependent RNA polymerase. When the cell is infected by the virus, L polymerase is associated with the viral RNP and initiates the transcription of the genomic RNA. The 5' and 3' terminal 19 nt viral promoter regions of both RNA segments are necessary for recognition and binding of the viral polymerase . The primary transcription first transcribes mRNAs from the genomic S and L RNAs, which code NP and L proteins, respectively. Transcription terminates at the stem-loop (SL) structure within the intergenomic region. Arenaviruses use a cap snatching strategy to gain the cap structures from the cellular mRNAs, and it is mediated by the endonuclease activity of the L polymerase and the cap binding activity of NP. Antigenomic RNA transcribes viral genes GPC and Z, encoded in genomic orientation, from S and L segments respectively. The antigenomic RNA also serves as the template for the replication. After translation of GPC, it is posttranslationally modified in the endoplasmic reticulum . GPC is cleaved into GP1 and GP2 at the later stage of the secretory pathway. It has been reported that the cellular protease SKI-1/S1P is responsible for this cleavage. The cleaved glycoproteins are incorporated into the virion envelope when the virus buds and release from the cell membrane. Lassa fever is caused by the Lassa mammarenavirus . The symptoms include flu-like illness characterized by fever, general weakness, cough, sore throat, headache, and gastrointestinal manifestations. Hemorrhagic manifestations include vascular permeability. Upon entry, the Lassa mammarenavirus infects almost every tissue in the human body. It starts with the mucosa , intestine, lungs and urinary system, and then progresses to the vascular system. The main targets of the virus are antigen-presenting cells , mainly dendritic cells and endothelial cells. In 2012 it was reported how Lassa mammarenavirus nucleoprotein (NP) sabotages the host's innate immune system response. Generally, when a pathogen enters into a host, innate defense system recognizes the pathogen-associated molecular patterns (PAMP) and activates an immune response. One of the mechanisms detects double stranded RNA (dsRNA), which is only synthesized by negative-sense viruses . In the cytoplasm, dsRNA receptors, such as RIG-I (retinoic acid-inducible gene I) and MDA-5 (melanoma differentiation associated gene 5), detect dsRNAs and initiate signaling pathways that translocate IRF-3 ( interferon regulatory factor 3) and other transcription factors to the nucleus. Translocated transcription factors activate expression of interferons 𝛂 and 𝛃, and these initiate adaptive immunity . NP encoded in Lassa mammarenavirus is essential in viral replication and transcription, but it also suppresses host innate IFN response by inhibiting translocation of IRF-3. NP of Lassa mammarenavirus is reported to have an exonuclease activity to only dsRNAs. the NP dsRNA exonuclease activity counteracts IFN responses by digesting the PAMPs thus allowing the virus to evade host immune responses.

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Rift Valley fever

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Riboviria

Riboviria is a realm of viruses that includes all viruses that use a homologous RNA-dependent polymerase for replication. It includes RNA viruses that encode an RNA-dependent RNA polymerase , as well as reverse-transcribing viruses (with either RNA or DNA genomes) that encode an RNA-dependent DNA polymerase . RNA-dependent RNA polymerase (RdRp), also called RNA replicase, produces RNA ( ribonucleic acid ) from RNA. RNA-dependent DNA polymerase (RdDp), also called reverse transcriptase (RT), produces DNA ( deoxyribonucleic acid ) from RNA. These enzymes are essential for replicating the viral genome and transcribing viral genes into messenger RNA (mRNA) for translation of viral proteins . Riboviria was established in 2018 to accommodate all RdRp-encoding RNA viruses and was expanded a year later to also include RdDp-encoding retroviruses . These two groups of viruses are assigned to two separate kingdoms: Orthornavirae for RdRp-encoding RNA viruses, and Pararnavirae for RdDp-encoding viruses, i.e. all reverse-transcribing viruses. While the realm has few prokaryotic viruses, it includes most eukaryotic viruses, including most human, animal, and plant viruses, however, metagenomic studies are changing this perspective. Many of the most widely known viral diseases are caused by viruses in Riboviria , which includes coronaviruses , ebola virus , HIV , influenza viruses , and the rabies virus . These viruses and others have been prominent throughout history, including Tobacco mosaic virus , which was the first virus to be discovered. Many reverse transcribing viruses notably become integrated into the genome of their host as part of their replication cycle. As a result of that, it is estimated that about 7–8% of the human genome originates from these viruses.Riboviria is a portmanteau of ribo , referencing ribonucleic acid, and the suffix - viria , which is the suffix used for virus realms. All members of Riboviria contain a gene that encodes for an RNA-dependent polymerase, also called RNA-directed polymerase. There are two types of RNA-dependent polymerases: RNA-dependent RNA polymerase (RdRp), also called RNA replicase, which synthesizes RNA from RNA, and RNA-dependent DNA polymerase (RdDp), also called reverse transcriptase (RT), which synthesizes DNA from RNA. In a typical virus particle, called a virion, the RNA-dependent polymerase is bound to the viral genome in some manner and begins transcription of the viral genome after entering a cell . As part of a virus's life cycle , the RNA-dependent polymerase also synthesizes copies of the viral genome as part of the process of creating new viruses. Viruses that replicate via RdRp belong to three groups in the Baltimore classification system, all of which are in the kingdom Orthornavirae : single-stranded RNA (ssRNA) viruses, which are either positive (+) or negative (-) sense , and double-stranded RNA viruses (dsRNA). +ssRNA viruses have genomes that can functionally act as mRNA, and a negative sense strand can also be created to form dsRNA from which mRNA is transcribed from the negative strand. The genomes of -ssRNA viruses and dsRNA viruses act as templates from which RdRp creates mRNA. Viruses that replicate via reverse transcription belong to two Baltimore groups, both of which are in the kingdom Pararnavirae : single-stranded RNA (ssRNA-RT) viruses, all of which belong to the order Ortervirales , and double-stranded DNA (dsDNA-RT) viruses, which belong to the family Caulimoviridae , also in Ortervirales , and the family Hepadnaviridae of the order Blubervirales . ssRNA-RT viruses have their positive-sense genome transcribed by RdDp to synthesize a negative sense complementary DNA (-cDNA) strand. The +RNA strand is degraded and later replaced by RdDp with a +DNA strand to synthesize a linear dsDNA copy of the viral genome. This genome is then integrated into the host cell's DNA. For dsDNA-RT viruses, a pregenomic +RNA strand is transcribed from the relaxed circular DNA (rcDNA), which is in turn used by RdDp to transcribe a -cDNA strand. The +RNA strand is degraded and replaced in a similar manner as +ssRNA-RT viruses to synthesize the rcDNA. The rcDNA genome is later repaired by the host cell's DNA repair mechanisms to synthesize a covalently closed circular DNA (cccDNA) genome. The integrated genome of +ssRNA-RT viruses and the cccDNA of dsDNA-RT viruses are then transcribed into mRNA by the host cell enzyme RNA polymerase II . Viral mRNA is translated by the host cell's ribosomes to produce viral proteins. In order to produce more viruses, viral RNA-dependent polymerases use copies of the viral genome as templates to replicate the viral genome. For +ssRNA viruses, an intermediate dsRNA genome is created from which +ssRNA is synthesized from the negative strand. For -ssRNA viruses, genomes are synthesized from complementary positive sense strands. dsRNA viruses replicate their genomes from mRNA by synthesizing a complementary negative sense strand to form genomic dsRNA. For dsDNA-RT viruses, pregenomic RNA created from the cccDNA is retrotranscribed into new dsDNA genomes. For +ssRNA-RT viruses, the genome is replicated from the integrated genome. After replication and translation, the genome and the viral proteins are assembled into complete virions, which then leave the host cell .Both kingdoms in Riboviria show a relation to the reverse transcriptases of group II introns that encode RTs and retrotransposons , which are self-replicating DNA sequences, the latter of which self-replicate via reverse transcription and integrate themselves into other parts of the same DNA molecule. Reverse transcribing viruses, assigned to Pararnavirae , appear to have evolved from a retrotransposon on a single occasion. The origin of the RdRps of Orthornavirae is less clear due to a lack of information, that they originate from a reverse transcriptase from bacterial group II intron before the emergence of eukaryotes or originated before the last universal common ancestor (LUCA) being descendants of the ancient RNA world and that they preceded the retroelement reverse transcriptases. A larger study (2022) where new lineages (phyla) were described, was in favor of the hypothesis that RNA viruses descend from the RNA world, suggesting that retroelements originated from an ancestor related to the phylum Lenarviricota and that members of a newly discovered Taraviricota lineage (phylum) would be the ancestors of all RNA viruses. Riboviria contains two kingdoms: Orthornavirae and Pararnavirae . Orthornavirae contains multiple phyla and unassigned taxa, whereas Pararnavirae is monotypic down to the rank of class. This taxonomy can be visualized hereafter. Additionally, Riboviria contains two incertae sedis families and four incertae sedis genera. Additional information about them is needed to know their exact placement in higher taxa. Metagenomic studies have suggested the existence of six new phyla not in the ICTV: Arctiviricota , Taraviricota , Pomiviricota , Paraxenoviricota , Wamoviricota and Artimaviricota . Riboviria partially merges Baltimore classification with virus taxonomy, including the Baltimore groups for RNA viruses and reverse transcribing viruses in the realm. Baltimore classification is a classification system used for viruses based on their manner of mRNA production, often used alongside standard virus taxonomy, which is based on evolutionary history. All members of five Baltimore groups belong to Riboviria : Group III: dsRNA viruses, Group IV: +ssRNA viruses, Group V: -ssRNA viruses, Group VI: ssRNA-RT viruses, and Group VII: dsDNA-RT viruses. Realms are the highest level of taxonomy used for viruses and Riboviria is one of four, the other three being Duplodnaviria , Monodnaviria , and Varidnaviria . Most identified eukaryotic viruses are RNA viruses, and for that reason most eukaryotic viruses belong to Riboviria , including most human, animal, and plant viruses. Other major branches of eukaryotic viruses include herpesviruses in Duplodnaviria , the kingdom Shotokuvirae in Monodnaviria , and many viruses in Varidnaviria . In contrast, only three groups of prokaryotic RNA viruses have been identified: the class Leviviricetes , the family Cystoviridae and the phylum Artimaviricota . They also suggest that families Picobirnaviridae and Partitiviridae previously associated with eukaryotes also infect prokaryotes and also the phylum Taraviricota . Studies of metagenomic samples have uncovered new prokaryotic RNA virus taxa including two new phyla that infect only prokaryotes, suggesting that their diversity is greater than previously thought and challenging the traditional view that RNA viruses only infect mostly eukaryotes. Viruses in Riboviria are associated with a wide range of diseases, including many of the most widely known viral diseases. Notable disease-causing viruses in the realm include: Animal viruses in Riboviria include orbiviruses , which cause various diseases in ruminants and horses, including Bluetongue virus , African horse sickness virus , Equine encephalosis virus , and epizootic hemorrhagic disease virus . The vesicular stomatitis virus causes disease in cattle, horses, and pigs. Bats harbor many viruses including ebolaviruses and henipaviruses , which also can cause disease in humans. Similarly, arthropod viruses in the Flavivirus and Phlebovirus genera are numerous and often transmitted to humans. Coronaviruses and influenza viruses cause disease in various vertebrates, including bats, birds, and pigs. The family Retroviridae contains many viruses that cause leukemia , immunodeficiency , and other cancers and immune system-related diseases in animals. Plant viruses in the realm are numerous and infect many economically important crops. Tomato spotted wilt virus is estimated to cause more than US$1 billion in damages annually, affecting more than 800 plant species including chrysanthemum, lettuce, peanut, pepper, and tomato. Cucumber mosaic virus infects more than 1,200 plant species and likewise causes significant crop losses. Potato virus Y causes significant reductions in yield and quality for pepper, potato, tobacco, and tomato, and Plum pox virus is the most important virus among stone fruit crops. Brome mosaic virus , while not causing significant economic losses, is found throughout much of the world and primarily infects grasses, including cereals. Many reverse transcribing viruses, called retroviruses, in Riboviria are able to become integrated into the DNA of their host. These viruses become endogenized as part of their replication cycle. Namely, the viral genome is integrated into the host genome by the retroviral enzyme integrase, and viral mRNA is produced from that DNA. Endogenization is a form of horizontal gene transfer between unrelated organisms, and it is estimated that about 7–8% of the human genome consists of retroviral DNA. Endogenization can also be used to study the evolutionary history of viruses, showing an approximate time period when a virus first became endogenized into the host's genome as well as the rate of evolution for the viruses since endogenization first occurred. Viruses in Riboviria are associated with a wide range of diseases, including many of the most widely known viral diseases. Notable disease-causing viruses in the realm include: Animal viruses in Riboviria include orbiviruses , which cause various diseases in ruminants and horses, including Bluetongue virus , African horse sickness virus , Equine encephalosis virus , and epizootic hemorrhagic disease virus . The vesicular stomatitis virus causes disease in cattle, horses, and pigs. Bats harbor many viruses including ebolaviruses and henipaviruses , which also can cause disease in humans. Similarly, arthropod viruses in the Flavivirus and Phlebovirus genera are numerous and often transmitted to humans. Coronaviruses and influenza viruses cause disease in various vertebrates, including bats, birds, and pigs. The family Retroviridae contains many viruses that cause leukemia , immunodeficiency , and other cancers and immune system-related diseases in animals. Plant viruses in the realm are numerous and infect many economically important crops. Tomato spotted wilt virus is estimated to cause more than US$1 billion in damages annually, affecting more than 800 plant species including chrysanthemum, lettuce, peanut, pepper, and tomato. Cucumber mosaic virus infects more than 1,200 plant species and likewise causes significant crop losses. Potato virus Y causes significant reductions in yield and quality for pepper, potato, tobacco, and tomato, and Plum pox virus is the most important virus among stone fruit crops. Brome mosaic virus , while not causing significant economic losses, is found throughout much of the world and primarily infects grasses, including cereals. Many reverse transcribing viruses, called retroviruses, in Riboviria are able to become integrated into the DNA of their host. These viruses become endogenized as part of their replication cycle. Namely, the viral genome is integrated into the host genome by the retroviral enzyme integrase, and viral mRNA is produced from that DNA. Endogenization is a form of horizontal gene transfer between unrelated organisms, and it is estimated that about 7–8% of the human genome consists of retroviral DNA. Endogenization can also be used to study the evolutionary history of viruses, showing an approximate time period when a virus first became endogenized into the host's genome as well as the rate of evolution for the viruses since endogenization first occurred. Diseases caused by viruses in Riboviria have been known for much of recorded history, though their cause was only discovered in modern times. Tobacco mosaic virus was discovered in 1898 and was the first virus to be discovered. Viruses transmitted by arthropods have been central in the development of vector control , which often aims to prevent viral infections. In modern history, numerous disease outbreaks have been caused by various members of the realm, including coronaviruses, ebola, and influenza. HIV especially has had dramatic effects on society as it causes a sharp decline in life expectancy and significant stigma for infected persons. For a long time, the relation between many viruses in Riboviria could not be established due to the high amount of genetic divergence among RNA viruses. With the development of viral metagenomics , many additional RNA viruses were identified, helping to fill in the gaps of their relations. This led to the establishment of Riboviria in 2018 to accommodate all RdRp-encoding RNA viruses based on phylogenetic analysis that they were related. A year later, all reverse transcribing viruses were added to the realm. The kingdoms were also established in 2019, separating the two RNA-dependent polymerase branches. When the realm was founded, it mistakenly included two viroid families, Avsunviroidae and Pospiviroidae , and the genus Deltavirus , which were promptly removed in 2019 because they use host cell enzymes for replication.

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Rift Valley fever

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List of diseases (R)

This is a list of diseases starting with the letter "R".

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Rift Valley fever

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Henipavirus

Henipavirus is a genus of negative-strand RNA viruses in the family Paramyxoviridae , order Mononegavirales containing six established species, and numerous others still under study. Henipaviruses are naturally harboured by several species of small mammals, notably pteropid fruit bats (flying foxes), microbats of several species, and shrews . Henipaviruses are characterised by long genomes and a wide host range. Their recent emergence as zoonotic pathogens capable of causing illness and death in domestic animals and humans is a cause of concern. In 2009, RNA sequences of three novel viruses in phylogenetic relationship to known henipaviruses were detected in African straw-colored fruit bats ( Eidolon helvum ) in Ghana . The finding of these novel henipaviruses outside Australia and Asia indicates that the region of potential endemicity of henipaviruses may be worldwide. These African henipaviruses are slowly being characterised. Nipah and Hendra henipaviruses are both considered category C (USDA-HHS overlap) select agents . Henipavirions are pleomorphic (variably shaped), ranging in size from 40 to 600 nm in diameter. They possess a lipid membrane overlying a shell of viral matrix protein . At the core is a single helical strand of genomic RNA tightly bound to N ( nucleocapsid ) protein and associated with the L (large) and P (phosphoprotein) proteins, which provide RNA polymerase activity during replication. Embedded within the lipid membrane are spikes of F (fusion) protein trimers and G (attachment) protein tetramers. The function of the G protein (except in the case of MojV-G) is to attach the virus to the surface of a host cell via Ephrin B1, B2, or B3 , a family of highly conserved mammalian proteins. The structure of the attachment glycoprotein has been determined by X-ray crystallography. The F protein fuses the viral membrane with the host cell membrane, releasing the virion contents into the cell. It also causes infected cells to fuse with neighbouring cells to form large, multinucleated syncytia .As all mononegaviral genomes, Hendra virus and Nipah virus genomes are non-segmented, single-stranded negative-sense RNA. Both genomes are 18.2 kb in length and contain six genes corresponding to six structural proteins. In common with other members of the Paramyxoviridae family, the number of nucleotides in the henipavirus genome is a multiple of six, consistent with what is known as the ' rule of six '. Deviation from the rule of six, through mutation or incomplete genome synthesis, leads to inefficient viral replication, probably due to structural constraints imposed by the binding between the RNA and the N protein. Three additional protein products are produced from the henipavirus P gene: V, W, and C. The V and W proteins are generated through an unusual process called RNA editing . This specific process in henipaviruses involves the insertion of extra guanosine residues into the P gene mRNA prior to translation . The addition of a single guanosine results in production of V, and the addition of two guanosines residues produces W. The C protein is not produced through RNA editing but instead by leaky scanning of the host cell ribosome during translation of viral mRNA. P, V, and W possess an alternate open reading frame which results in production of C. P, V, W, and C are known to disrupt the host innate antiviral immune response through several different mechanisms. P, V, and W contain STAT1 binding domains, and act as interferon antagonists by sequestering STAT1 in the nucleus and cytoplasm. The C protein controls the early pro-inflammatory response and is also known to promote the viral budding process via a ESCRT -dependent pathway. Cell receptor ephrin-B2, which is located on epithelial cells around smaller arteries, neurons, and smooth muscle cells, is targeted by the viral protein G. Once the protein G binds to ephrin-B2, the viral protein F facilitates fusion with the host cell membrane and releases viral RNA into the host cell cytoplasm. Upon entry, transcription of viral mRNA takes place using the viral RNA as a template. This process is started and stopped by the polymerase complex. Viral proteins are gathering in the cell as transcription occurs until the polymerase complex stops transcription and starts genome replication. Transcription of the viral RNA makes positive sense strands of RNA, which are then used as templates to make more negative sense viral RNA . Genome replication is halted before the viral particles can assemble to make a virion. Once the cell membrane is ready, new virions exit the host cell through budding. Henipaviruses have high mortality rates in mammalian hosts, both human and animal. Because of this, there is a need for immunization against HeV and NiV. The World Health Organization has classified henipaviral agents as R&D Blueprint Priority Pathogens, indicating that they pose a significant risk due to their epidemic potential. The broad species tropism of NiV and HeV have resulted in mortality in livestock species in addition to humans, and as a result veterinary vaccines are in various stages of development or licensure. EquiVac HeV, a veterinary vaccine for horses was licensed in Australia in 2012. A number of experimental vaccines designed for humans are in preclinical development, but none have yet been licensed. A soluble HeV attachment glycoprotein vaccine designed to protect against NiV completed a phase I clinical trial in November 2022, but results have not yet been published. The primary mechanism of protection against NiV and HeV induced by vaccination is thought to be neutralizing antibodies. However, a number of preclinical vaccine studies in animal models of disease have identified that the cell-mediated immune response including CD8+ and CD4+ T-cells may play a role in protection. The emergence of henipaviruses parallels the emergence of other zoonotic viruses in recent decades. SARS coronavirus , Australian bat lyssavirus , Menangle virus , Marburg virus , COVID 19 and possibly Ebola viruses are also harboured by bats, and are capable of infecting a variety of other species. The emergence of each of these viruses has been linked to an increase in contact between bats and humans, sometimes involving an intermediate domestic animal host. The increased contact is driven both by human encroachment into the bats' territory (in the case of Nipah, specifically pigpens in said territory) and by movement of bats towards human populations due to changes in food distribution and loss of habitat. There is evidence that habitat loss for flying foxes, both in South Asia and Australia (particularly along the east coast) as well as encroachment of human dwellings and agriculture into the remaining habitats, is creating greater overlap of human and flying fox distributions.

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Rift Valley fever

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Crimean–Congo hemorrhagic fever

Crimean–Congo hemorrhagic fever ( CCHF ) is a viral disease . Symptoms of CCHF may include fever , muscle pains , headache , vomiting, diarrhea , and bleeding into the skin . Onset of symptoms is less than two weeks following exposure. Complications may include liver failure . Survivors generally recover around two weeks after onset. The CCHF virus is typically spread by tick bites or close contact with the blood, secretions, organs or other bodily fluids of infected persons or animals. Groups that are at high risk of infection are farmers and those who work in slaughterhouses . The virus can also spread between people via body fluids . Diagnosis can be made by detecting antibodies , the virus's RNA , or viral proteins (antigens). It is a type of viral hemorrhagic fever . There are no FDA - or WHO -approved therapeutics for CCHF, and a vaccine is not commercially available. Prevention involves avoiding tick bites, following safe practices in meat processing plants, and observing universal healthcare precautions. Treatment is typically with supportive care , and the medication ribavirin may also help. CCHF cases are observed in a wide geographic range including Africa , Russia , the Balkans , the Middle East , and Asia . Typically small outbreaks are seen in areas where the virus is endemic. In 2013 Iran , Russia, Turkey , and Uzbekistan documented more than 50 cases. The fatality rate is typically between 10 and 40%, though fatalities as high as 80% have been observed in some outbreaks. The virus was first observed in Crimea in the 1940s and was later identified as the same agent of what had been called Congo Hemorrhagic Fever. In the past 20 years, CCHF outbreaks have been reported in eastern Europe, particularly in the former Soviet Union , throughout the Mediterranean, in northwestern China , central Asia, southern Europe, Africa, the Middle East, and the Indian subcontinent . CCHF is on WHO's priority list for Research and Development and the US National Institute of Allergy and Infectious Diseases (NIH/NIAID) priority A list, as a disease posing the highest level of risk to national security and public health.The clinical illness associated with CCHFV (the CCHF virus) is a severe form of hemorrhagic fever . Following infection by a tick bite, the incubation period is typically two to three days but can last as long as nine days, while the incubation period following contact with infected blood or tissues is usually five to six days with a documented maximum of 13 days. The onset of symptoms ushering in the pre-hemorrhagic phase is sudden, with fever, myalgia (muscle ache), dizziness, neck pain and stiffness, backache, headache, sore eyes and photophobia (sensitivity to light). Typical symptoms include nausea, vomiting (which may progress to severe bleeding and can be fatal if not treated), diarrhea, abdominal pain and sore throat early in the acute infection phase, followed by sharp mood swings, agitations and confusion. After several days, agitation may be replaced by sleepiness, depression and lassitude, and the abdominal pain may localize to the upper right quadrant, with detectable liver enlargement. As the illness progresses into the hemorrhagic phase, large areas of severe bruising, severe nosebleeds, and uncontrolled bleeding at injection sites can be seen, beginning on about the fourth day of illness and lasting for about two weeks. Other clinical signs include tachycardia (fast heart rate), lymphadenopathy (enlarged lymph nodes), and a petechiae (a rash caused by bleeding into the skin) on internal mucosal surfaces, such as in the mouth and throat, and on the skin. The petechiae may give way to larger rashes called ecchymoses, and other haemorrhagic phenomena. There is usually evidence of hepatitis, and severely ill patients may experience rapid kidney deterioration, liver failure or pulmonary failure after the fifth day of illness. In documented outbreaks of CCHF, fatality rates in hospitalized patients have ranged from 9% to as high as 70%, though the WHO notes a typical range of 10–40%, with death often occurring in the second week of illness. In patients who recover, improvement generally begins on the ninth or tenth day after the onset of illness. The long-term effects of CCHF infection have not been studied well enough in survivors to determine whether or not specific complications exist. However, recovery is slow.The Crimean–Congo hemorrhagic fever orthonairovirus (CCHFV) is a member of the genus Orthonairovirus , family Nairoviridae of RNA viruses . The virions are 80–120 nanometers (nm) in diameter and are pleomorphic . There are no host ribosomes within the virion. Each virion contains three distinct RNA sequences, which together make up the viral genome. The envelope is single layered and is formed from a lipid bilayer 5 nm thick. It has no external protrusions. The envelope proteins form small projections ~5–10 nm long. The nucleocapsids are filamentous and circular with a length of 200–3000 nm. Viral entry is thought to be clathrin-mediated with the cell surface protein nucleolin playing a role. The genome is circular, negative-sense RNA in three parts – Small (S), Medium (M) and Large (L). The L segment is 11–14.4 kilobases in length while the M and S segments are 4.4–6.3 and 1.7–2.1 kilobases long respectively. The L segment encodes the RNA polymerase , the M segment encodes the envelope glycoproteins (Gc and Gn), and the S segment encodes the nucleocapsid protein. The mutation rates for the three parts of the genome were estimated to be: 1.09 × 10 −4 , 1.52 × 10 −4 and 0.58 × 10 −4 substitutions/site/year for the S, M, and L segments respectively. CCHFV is the most genetically diverse of the arboviruses : its nucleotide sequences frequently differ between different strains, ranging from a 20% variability for the viral S segment to 31% for the M segment. Viruses with diverse sequences can be found within the same geographic area; closely related viruses have been isolated from widely separated regions, suggesting that viral dispersion has occurred possibly by ticks carried on migratory birds or through international livestock trade. Reassortment among genome segments during coinfection of ticks or vertebrates seems likely to have played a role in generating diversity in this virus. [ citation needed ] Based on the sequence data, seven genotypes of CCHFV have been recognised: Africa 1 ( Senegal ), Africa 2 ( Democratic Republic of the Congo and South Africa), Africa 3 (southern and western Africa), Europe 1 ( Albania , Bulgaria , Kosovo , Russia and Turkey ), Europe 2 ( Greece ), Asia 1 ( the Middle East , Iran and Pakistan ) and Asia 2 ( China , Kazakhstan , Tajikistan and Uzbekistan ). [ citation needed ] Ticks are both "environmental reservoir" and vector for the virus, carrying it from wild animals to domestic animals and humans. Tick species identified as infected with the virus include Argas reflexus , Hyalomma anatolicum , Hyalomma detritum , Hyalomma marginatum marginatum and Rhipicephalus sanguineus . [ citation needed ] At least 31 different species of ticks from the genera Haemaphysalis and Hyalomma in southeastern Iran have been found to carry the virus. Wild animals and small mammals, particularly European hare , Middle-African hedgehogs and multimammate rats are the "amplifying hosts" of the virus. Birds are generally resistant to CCHF, with the exception of ostriches . Domestic animals like sheep, goats and cattle can develop high titers of virus in their blood, but tend not to fall ill. The "sporadic infection" of humans is usually caused by a Hyalomma tick bite. Animals can transmit the virus to humans, but this would usually be as part of a disease cluster . When clusters of illness occur, it is typically after people treat, butcher or eat infected livestock, particularly ruminants and ostriches . Outbreaks have occurred in abattoirs and other places where workers have been exposed to infected human or animal blood and fomites [ citation needed ] Humans can infect humans and outbreaks also occur in clinical facilities through infected blood and unclean medical instruments. The Crimean–Congo hemorrhagic fever orthonairovirus (CCHFV) is a member of the genus Orthonairovirus , family Nairoviridae of RNA viruses . The virions are 80–120 nanometers (nm) in diameter and are pleomorphic . There are no host ribosomes within the virion. Each virion contains three distinct RNA sequences, which together make up the viral genome. The envelope is single layered and is formed from a lipid bilayer 5 nm thick. It has no external protrusions. The envelope proteins form small projections ~5–10 nm long. The nucleocapsids are filamentous and circular with a length of 200–3000 nm. Viral entry is thought to be clathrin-mediated with the cell surface protein nucleolin playing a role. The genome is circular, negative-sense RNA in three parts – Small (S), Medium (M) and Large (L). The L segment is 11–14.4 kilobases in length while the M and S segments are 4.4–6.3 and 1.7–2.1 kilobases long respectively. The L segment encodes the RNA polymerase , the M segment encodes the envelope glycoproteins (Gc and Gn), and the S segment encodes the nucleocapsid protein. The mutation rates for the three parts of the genome were estimated to be: 1.09 × 10 −4 , 1.52 × 10 −4 and 0.58 × 10 −4 substitutions/site/year for the S, M, and L segments respectively. CCHFV is the most genetically diverse of the arboviruses : its nucleotide sequences frequently differ between different strains, ranging from a 20% variability for the viral S segment to 31% for the M segment. Viruses with diverse sequences can be found within the same geographic area; closely related viruses have been isolated from widely separated regions, suggesting that viral dispersion has occurred possibly by ticks carried on migratory birds or through international livestock trade. Reassortment among genome segments during coinfection of ticks or vertebrates seems likely to have played a role in generating diversity in this virus. [ citation needed ] Based on the sequence data, seven genotypes of CCHFV have been recognised: Africa 1 ( Senegal ), Africa 2 ( Democratic Republic of the Congo and South Africa), Africa 3 (southern and western Africa), Europe 1 ( Albania , Bulgaria , Kosovo , Russia and Turkey ), Europe 2 ( Greece ), Asia 1 ( the Middle East , Iran and Pakistan ) and Asia 2 ( China , Kazakhstan , Tajikistan and Uzbekistan ). [ citation needed ]The genome is circular, negative-sense RNA in three parts – Small (S), Medium (M) and Large (L). The L segment is 11–14.4 kilobases in length while the M and S segments are 4.4–6.3 and 1.7–2.1 kilobases long respectively. The L segment encodes the RNA polymerase , the M segment encodes the envelope glycoproteins (Gc and Gn), and the S segment encodes the nucleocapsid protein. The mutation rates for the three parts of the genome were estimated to be: 1.09 × 10 −4 , 1.52 × 10 −4 and 0.58 × 10 −4 substitutions/site/year for the S, M, and L segments respectively. CCHFV is the most genetically diverse of the arboviruses : its nucleotide sequences frequently differ between different strains, ranging from a 20% variability for the viral S segment to 31% for the M segment. Viruses with diverse sequences can be found within the same geographic area; closely related viruses have been isolated from widely separated regions, suggesting that viral dispersion has occurred possibly by ticks carried on migratory birds or through international livestock trade. Reassortment among genome segments during coinfection of ticks or vertebrates seems likely to have played a role in generating diversity in this virus. [ citation needed ] Based on the sequence data, seven genotypes of CCHFV have been recognised: Africa 1 ( Senegal ), Africa 2 ( Democratic Republic of the Congo and South Africa), Africa 3 (southern and western Africa), Europe 1 ( Albania , Bulgaria , Kosovo , Russia and Turkey ), Europe 2 ( Greece ), Asia 1 ( the Middle East , Iran and Pakistan ) and Asia 2 ( China , Kazakhstan , Tajikistan and Uzbekistan ). [ citation needed ]Ticks are both "environmental reservoir" and vector for the virus, carrying it from wild animals to domestic animals and humans. Tick species identified as infected with the virus include Argas reflexus , Hyalomma anatolicum , Hyalomma detritum , Hyalomma marginatum marginatum and Rhipicephalus sanguineus . [ citation needed ] At least 31 different species of ticks from the genera Haemaphysalis and Hyalomma in southeastern Iran have been found to carry the virus. Wild animals and small mammals, particularly European hare , Middle-African hedgehogs and multimammate rats are the "amplifying hosts" of the virus. Birds are generally resistant to CCHF, with the exception of ostriches . Domestic animals like sheep, goats and cattle can develop high titers of virus in their blood, but tend not to fall ill. The "sporadic infection" of humans is usually caused by a Hyalomma tick bite. Animals can transmit the virus to humans, but this would usually be as part of a disease cluster . When clusters of illness occur, it is typically after people treat, butcher or eat infected livestock, particularly ruminants and ostriches . Outbreaks have occurred in abattoirs and other places where workers have been exposed to infected human or animal blood and fomites [ citation needed ] Humans can infect humans and outbreaks also occur in clinical facilities through infected blood and unclean medical instruments. Where mammalian tick infection is common, agricultural regulations require de-ticking farm animals before transportation or delivery for slaughter. Personal tick avoidance measures are recommended, such as use of insect repellents, adequate clothing, and body inspection for adherent ticks. [ citation needed ] When feverish patients with evidence of bleeding require resuscitation or intensive care , body substance isolation precautions should be taken. [ citation needed ] Since the 1970s, several vaccine trials around the world against CCHF have been terminated due to high toxicity. As of March 2011 [ update ] , the only available and probably somewhat efficacious CCHF vaccine has been an inactivated antigen preparation then used in Bulgaria. No publication in the scientific literature related to this vaccine exists, which a Turkish virologist called suspicious both because antiquated technology and mouse brain were used to manufacture it. More vaccines are under development, but the sporadic nature of the disease, even in endemic countries, suggests that large trials of vaccine efficacy will be difficult to perform. Finding volunteers may prove challenging, given growing anti-vaccination sentiment and resistance of populations to vaccination against contagious diseases. The number of people to be vaccinated, and the length of time they would have to be followed to confirm protection would have to be carefully defined. Alternatively, many scientists appear to believe that treatment of CCHF with ribavirin is more practical than prevention, but some recently conducted clinical trials appear to counter assumptions of drug efficacy. In 2011, a Turkish research team led by Erciyes University successfully developed the first non-toxic preventive vaccine, which passed clinical trials. As of 2012, the vaccine was pending approval by the US FDA. Since the Ebola epidemic, the WHO jumpstarted a "Blueprint for Research and Development preparedness" on emerging pathogens with epidemic potential, against which there are no medical treatments. CCHF was the top priority on the initial list from December 2015, and is second as of January 2017. Since the 1970s, several vaccine trials around the world against CCHF have been terminated due to high toxicity. As of March 2011 [ update ] , the only available and probably somewhat efficacious CCHF vaccine has been an inactivated antigen preparation then used in Bulgaria. No publication in the scientific literature related to this vaccine exists, which a Turkish virologist called suspicious both because antiquated technology and mouse brain were used to manufacture it. More vaccines are under development, but the sporadic nature of the disease, even in endemic countries, suggests that large trials of vaccine efficacy will be difficult to perform. Finding volunteers may prove challenging, given growing anti-vaccination sentiment and resistance of populations to vaccination against contagious diseases. The number of people to be vaccinated, and the length of time they would have to be followed to confirm protection would have to be carefully defined. Alternatively, many scientists appear to believe that treatment of CCHF with ribavirin is more practical than prevention, but some recently conducted clinical trials appear to counter assumptions of drug efficacy. In 2011, a Turkish research team led by Erciyes University successfully developed the first non-toxic preventive vaccine, which passed clinical trials. As of 2012, the vaccine was pending approval by the US FDA. Since the Ebola epidemic, the WHO jumpstarted a "Blueprint for Research and Development preparedness" on emerging pathogens with epidemic potential, against which there are no medical treatments. CCHF was the top priority on the initial list from December 2015, and is second as of January 2017. Treatment is mostly supportive . Ribavirin has shown some efficacy in vitro and has been used by mouth during outbreaks, [ citation needed ] but there is uncertain evidence to support its use, and this medication can cause serious side effects including hemolytic anemia and liver damage. As of 2011 [ update ] the use of Immunoglobulin preparations has remained unproven and antibody engineering, which raised hopes for monoclonal antibody therapy, has remained in its infancy. CCHF occurs most frequently among agricultural workers, following the bite of an infected tick, and to a lesser extent among slaughterhouse workers exposed to the blood and tissues of infected livestock, and medical personnel through contact with the body fluids of infected persons. As of 2013 [ update ] the northern limit of CCHF has been 50 degrees northern latitude, north of which the Hyalomma ticks have not been found. Per a WHO map from 2008, Hyalomma ticks occurred south of this latitude across all of the Eurasian continent and Africa, sparing only the islands of Sri Lanka , Indonesia and Japan . Serological or virological evidence of CCHF was widespread in Asia, Eastern Europe, the Middle East (except Israel, Lebanon and Jordan), central Africa, Western Africa, South Africa and Madagascar. In 2008, more than 50 cases/year were reported from only 4 countries: Turkey, Iran, Russia and Uzbekistan. 5-49 cases/year were present in South Africa, Central Asia including Pakistan and Afghanistan (but sparing Turkmenistan), in the Middle East only the UAE and the Balkan countries limited to Romania, Bulgaria, Serbia, Montenegro and Albania. In Russia, the disease is limited to Southern and North Caucasian Federal Districts , but climate change may cause it to spread into more northerly areas. A 2014 map by the CDC shows endemic areas (in red) largely unchanged in Africa and the Middle East, but different for the Balkan, including all countries of the former Yugoslavia, and also Greece, but no longer Romania. India 's Northwestern regions of Rajasthan and Gujarat saw their first cases. From 1995 to 2013, 228 cases of CCHF were reported in the Republic of Kosovo, with a case-fatality rate of 25.5%. Between 2002–2008 the Ministry of Health of Turkey reported 3,128 CCHF cases, with a 5% death rate. [ citation needed ] In July 2005, authorities reported 41 cases of CCHF in central Turkey's Yozgat Province , with one death. [ clarification needed ] As of August 2008, a total of 50 deaths were reported for the year thus far in various cities in Turkey due to CCHF. [ clarification needed ] In 2003, 38 people were infected with CCHF in Mauritania , including 35 residents of Nouakchott. In September 2010, an outbreak was reported in Pakistan's Khyber Pakhtunkhwa province. Poor diagnosis and record keeping caused the extent of the outbreak to be uncertain, though some reports indicated over 100 cases, with a case-fatality rate above 10%. [ citation needed ] In January 2011, the first human cases of CCHF in India was reported in Sanand , Gujarat, India, with 4 reported deaths, which included the index patient , treating physician and nurse. As of May 2012 [ update ] , 71 people were reported to have contracted the disease in Iran, resulting in 8 fatalities. [ citation needed ] In October 2012, a British man died from the disease at the Royal Free Hospital in London. He had earlier been admitted to Gartnavel General Hospital in Glasgow , after returning on a flight from Kabul in Afghanistan . In July 2013, seven people died of CCHF in the Karyana village of Babra , Gujarat, India. In August 2013, a farmer from Agago , Uganda was treated at Kalongo Hospital for a confirmed CCHF infection. The deaths of three other individuals in the northern region were suspected to have been caused by the virus. Another unrelated CCHF patient was admitted to Mulago Hospital on the same day. The Ministry of Health announced on the 19th that the outbreak was under control, but the second patient, a 27-year-old woman from Nansana , died on the 21st. She is believed to have contracted the virus from her husband, who returned to Kampala after being treated for CCHF in Juba , South Sudan. In June 2014, cases were diagnosed in Kazakhstan. Ten people, including an ambulance crew, were admitted on to hospital in southern Kazakhstan with suspected CCHF. [ citation needed ] In July 2014 an 8th person was found to be infected with CCHF at Hayatabad Medical Complex (HMC), Pakistan. The eight patients, including a nurse and 6 Afghan nationals, died between April and July 2014. As of 2015 [ update ] , sporadic confirmed cases have been reported from Bhuj , Amreli , Sanand , Idar and Vadnagar in Gujarat, India. In November 2014, a doctor and a labourer in north Gujarat tested positive for the disease. In the following weeks, three more people died from CCHF. In March 2015, one more person died of CCHF in Gujarat. As of 2015, among livestock, CCHF was recognized as "widespread" in India, only 4 years after the first human case had been diagnosed. In August 2016, the first local case of CCHF in Western Europe occurred in Western Spain. A 62-year-old man, who had been bitten by a tick in Spain died on August 25, having infected a nurse. The tick bite occurred in the province of Ávila , 300 km away from the province of Cáceres , where CCHF viral RNA from ticks was amplified in 2010. As of July 2017 [ update ] it was unclear what specific ecology led to the Spanish cases. In August 2016, a number of Pakistani news sources raised concerns regarding the disease. Between January and October 2016, CCHF outbreaks in Pakistan were reported with highest numbers of cases and deaths during August 2016, just before the festival of Eid-al-Adha (held on September 13–15 in 2016). It was hypothesized that the festival could play an important part as people could come into contact with domestic or imported animals potentially infected with CCHF virus. The Pakistani NIH showed there was no correlation, and that CCHF cases have coincided with the peak tick proliferation during the preceding 8–10 years. In 2017, the General Directorate of Public Health in Turkey published official records of infections and casualties involving CCHF between 2008 and 2017. Cases declined form 1,318 in 2009 to 343 in 2017 alongside a lowered mortality rate. Cases are concentrated in rural areas of the Southern Black Sea Region , Central Anatolia Region , and Eastern Anatolia Region during early summer months. On February 2, 2020, an outbreak was reported in Mali involving fourteen cases and seven deaths, days before the COVID-19 pandemic in Africa . In May 2020, a single case was reported in Mauritania. In 2022, an outbreak occurred in Iraq . Between 1 January and 22 May, 212 cases of CCHF were reported to the WHO. Of the 212 cases, 115 were suspected and 97 laboratory confirmed. Twenty seven deaths were recorded, of which 13 were in laboratory confirmed cases. In July 2023, there was a single confirmed fatality of tick-borne CCHF in North Macedonia . As of 2013 [ update ] the northern limit of CCHF has been 50 degrees northern latitude, north of which the Hyalomma ticks have not been found. Per a WHO map from 2008, Hyalomma ticks occurred south of this latitude across all of the Eurasian continent and Africa, sparing only the islands of Sri Lanka , Indonesia and Japan . Serological or virological evidence of CCHF was widespread in Asia, Eastern Europe, the Middle East (except Israel, Lebanon and Jordan), central Africa, Western Africa, South Africa and Madagascar. In 2008, more than 50 cases/year were reported from only 4 countries: Turkey, Iran, Russia and Uzbekistan. 5-49 cases/year were present in South Africa, Central Asia including Pakistan and Afghanistan (but sparing Turkmenistan), in the Middle East only the UAE and the Balkan countries limited to Romania, Bulgaria, Serbia, Montenegro and Albania. In Russia, the disease is limited to Southern and North Caucasian Federal Districts , but climate change may cause it to spread into more northerly areas. A 2014 map by the CDC shows endemic areas (in red) largely unchanged in Africa and the Middle East, but different for the Balkan, including all countries of the former Yugoslavia, and also Greece, but no longer Romania. India 's Northwestern regions of Rajasthan and Gujarat saw their first cases. From 1995 to 2013, 228 cases of CCHF were reported in the Republic of Kosovo, with a case-fatality rate of 25.5%. Between 2002–2008 the Ministry of Health of Turkey reported 3,128 CCHF cases, with a 5% death rate. [ citation needed ] In July 2005, authorities reported 41 cases of CCHF in central Turkey's Yozgat Province , with one death. [ clarification needed ] As of August 2008, a total of 50 deaths were reported for the year thus far in various cities in Turkey due to CCHF. [ clarification needed ] In 2003, 38 people were infected with CCHF in Mauritania , including 35 residents of Nouakchott. In September 2010, an outbreak was reported in Pakistan's Khyber Pakhtunkhwa province. Poor diagnosis and record keeping caused the extent of the outbreak to be uncertain, though some reports indicated over 100 cases, with a case-fatality rate above 10%. [ citation needed ] In January 2011, the first human cases of CCHF in India was reported in Sanand , Gujarat, India, with 4 reported deaths, which included the index patient , treating physician and nurse. As of May 2012 [ update ] , 71 people were reported to have contracted the disease in Iran, resulting in 8 fatalities. [ citation needed ] In October 2012, a British man died from the disease at the Royal Free Hospital in London. He had earlier been admitted to Gartnavel General Hospital in Glasgow , after returning on a flight from Kabul in Afghanistan . In July 2013, seven people died of CCHF in the Karyana village of Babra , Gujarat, India. In August 2013, a farmer from Agago , Uganda was treated at Kalongo Hospital for a confirmed CCHF infection. The deaths of three other individuals in the northern region were suspected to have been caused by the virus. Another unrelated CCHF patient was admitted to Mulago Hospital on the same day. The Ministry of Health announced on the 19th that the outbreak was under control, but the second patient, a 27-year-old woman from Nansana , died on the 21st. She is believed to have contracted the virus from her husband, who returned to Kampala after being treated for CCHF in Juba , South Sudan. In June 2014, cases were diagnosed in Kazakhstan. Ten people, including an ambulance crew, were admitted on to hospital in southern Kazakhstan with suspected CCHF. [ citation needed ] In July 2014 an 8th person was found to be infected with CCHF at Hayatabad Medical Complex (HMC), Pakistan. The eight patients, including a nurse and 6 Afghan nationals, died between April and July 2014. As of 2015 [ update ] , sporadic confirmed cases have been reported from Bhuj , Amreli , Sanand , Idar and Vadnagar in Gujarat, India. In November 2014, a doctor and a labourer in north Gujarat tested positive for the disease. In the following weeks, three more people died from CCHF. In March 2015, one more person died of CCHF in Gujarat. As of 2015, among livestock, CCHF was recognized as "widespread" in India, only 4 years after the first human case had been diagnosed. In August 2016, the first local case of CCHF in Western Europe occurred in Western Spain. A 62-year-old man, who had been bitten by a tick in Spain died on August 25, having infected a nurse. The tick bite occurred in the province of Ávila , 300 km away from the province of Cáceres , where CCHF viral RNA from ticks was amplified in 2010. As of July 2017 [ update ] it was unclear what specific ecology led to the Spanish cases. In August 2016, a number of Pakistani news sources raised concerns regarding the disease. Between January and October 2016, CCHF outbreaks in Pakistan were reported with highest numbers of cases and deaths during August 2016, just before the festival of Eid-al-Adha (held on September 13–15 in 2016). It was hypothesized that the festival could play an important part as people could come into contact with domestic or imported animals potentially infected with CCHF virus. The Pakistani NIH showed there was no correlation, and that CCHF cases have coincided with the peak tick proliferation during the preceding 8–10 years. In 2017, the General Directorate of Public Health in Turkey published official records of infections and casualties involving CCHF between 2008 and 2017. Cases declined form 1,318 in 2009 to 343 in 2017 alongside a lowered mortality rate. Cases are concentrated in rural areas of the Southern Black Sea Region , Central Anatolia Region , and Eastern Anatolia Region during early summer months. On February 2, 2020, an outbreak was reported in Mali involving fourteen cases and seven deaths, days before the COVID-19 pandemic in Africa . In May 2020, a single case was reported in Mauritania. In 2022, an outbreak occurred in Iraq . Between 1 January and 22 May, 212 cases of CCHF were reported to the WHO. Of the 212 cases, 115 were suspected and 97 laboratory confirmed. Twenty seven deaths were recorded, of which 13 were in laboratory confirmed cases. In July 2023, there was a single confirmed fatality of tick-borne CCHF in North Macedonia . In ancient Celtic settlements in the Upper Danube area in Germany, the CCHF virus was detected in archaeological blood samples, indicating that it was endemic at the time. The virus may have evolved around 1500–1100 BC. It is thought that changing climate and agricultural practices around this time could be behind its evolution. In the 12th century a case of a hemorrhagic disease reported from what is now Tajikistan may have been the first known case of Crimean–Congo hemorrhagic fever. [ citation needed ] In 1944, roughly 200 Soviet military agricultural workers were infected by Crimean hemorrhagic fever (CHF), leading to experiments showing a tick-borne viral etiology. In February 1967, virologists John P. Woodall , David Simpson, Ghislaine Courtois and others published initial reports on a virus they called the Congo virus. In 1956, the Congo virus had first been isolated by physician Ghislaine Courtois, head of the Provincial Medical Laboratory, Stanleyville , in the Belgian Congo . Strain V3010, isolated by Courtois, was sent to the Rockefeller Foundation Virus Laboratory (RFVL) in New York City and found to be identical to another strain from Uganda , but to no other named virus at that time. [ citation needed ] In June 1967, Soviet virologist Mikhail Chumakov registered an isolate from a fatal case that occurred in Samarkand in the Catalogue of Arthropod-borne Viruses. In 1969, the Russian strain, which Chumakov had sent to the RFVL, was found to be antigenically indistinguishable from the Congo virus. In 1973, the International Committee on Taxonomy of Viruses adopted Crimean–Congo hemorrhagic fever virus as the official name. These reports include records of the occurrence of the virus or antibodies to the virus from Greece, Portugal, South Africa, Madagascar (the first isolation from there), the Maghreb , Dubai , Saudi Arabia , Kuwait and Iraq.

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Zika fever

Zika fever , also known as Zika virus disease or simply Zika , is an infectious disease caused by the Zika virus . Most cases have no symptoms, but when present they are usually mild and can resemble dengue fever . Symptoms may include fever , red eyes , joint pain , headache, and a maculopapular rash . Symptoms generally last less than seven days. It has not caused any reported deaths during the initial infection. Mother-to-child transmission during pregnancy can cause microcephaly and other brain malformations in some babies. Infections in adults have been linked to Guillain–Barré syndrome (GBS). Zika fever is mainly spread via the bite of mosquitoes of the Aedes type. It can also be sexually transmitted and potentially spread by blood transfusions . Infections in pregnant women can spread to the baby. Diagnosis is by testing the blood, urine, or saliva for the presence of the virus's RNA when the person is sick, or the blood for antibodies after symptoms are present more than a week. Prevention involves decreasing mosquito bites in areas where the disease occurs and proper use of condoms. Efforts to prevent bites include the use of insect repellent , covering much of the body with clothing, mosquito nets , and getting rid of standing water where mosquitoes reproduce. There is no effective vaccine . Health officials recommended that women in areas affected by the 2015–16 Zika outbreak consider putting off pregnancy and that pregnant women not travel to these areas. While there is no specific treatment, paracetamol (acetaminophen) may help with the symptoms. Admission to hospital is rarely necessary. The virus that causes the disease was first isolated in Africa in 1947. The first documented outbreak among people occurred in 2007 in the Federated States of Micronesia . An outbreak started in Brazil in 2015, and spread to the Americas, Pacific, Asia, and Africa. This led the World Health Organization to declare it a Public Health Emergency of International Concern in February 2016. The emergency was lifted in November 2016, but 84 countries still reported cases as of March 2017. The last proven case of Zika spread in the Continental United States was in 2017. Most people who are infected have no or few symptoms. Otherwise the most common signs and symptoms of Zika fever are fever , rash , conjunctivitis (red eyes), muscle and joint pain , and headache, which are similar to signs and symptoms of dengue and chikungunya fever. The time from a mosquito bite to developing symptoms is not yet known, but is probably a few days to a week. The disease lasts for several days to a week and is usually mild enough that people do not have to go to a hospital. Due to being in the same family as dengue, there has been concern that it could cause similar bleeding disorders. However that has only been documented in one case, with blood seen in semen, also known as hematospermia . Zika virus infections have been strongly associated with Guillain–Barré syndrome (GBS), which is a rapid onset of muscle weakness caused by the immune system damaging the peripheral nervous system, and which can progress to paralysis. While both GBS and Zika infection can simultaneously occur in the same individual, it is difficult to definitively identify Zika virus as the cause of GBS. Though Zika virus has been shown to infect human Schwann cells . Several countries affected by Zika outbreaks have reported increases in the rate of new cases of GBS. During the 2013–2014 outbreak in French Polynesia there were 42 reported cases of GBS over a 3-month period, compared to between 3 and 10 annually prior to the outbreak. The disease spreads from mother to child in the womb and can cause multiple problems, most notably microcephaly , in the baby. The full range of birth defects caused by infection during pregnancy is not known, but they appear to be common, with large scale abnormalities seen in up to 42% of live births. The most common observed associations have been abnormalities with brain and eye development such as microcephaly and chorioretinal scarring. Less commonly there have been systemic abnormalities such as hydrops fetalis , where there is abnormal accumulation of fluid in the fetus. These abnormalities can lead to intellectual problems, seizures , vision problems , hearing problems , problems feeding and slow development. Whether the stage of pregnancy at which the mother becomes infected affects the risk to the fetus is not well understood, nor is whether other risk factors affect outcomes. One group has estimated the risk of a baby developing microcephaly at about 1% when the mother is infected during the first trimester, with the risk of developing microcephaly becoming uncertain beyond the first trimester. Affected babies might appear normal but actually have brain abnormalities; infection in newborns could also lead to brain damage. Zika virus infections have been strongly associated with Guillain–Barré syndrome (GBS), which is a rapid onset of muscle weakness caused by the immune system damaging the peripheral nervous system, and which can progress to paralysis. While both GBS and Zika infection can simultaneously occur in the same individual, it is difficult to definitively identify Zika virus as the cause of GBS. Though Zika virus has been shown to infect human Schwann cells . Several countries affected by Zika outbreaks have reported increases in the rate of new cases of GBS. During the 2013–2014 outbreak in French Polynesia there were 42 reported cases of GBS over a 3-month period, compared to between 3 and 10 annually prior to the outbreak. The disease spreads from mother to child in the womb and can cause multiple problems, most notably microcephaly , in the baby. The full range of birth defects caused by infection during pregnancy is not known, but they appear to be common, with large scale abnormalities seen in up to 42% of live births. The most common observed associations have been abnormalities with brain and eye development such as microcephaly and chorioretinal scarring. Less commonly there have been systemic abnormalities such as hydrops fetalis , where there is abnormal accumulation of fluid in the fetus. These abnormalities can lead to intellectual problems, seizures , vision problems , hearing problems , problems feeding and slow development. Whether the stage of pregnancy at which the mother becomes infected affects the risk to the fetus is not well understood, nor is whether other risk factors affect outcomes. One group has estimated the risk of a baby developing microcephaly at about 1% when the mother is infected during the first trimester, with the risk of developing microcephaly becoming uncertain beyond the first trimester. Affected babies might appear normal but actually have brain abnormalities; infection in newborns could also lead to brain damage. Zika virus is a mosquito - borne flavivirus closely related to the dengue and yellow fever viruses. While mosquitoes are the vector , the main reservoir species remains unknown, though serological evidence has been found in both West African monkeys and rodents. Transmission is via the bite of mosquitoes from the genus Aedes , primarily Aedes aegypti in tropical regions. It has also been isolated from Ae. africanus , Ae. apicoargenteus , Ae. luteocephalus , Ae. albopictus , Ae. vittatus and Ae. furcifer . During the 2007 outbreak on Yap Island in the South Pacific, Aedes hensilli was the vector, while Aedes polynesiensis spread the virus in French Polynesia in 2013. Zika virus can also spread by sexual transmission from infected men to their partners. Zika virus has been isolated from semen samples, with one person having 100,000 times more virus in semen than blood or urine, two weeks after being infected. It is unclear why levels in semen can be higher than other body fluids, and it is also unclear how long infectious virus can remain in semen. There have also been cases of men with no symptoms of Zika virus infection transmitting the disease. The CDC has recommended that all men who have travelled to affected areas should wait at least 6 months before trying to attempt conception , regardless of whether they were ill. To date there have been no reported sexual transmissions from women to their sexual partners. Oral, anal or vaginal sex can spread the disease. Cases of vertical perinatal transmission have been reported. The CDC recommends that women with Zika fever should wait at least 8 weeks after they start having symptoms of disease before attempting to conceive. There have been no reported cases of transmission from breastfeeding, but infectious virus has been found in breast milk. Like other flaviviruses it could potentially be transmitted by blood transfusion and several affected countries have developed strategies to screen blood donors. The U.S. FDA has recommended universal screening of blood products for Zika. The virus is detected in 3% of asymptomatic blood donors in French Polynesia. Zika virus is a mosquito - borne flavivirus closely related to the dengue and yellow fever viruses. While mosquitoes are the vector , the main reservoir species remains unknown, though serological evidence has been found in both West African monkeys and rodents. Transmission is via the bite of mosquitoes from the genus Aedes , primarily Aedes aegypti in tropical regions. It has also been isolated from Ae. africanus , Ae. apicoargenteus , Ae. luteocephalus , Ae. albopictus , Ae. vittatus and Ae. furcifer . During the 2007 outbreak on Yap Island in the South Pacific, Aedes hensilli was the vector, while Aedes polynesiensis spread the virus in French Polynesia in 2013. Zika virus can also spread by sexual transmission from infected men to their partners. Zika virus has been isolated from semen samples, with one person having 100,000 times more virus in semen than blood or urine, two weeks after being infected. It is unclear why levels in semen can be higher than other body fluids, and it is also unclear how long infectious virus can remain in semen. There have also been cases of men with no symptoms of Zika virus infection transmitting the disease. The CDC has recommended that all men who have travelled to affected areas should wait at least 6 months before trying to attempt conception , regardless of whether they were ill. To date there have been no reported sexual transmissions from women to their sexual partners. Oral, anal or vaginal sex can spread the disease. Cases of vertical perinatal transmission have been reported. The CDC recommends that women with Zika fever should wait at least 8 weeks after they start having symptoms of disease before attempting to conceive. There have been no reported cases of transmission from breastfeeding, but infectious virus has been found in breast milk. Like other flaviviruses it could potentially be transmitted by blood transfusion and several affected countries have developed strategies to screen blood donors. The U.S. FDA has recommended universal screening of blood products for Zika. The virus is detected in 3% of asymptomatic blood donors in French Polynesia. In fruit flies microcephaly appears to be caused by the flavivirid virus protein NS4A , which can disrupt brain growth by hijacking a pathway which regulates growth of new neurons. It is difficult to diagnose Zika virus infection based on clinical signs and symptoms alone due to overlaps with other arboviruses that are endemic to similar areas. The US Centers for Disease Control and Prevention (CDC) advises that "based on the typical clinical features, the differential diagnosis for Zika virus infection is broad. In addition to dengue, other considerations include leptospirosis , malaria , rickettsia , group A streptococcus , rubella , measles , and parvovirus , enterovirus , adenovirus , and alphavirus infections (e.g., chikungunya, Mayaro , Ross River , Barmah Forest , O'nyong'nyong , and Sindbis viruses)." In small case series, routine chemistry and complete blood counts have been normal in most patients. A few have been reported to have mild leukopenia , thrombocytopenia , and elevated liver transaminases . Zika virus can be identified by reverse transcriptase PCR (RT-PCR) in acutely ill patients. However, the period of viremia can be short and the World Health Organization (WHO) recommends RT-PCR testing be done on serum collected within 1 to 3 days of symptom onset or on saliva samples collected during the first 3 to 5 days. When evaluating paired samples, Zika virus was detected more frequently in saliva than serum. Urine samples can be collected and tested up to 14 days after the onset of symptoms, as the virus has been seen to survive longer in the urine than either saliva or serum. The longest period of detectable virus has been 11 days and Zika virus does not appear to establish latency. Later on, serology for the detection of specific IgM and IgG antibodies to Zika virus can be used. IgM antibodies can be detectable within 3 days of the onset of illness. Serological cross-reactions with closely related flaviviruses such as dengue and West Nile virus as well as vaccines to flaviviruses are possible. As of 2019, the FDA has authorized two tests to detect Zika virus antibodies. The CDC recommends screening some pregnant women even if they do not have symptoms of infection. Pregnant women who have traveled to affected areas should be tested between two and twelve weeks after their return from travel. Due to the difficulties with ordering and interpreting tests for Zika virus, the CDC also recommends that healthcare providers contact their local health department for assistance. For women living in affected areas, the CDC has recommended testing at the first prenatal visit with a doctor as well as in the mid-second trimester , though this may be adjusted based on local resources and the local burden of Zika virus. Additional testing should be done if there are any signs of Zika virus disease. Women with positive test results for Zika virus infection should have their fetus monitored by ultrasound every three to four weeks to monitor fetal anatomy and growth. For infants with suspected congenital Zika virus disease, the CDC recommends testing with both serologic and molecular assays such as RT-PCR, IgM ELISA and plaque reduction neutralization test (PRNT). RT-PCR of the infants serum and urine should be performed in the first two days of life. Newborns with a mother who was potentially exposed and who have positive blood tests, microcephaly or intracranial calcifications should have further testing including a thorough physical investigation for neurologic abnormalities, dysmorphic features, splenomegaly, hepatomegaly, and rash or other skin lesions. Other recommended tests are cranial ultrasound, hearing evaluation, and eye examination. Testing should be done for any abnormalities encountered as well as for other congenital infections such as syphilis , toxoplasmosis , rubella, cytomegalovirus infection, lymphocytic choriomeningitis virus infection, and herpes simplex virus . Some tests should be repeated up to 6 months later as there can be delayed effects, particularly with hearing. In response to the widespread transmission of Zika virus during the 2016 outbreak and concerns of viral genetic material detected in breast milk the World Health Organization (WHO) released a Guideline of infant feeding in areas of Zika virus transmission, first in 2016 and updated in 2021, where the evidence showed that despite the detection of Zika virus in breast milk, there is unclear evidence of transmission to the infant, and considering that Zika virus infection among infants is mild, the balance between desirable and undesirable effects favours breastfeeding versus not breastfeeding. According to the 2021WHO guidelines: The CDC recommends screening some pregnant women even if they do not have symptoms of infection. Pregnant women who have traveled to affected areas should be tested between two and twelve weeks after their return from travel. Due to the difficulties with ordering and interpreting tests for Zika virus, the CDC also recommends that healthcare providers contact their local health department for assistance. For women living in affected areas, the CDC has recommended testing at the first prenatal visit with a doctor as well as in the mid-second trimester , though this may be adjusted based on local resources and the local burden of Zika virus. Additional testing should be done if there are any signs of Zika virus disease. Women with positive test results for Zika virus infection should have their fetus monitored by ultrasound every three to four weeks to monitor fetal anatomy and growth. For infants with suspected congenital Zika virus disease, the CDC recommends testing with both serologic and molecular assays such as RT-PCR, IgM ELISA and plaque reduction neutralization test (PRNT). RT-PCR of the infants serum and urine should be performed in the first two days of life. Newborns with a mother who was potentially exposed and who have positive blood tests, microcephaly or intracranial calcifications should have further testing including a thorough physical investigation for neurologic abnormalities, dysmorphic features, splenomegaly, hepatomegaly, and rash or other skin lesions. Other recommended tests are cranial ultrasound, hearing evaluation, and eye examination. Testing should be done for any abnormalities encountered as well as for other congenital infections such as syphilis , toxoplasmosis , rubella, cytomegalovirus infection, lymphocytic choriomeningitis virus infection, and herpes simplex virus . Some tests should be repeated up to 6 months later as there can be delayed effects, particularly with hearing. In response to the widespread transmission of Zika virus during the 2016 outbreak and concerns of viral genetic material detected in breast milk the World Health Organization (WHO) released a Guideline of infant feeding in areas of Zika virus transmission, first in 2016 and updated in 2021, where the evidence showed that despite the detection of Zika virus in breast milk, there is unclear evidence of transmission to the infant, and considering that Zika virus infection among infants is mild, the balance between desirable and undesirable effects favours breastfeeding versus not breastfeeding. According to the 2021WHO guidelines: The virus is spread by mosquitoes, making mosquito avoidance an important element to disease control. The CDC recommends that individuals: The CDC also recommends strategies for controlling mosquitoes such as eliminating standing water, repairing septic tanks and using screens on doors and windows. Spraying insecticide is used to kill flying mosquitoes and larvicide can be used in water containers. Because Zika virus can be sexually transmitted, men who have gone to an area where Zika fever is occurring should be counseled to either abstain from sex or use condoms for 6 months after travel if their partner is pregnant or could potentially become pregnant. Breastfeeding is still recommended by the WHO, even by women who have had Zika fever. There have been no recorded cases of Zika transmission to infants through breastfeeding, though the replicative virus has been detected in breast milk. When returning from travel, with or without symptoms, it is suggested that prevention of mosquito bites continue for 3 weeks in order reduce the risk of virus transmission to uninfected mosquitos. Because of the "growing evidence of a link between Zika and microcephaly", in January 2016, the CDC issued a travel alert advising pregnant women to consider postponing travel to countries and territories with ongoing local transmission of Zika virus. Later, the advice was updated to caution pregnant women to avoid these areas entirely if possible and, if travel is unavoidable, to protect themselves from mosquito bites. Male partners of pregnant women and couples contemplating pregnancy who must travel to areas where Zika is active are advised to use condoms or abstain from sex. The agency also suggested that women thinking about becoming pregnant should consult with their physicians before traveling. In September 2016, the CDC travel advisories included: Cape Verde Many parts of the Caribbean: Anguilla, Antigua and Barbuda, Aruba, The Bahamas, Barbados, Bonaire, British Virgin Islands, Cayman Islands, Cuba, Curaçao, Dominica, Dominican Republic, Grenada, Guadeloupe, Haiti, Jamaica, Martinique, Puerto Rico, Saba, Saint Saint Barthélemy, Saint Lucia, Saint Martin, Saint Vincent and the Grenadines, Sint Eustatius, Sint Maarten, Trinidad and Tobago, and the U.S. Virgin Islands Central America: Belize, Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, and Panama Mexico Most of South America: Argentina, Bolivia, Brazil, Colombia, Ecuador, French Guiana, Guyana, Paraguay, Peru, Suriname, and Venezuela Several Pacific Islands: American Samoa, Fiji, Marshall Islands, Micronesia, New Caledonia, Papua New Guinea, Samoa, and Tonga In Asia: Singapore, Malaysia, Brunei In December 2020, no active Zika outbreaks were reported by the CDC. Both the regional Pan American Health Organization (PAHO) as well as the WHO have issued statements of concern about the widespread public health impact of the Zika virus and its links to GBS and microcephaly. The WHO Director-General, Margaret Chan , issued a statement in February 2016 "declaring that the recent cluster of microcephaly cases and other neurological disorders reported in Brazil, following a similar cluster in French Polynesia in 2014, constitutes a Public Health Emergency of International Concern." The declaration allowed the WHO to coordinate international response to the virus as well as gave its guidance the force of international law under the International Health Regulations . The declaration was ended in November 2016. As of 2016 there was no available vaccine. Development was a priority of the US National Institutes of Health (NIH), but officials stated that development of a vaccine could take years. To speed new drug development regulatory strategies were proposed by the WHO and NIH. Animal and early human studies were underway as of September 2016. As of December 2019, there were several vaccine candidates in various stages of development. Disease control in the affected countries currently centres around mosquito control. Several approaches are available for the management of Aedes aegypti mosquito populations, including the destruction of larval breeding sites (the aquatic pools in which eggs are laid and larvae hatch prior to mosquito development into flying adults); and, insecticides targeting either the larval stages, adult mosquitoes or both. Additionally, a whole host of novel technologies are under current development for mosquito control and the World Health Organization has recently lent its support for the accelerated development of modern methods for mosquito control such as the use of Wolbachia bacteria to render mosquitoes resistant to the virus, and, the release of sterilized male mosquitoes that breed with wild female mosquitoes to give rise to non-viable offspring (offspring that do not survive to the biting, adult stage). Oxitec 's genetically modified OX513A mosquito was approved by Brazil's National Biosecurity Technical Commission (CTNBio) in April 2014 and it was being used to try to combat mosquitoes carrying the Zika virus in the town of Piracicaba , São Paulo in 2016. In the 1940s and 1950s, the Aedes aegypti mosquito was eradicated on some Caribbean islands and in at least eighteen Latin American countries. Decreasing political will and presumably available money, mosquito resistance to insecticide, and a pace of urbanization which exceeded eradication efforts led to this mosquito's comeback. Because of the "growing evidence of a link between Zika and microcephaly", in January 2016, the CDC issued a travel alert advising pregnant women to consider postponing travel to countries and territories with ongoing local transmission of Zika virus. Later, the advice was updated to caution pregnant women to avoid these areas entirely if possible and, if travel is unavoidable, to protect themselves from mosquito bites. Male partners of pregnant women and couples contemplating pregnancy who must travel to areas where Zika is active are advised to use condoms or abstain from sex. The agency also suggested that women thinking about becoming pregnant should consult with their physicians before traveling. In September 2016, the CDC travel advisories included: Cape Verde Many parts of the Caribbean: Anguilla, Antigua and Barbuda, Aruba, The Bahamas, Barbados, Bonaire, British Virgin Islands, Cayman Islands, Cuba, Curaçao, Dominica, Dominican Republic, Grenada, Guadeloupe, Haiti, Jamaica, Martinique, Puerto Rico, Saba, Saint Saint Barthélemy, Saint Lucia, Saint Martin, Saint Vincent and the Grenadines, Sint Eustatius, Sint Maarten, Trinidad and Tobago, and the U.S. Virgin Islands Central America: Belize, Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, and Panama Mexico Most of South America: Argentina, Bolivia, Brazil, Colombia, Ecuador, French Guiana, Guyana, Paraguay, Peru, Suriname, and Venezuela Several Pacific Islands: American Samoa, Fiji, Marshall Islands, Micronesia, New Caledonia, Papua New Guinea, Samoa, and Tonga In Asia: Singapore, Malaysia, Brunei In December 2020, no active Zika outbreaks were reported by the CDC. Both the regional Pan American Health Organization (PAHO) as well as the WHO have issued statements of concern about the widespread public health impact of the Zika virus and its links to GBS and microcephaly. The WHO Director-General, Margaret Chan , issued a statement in February 2016 "declaring that the recent cluster of microcephaly cases and other neurological disorders reported in Brazil, following a similar cluster in French Polynesia in 2014, constitutes a Public Health Emergency of International Concern." The declaration allowed the WHO to coordinate international response to the virus as well as gave its guidance the force of international law under the International Health Regulations . The declaration was ended in November 2016. As of 2016 there was no available vaccine. Development was a priority of the US National Institutes of Health (NIH), but officials stated that development of a vaccine could take years. To speed new drug development regulatory strategies were proposed by the WHO and NIH. Animal and early human studies were underway as of September 2016. As of December 2019, there were several vaccine candidates in various stages of development. Disease control in the affected countries currently centres around mosquito control. Several approaches are available for the management of Aedes aegypti mosquito populations, including the destruction of larval breeding sites (the aquatic pools in which eggs are laid and larvae hatch prior to mosquito development into flying adults); and, insecticides targeting either the larval stages, adult mosquitoes or both. Additionally, a whole host of novel technologies are under current development for mosquito control and the World Health Organization has recently lent its support for the accelerated development of modern methods for mosquito control such as the use of Wolbachia bacteria to render mosquitoes resistant to the virus, and, the release of sterilized male mosquitoes that breed with wild female mosquitoes to give rise to non-viable offspring (offspring that do not survive to the biting, adult stage). Oxitec 's genetically modified OX513A mosquito was approved by Brazil's National Biosecurity Technical Commission (CTNBio) in April 2014 and it was being used to try to combat mosquitoes carrying the Zika virus in the town of Piracicaba , São Paulo in 2016. In the 1940s and 1950s, the Aedes aegypti mosquito was eradicated on some Caribbean islands and in at least eighteen Latin American countries. Decreasing political will and presumably available money, mosquito resistance to insecticide, and a pace of urbanization which exceeded eradication efforts led to this mosquito's comeback. There is currently no specific treatment for Zika virus infection. Care is supportive with treatment of pain, fever, and itching. Some authorities have recommended against using aspirin and other NSAIDs as these have been associated with hemorrhagic syndrome when used for other flaviviruses. Additionally, aspirin use is generally avoided in children when possible due to the risk of Reye syndrome . Zika virus had been relatively little studied until the major outbreak in 2015, and no specific antiviral treatments are available as yet. Advice to pregnant women is to avoid any risk of infection so far as possible, as once infected there is little that can be done beyond supportive treatment. Most of the time, Zika fever resolves on its own in two to seven days, but rarely, some people develop Guillain–Barré syndrome . The fetus of a pregnant woman who has Zika fever may die or be born with congenital central nervous system malformations, like microcephaly . In April 1947, as part of studies sponsored by the Rockefeller Foundation into yellow fever , 6 caged rhesus monkeys were placed in the canopy of the Zika Forest of Uganda. On April 18 one of the monkeys (no. 776) developed a fever and blood samples revealed the first known case of Zika fever. Population surveys at the time in Uganda found 6.1% of individuals to be seropositive for Zika. The first human cases were reported in Nigeria in 1954. A few outbreaks have been reported in tropical Africa and in some areas in Southeast Asia. Until recently there were no documented cases of Zika virus in the Indian subcontinent , however, the first cases were reported in 2017 from Gujarat state and Tamil Nadu, more cases were reported in Rajasthan state involving an outbreak of 153 reported cases and in a pregnant women living in Kerala state. A 1954 study assessing blood samples from several people from different states found antibodies to Zika in healthy people in India which could indicate past exposure, though it could also be due to cross-reaction with other flaviviruses. By using phylogenetic analysis of Asian strains, it was estimated that Zika virus had moved to Southeast Asia by 1945. In 1977–1978, Zika virus infection was described as a cause of fever in Indonesia. Before 2007, there were only 13 reported natural infections with Zika virus, all with a mild, self-limited febrile illness. As of July 2019, evidence of local transmission from mosquitoes to humans has been reported in a total of 87 countries from four of six WHO Regions ; African, Americas, South-East Asia and Western Pacific. The first major outbreak, with 185 confirmed cases, was reported in 2007 in the Yap Islands of the Federated States of Micronesia. A total of 108 cases were confirmed by PCR or serology and 72 additional cases were suspected. The most common symptoms were rash, fever, arthralgia, and conjunctivitis, and no deaths were reported. The mosquito Aedes hensilli , which was the predominant species identified in Yap during the outbreak, was probably the main vector of transmission. While the way of introduction of the virus on Yap Island remains uncertain, it is likely to have happened through introduction of infected mosquitoes or a human infected with a strain related to those in Southeast Asia. This was also the first time Zika fever had been reported outside Africa and Asia. Before the Yap Island outbreak, only 14 human cases had ever been reported. In 2013–2014, several outbreaks of Zika were reported in French Polynesia , New Caledonia , Easter Island and the Cook Islands . The source of the virus was thought to be an independent introduction of the virus from Southeast Asia , unrelated to the Yap Islands outbreak. Genetic analyses of Zika virus strains suggest that Zika first entered the Americas between May and December 2013. It was first detected in the Western Hemisphere in February 2014, and rapidly spread throughout South and Central America, reaching Mexico in November 2015. In 2016 it established local transmission in Florida and Texas. The first death in the United States due to Zika occurred in February 2016. In May 2015, Brazil officially reported its first 16 cases of the illness. Although, a case of illness was reported in March 2015 in a returning traveller. According to the Brazilian Health Ministry, as of November 2015 there was no official count of the number of people infected with the virus in Brazil, since the disease is not subject to compulsory notification. Even so, cases were reported in 14 states of the country. Mosquito-borne Zika virus is suspected to be the cause of 2,400 possible cases of microcephaly and 29 infant deaths in Brazil in 2015 (of the 2400 or so notified cases in 2015, 2165 were under investigation in December 2015, 134 were confirmed and 102 were ruled out for microcephaly). The Brazilian Health Ministry has reported at least 2,400 suspected cases of microcephaly in the country in 2015 as of 12 December, and 29 fatalities. Before the Zika outbreak, only an average of 150 to 200 cases per year were reported in Brazil. In the state of Pernambuco the reported rates of microcephaly in 2015 are 77 times higher than in the previous 5 years. A model using data from a Zika outbreak in French Polynesia estimated the risk of microcephaly in children born to mothers who acquired Zika virus in the first trimester to be 1%. On 24 January 2016, the WHO warned that the virus is likely to spread to nearly all countries of the Americas, since its vector, the mosquito Aedes aegypti , is found in all countries in the region, except for Canada and continental Chile . The mosquito and dengue fever have been detected in Chile's Easter Island, some 3,500 km (2,200 mi) away from its closest point in mainland Chile, since 2002. In February 2016, WHO declared the outbreak a Public Health Emergency of International Concern as evidence grew that Zika is a cause of birth defects and neurological problems. In April 2016, WHO stated there is a scientific consensus, based on preliminary evidence, that Zika is a cause of microcephaly in infants and Guillain–Barré syndrome in adults. Studies of this and prior outbreaks have found Zika infection during pregnancy to be associated with early pregnancy loss and other pregnancy problems. In the Americas the number of cases peaked during the first half of 2016 and declined through 2017–2018, with a total of 31,587 suspected, probable, and confirmed cases of ZIKV disease were reported in the Region of the Americas. Of these, 3,473 (11%) were laboratory confirmed. In general, transmission persists at low levels in some areas and is not uniformly distributed within countries. In 2016 imported or locally transmitted Zika was reported in all the countries of Asia except Brunei, Hong Kong, Myanmar and Nepal. Serological surveys have indicated that Zika virus is endemic in most areas of Asia, though at a low level. While there was a sharp rise in the number of cases of Zika detected in Singapore after the 2016 Summer Olympics in Brazil, genetic analysis revealed that the strains were more closely related to strains from Thailand than from those causing the epidemic in the Americas. The first major outbreak, with 185 confirmed cases, was reported in 2007 in the Yap Islands of the Federated States of Micronesia. A total of 108 cases were confirmed by PCR or serology and 72 additional cases were suspected. The most common symptoms were rash, fever, arthralgia, and conjunctivitis, and no deaths were reported. The mosquito Aedes hensilli , which was the predominant species identified in Yap during the outbreak, was probably the main vector of transmission. While the way of introduction of the virus on Yap Island remains uncertain, it is likely to have happened through introduction of infected mosquitoes or a human infected with a strain related to those in Southeast Asia. This was also the first time Zika fever had been reported outside Africa and Asia. Before the Yap Island outbreak, only 14 human cases had ever been reported. In 2013–2014, several outbreaks of Zika were reported in French Polynesia , New Caledonia , Easter Island and the Cook Islands . The source of the virus was thought to be an independent introduction of the virus from Southeast Asia , unrelated to the Yap Islands outbreak. Genetic analyses of Zika virus strains suggest that Zika first entered the Americas between May and December 2013. It was first detected in the Western Hemisphere in February 2014, and rapidly spread throughout South and Central America, reaching Mexico in November 2015. In 2016 it established local transmission in Florida and Texas. The first death in the United States due to Zika occurred in February 2016. In May 2015, Brazil officially reported its first 16 cases of the illness. Although, a case of illness was reported in March 2015 in a returning traveller. According to the Brazilian Health Ministry, as of November 2015 there was no official count of the number of people infected with the virus in Brazil, since the disease is not subject to compulsory notification. Even so, cases were reported in 14 states of the country. Mosquito-borne Zika virus is suspected to be the cause of 2,400 possible cases of microcephaly and 29 infant deaths in Brazil in 2015 (of the 2400 or so notified cases in 2015, 2165 were under investigation in December 2015, 134 were confirmed and 102 were ruled out for microcephaly). The Brazilian Health Ministry has reported at least 2,400 suspected cases of microcephaly in the country in 2015 as of 12 December, and 29 fatalities. Before the Zika outbreak, only an average of 150 to 200 cases per year were reported in Brazil. In the state of Pernambuco the reported rates of microcephaly in 2015 are 77 times higher than in the previous 5 years. A model using data from a Zika outbreak in French Polynesia estimated the risk of microcephaly in children born to mothers who acquired Zika virus in the first trimester to be 1%. On 24 January 2016, the WHO warned that the virus is likely to spread to nearly all countries of the Americas, since its vector, the mosquito Aedes aegypti , is found in all countries in the region, except for Canada and continental Chile . The mosquito and dengue fever have been detected in Chile's Easter Island, some 3,500 km (2,200 mi) away from its closest point in mainland Chile, since 2002. In February 2016, WHO declared the outbreak a Public Health Emergency of International Concern as evidence grew that Zika is a cause of birth defects and neurological problems. In April 2016, WHO stated there is a scientific consensus, based on preliminary evidence, that Zika is a cause of microcephaly in infants and Guillain–Barré syndrome in adults. Studies of this and prior outbreaks have found Zika infection during pregnancy to be associated with early pregnancy loss and other pregnancy problems. In the Americas the number of cases peaked during the first half of 2016 and declined through 2017–2018, with a total of 31,587 suspected, probable, and confirmed cases of ZIKV disease were reported in the Region of the Americas. Of these, 3,473 (11%) were laboratory confirmed. In general, transmission persists at low levels in some areas and is not uniformly distributed within countries. In 2016 imported or locally transmitted Zika was reported in all the countries of Asia except Brunei, Hong Kong, Myanmar and Nepal. Serological surveys have indicated that Zika virus is endemic in most areas of Asia, though at a low level. While there was a sharp rise in the number of cases of Zika detected in Singapore after the 2016 Summer Olympics in Brazil, genetic analysis revealed that the strains were more closely related to strains from Thailand than from those causing the epidemic in the Americas. It is named after the Zika Forest near Entebbe , Uganda , where the Zika virus was first identified. Zika virus was first identified in the late 1940s in Kampala, Uganda, Africa but was first confirmed in Brazil. Since it was first identified, Zika has been found in more than 27 countries and territories. Following the initial Zika outbreak in Northeastern Brazil in May 2015, physicians observed a very large surge of reports of infants born with microcephaly , with 20 times the number of expected cases. Many of these cases have since been confirmed, leading WHO officials to project that approximately 2,500 infants will be found to have born in Brazil with Zika-related microcephaly. Proving that Zika causes these effects was difficult and complex for several reasons. For example, the effects on an infant might not be seen until months after the mother's initial infection, long after the time when Zika is easily detected in the body. In addition, research was needed to determine the mechanism by which Zika produced these effects. Since the initial outbreak, studies that use several different methods found evidence of a link, leading public health officials to conclude that it appears increasingly likely the virus is linked to microcephaly and miscarriage. On 1 February 2016, the World Health Organization declared recently reported clusters of microcephaly and other neurological disorders a Public Health Emergency of International Concern (PHEIC). On 8 March 2016, the WHO Committee reconfirmed that the association between Zika and neurological disorders is of global concern. The Zika virus was first linked with newborn microcephaly during the Brazil Zika virus outbreak. In 2015, there were 2,782 suspected cases of microcephaly compared with 147 in 2014 and 167 in 2013. Confirmation of many of the recent cases is pending, and it is difficult to estimate how many cases went unreported before the recent awareness of the risk of virus infections. In November 2015, the Zika virus was isolated in a newborn baby from the northeastern state of Ceará , Brazil, with microcephaly and other congenital disorders . The Lancet medical journal reported in January 2016 that the Brazilian Ministry of Health had confirmed 134 cases of microcephaly "believed to be associated with Zika virus infection" with an additional 2,165 cases in 549 counties in 20 states remaining under investigation. An analysis of 574 cases of microcephaly in Brazil during 2015 and the first week of 2016, reported in March 2016, found an association with maternal illness involving rash and fever during the first trimester of pregnancy. During this period, 12 Brazilian states reported increases of at least 3 standard deviations (SDs) in cases of microcephaly compared with 2000–14, with the northeastern states of Bahia, Paraíba and Pernambuco reporting increases of more than 20 SDs. In January 2016, a baby in Oahu , Hawaii, was born with microcephaly, the first case in the United States of brain damage linked to the virus. The baby and mother tested positive for a past Zika virus infection. The mother, who had probably acquired the virus while traveling in Brazil in May 2015 during the early stages of her pregnancy, had reported her bout of Zika. She recovered before relocating to Hawaii. Her pregnancy had progressed normally, and the baby's condition was not known until birth. In February 2016, ocular disorders in newborns have been linked to Zika virus infection. In one study in Pernambuco state in Brazil, about 40 percent of babies with Zika-related microcephaly also had scarring of the retina with spots, or pigment alteration . On 20 February 2016, Brazilian scientists announced that they had successfully sequenced the Zika virus genome and expressed hope that this would help in both developing a vaccine and in determining the nature of any link to birth defects. Also in February 2016, rumors that microcephaly is caused by the use of the larvicide pyriproxyfen in drinking water were refuted by scientists. "It's important to state that some localities that do not use pyriproxyfen also had reported cases of microcephaly", read a Brazilian government statement. The Brazilian government also refuted conspiracy theories that chickenpox and rubella vaccinations or genetically modified mosquitoes were causing increases in microcephaly. Researchers also suspected that Zika virus could be transmitted by a pregnant woman to her baby (" vertical transmission "). This remained unproven until February 2016, when a paper by Calvet et al. was published, showing not only was the Zika virus genome found in the amniotic fluid but also IgM antibodies against the virus. This means that not only can the virus cross the placental barrier, but also the antibodies produced by the mother can reach the fetus, which suggests that vertical transmission is plausible in these cases. One other study published in March 2016 by Mlakar and colleagues analyzed autopsy tissues from a fetus with microcephaly that was probably related to Zika virus; researchers found ZIKV in the brain tissue and suggested that the brain injuries were probably associated with the virus, which also shed a light on the vertical transmission theory. Also in March 2016, first solid evidence was reported on how the virus affects the development of the brain, indicating that it appears to preferentially kill developing brain cells. The first cases of birth defects linked to Zika in Colombia and in Panama were reported in March 2016. In the same month, researchers published a prospective cohort study that found profound impacts in 29 percent of infants of mothers infected with Zika, some of whom were infected late in pregnancy. This study did not suffer from some of the difficulties of studying Zika: the study followed women who presented to a Rio de Janeiro clinic with fever and rash within the last five days. The women were then tested for Zika using PCR, then the progress of the pregnancies were followed using ultrasound. A high rate of the autoimmune disease Guillain–Barré syndrome (GBS), noted in the French Polynesia outbreak, has also been found in the outbreak that began in Brazil. Laboratory analysis found Zika infections in some patients with GBS in Brazil, El Salvador, Suriname and Venezuela, and the WHO declared on 22 March 2016 that Zika appeared to be "implicated" in GBS infection and that if the pattern was confirmed it would represent a global public health crisis. It is named after the Zika Forest near Entebbe , Uganda , where the Zika virus was first identified. Zika virus was first identified in the late 1940s in Kampala, Uganda, Africa but was first confirmed in Brazil. Since it was first identified, Zika has been found in more than 27 countries and territories. Following the initial Zika outbreak in Northeastern Brazil in May 2015, physicians observed a very large surge of reports of infants born with microcephaly , with 20 times the number of expected cases. Many of these cases have since been confirmed, leading WHO officials to project that approximately 2,500 infants will be found to have born in Brazil with Zika-related microcephaly. Proving that Zika causes these effects was difficult and complex for several reasons. For example, the effects on an infant might not be seen until months after the mother's initial infection, long after the time when Zika is easily detected in the body. In addition, research was needed to determine the mechanism by which Zika produced these effects. Since the initial outbreak, studies that use several different methods found evidence of a link, leading public health officials to conclude that it appears increasingly likely the virus is linked to microcephaly and miscarriage. On 1 February 2016, the World Health Organization declared recently reported clusters of microcephaly and other neurological disorders a Public Health Emergency of International Concern (PHEIC). On 8 March 2016, the WHO Committee reconfirmed that the association between Zika and neurological disorders is of global concern. The Zika virus was first linked with newborn microcephaly during the Brazil Zika virus outbreak. In 2015, there were 2,782 suspected cases of microcephaly compared with 147 in 2014 and 167 in 2013. Confirmation of many of the recent cases is pending, and it is difficult to estimate how many cases went unreported before the recent awareness of the risk of virus infections. In November 2015, the Zika virus was isolated in a newborn baby from the northeastern state of Ceará , Brazil, with microcephaly and other congenital disorders . The Lancet medical journal reported in January 2016 that the Brazilian Ministry of Health had confirmed 134 cases of microcephaly "believed to be associated with Zika virus infection" with an additional 2,165 cases in 549 counties in 20 states remaining under investigation. An analysis of 574 cases of microcephaly in Brazil during 2015 and the first week of 2016, reported in March 2016, found an association with maternal illness involving rash and fever during the first trimester of pregnancy. During this period, 12 Brazilian states reported increases of at least 3 standard deviations (SDs) in cases of microcephaly compared with 2000–14, with the northeastern states of Bahia, Paraíba and Pernambuco reporting increases of more than 20 SDs. In January 2016, a baby in Oahu , Hawaii, was born with microcephaly, the first case in the United States of brain damage linked to the virus. The baby and mother tested positive for a past Zika virus infection. The mother, who had probably acquired the virus while traveling in Brazil in May 2015 during the early stages of her pregnancy, had reported her bout of Zika. She recovered before relocating to Hawaii. Her pregnancy had progressed normally, and the baby's condition was not known until birth. In February 2016, ocular disorders in newborns have been linked to Zika virus infection. In one study in Pernambuco state in Brazil, about 40 percent of babies with Zika-related microcephaly also had scarring of the retina with spots, or pigment alteration . On 20 February 2016, Brazilian scientists announced that they had successfully sequenced the Zika virus genome and expressed hope that this would help in both developing a vaccine and in determining the nature of any link to birth defects. Also in February 2016, rumors that microcephaly is caused by the use of the larvicide pyriproxyfen in drinking water were refuted by scientists. "It's important to state that some localities that do not use pyriproxyfen also had reported cases of microcephaly", read a Brazilian government statement. The Brazilian government also refuted conspiracy theories that chickenpox and rubella vaccinations or genetically modified mosquitoes were causing increases in microcephaly. Researchers also suspected that Zika virus could be transmitted by a pregnant woman to her baby (" vertical transmission "). This remained unproven until February 2016, when a paper by Calvet et al. was published, showing not only was the Zika virus genome found in the amniotic fluid but also IgM antibodies against the virus. This means that not only can the virus cross the placental barrier, but also the antibodies produced by the mother can reach the fetus, which suggests that vertical transmission is plausible in these cases. One other study published in March 2016 by Mlakar and colleagues analyzed autopsy tissues from a fetus with microcephaly that was probably related to Zika virus; researchers found ZIKV in the brain tissue and suggested that the brain injuries were probably associated with the virus, which also shed a light on the vertical transmission theory. Also in March 2016, first solid evidence was reported on how the virus affects the development of the brain, indicating that it appears to preferentially kill developing brain cells. The first cases of birth defects linked to Zika in Colombia and in Panama were reported in March 2016. In the same month, researchers published a prospective cohort study that found profound impacts in 29 percent of infants of mothers infected with Zika, some of whom were infected late in pregnancy. This study did not suffer from some of the difficulties of studying Zika: the study followed women who presented to a Rio de Janeiro clinic with fever and rash within the last five days. The women were then tested for Zika using PCR, then the progress of the pregnancies were followed using ultrasound. A high rate of the autoimmune disease Guillain–Barré syndrome (GBS), noted in the French Polynesia outbreak, has also been found in the outbreak that began in Brazil. Laboratory analysis found Zika infections in some patients with GBS in Brazil, El Salvador, Suriname and Venezuela, and the WHO declared on 22 March 2016 that Zika appeared to be "implicated" in GBS infection and that if the pattern was confirmed it would represent a global public health crisis. Early in the 2015–16 Zika virus epidemic , research was begun to better understand how Zika virus causes microcephaly and other neurological disorders. However, with the 2019 election of Jair Bolsonaro in Brazil, who cut funding for research, and the emergence of the COVID-19 pandemic in early 2020, most Zika-related research projects were abandoned or reduced. It may involve infection of the primary neural stem cells of the fetal brain, known as neural progenitor cells. The main roles of brain stem cells are to proliferate until the correct number is achieved, and then to produce neurons through the process of neurogenesis . Zika proteins NS4A and NS4B have also been shown to directly suppress neurogenesis. Infection of brain stem cells can cause cell death, which reduces the production of future neurons and leads to a smaller brain. Zika also appears to have an equal tropism for cells of the developing eye, leading to high rates of eye abnormalities as well. In addition to inducing cell death, infection of neural progenitor cells may alter the process of cell proliferation, causing a depletion in the pool of progenitor cells. A large number of cases of microcephaly have been associated with inherited gene mutations, and specifically with mutations that lead to dysfunction of the mitotic spindle . There is some evidence that Zika virus may directly or indirectly interfere with mitotic function, this may play a role in altering cell proliferation. Another line of research considers that Zika, unlike other flaviviruses, may target developing brain cells after it crosses the placenta, and considers the resulting damage likely to be the result of inflammation as a byproduct of the immune response to the infection of those cells. Some experimental methods of prevention include breeding and releasing mosquitoes that have been genetically modified to prevent them from transmitting pathogens, or have been infected with the Wolbachia bacterium, believed to inhibit the spread of viruses. A strain of Wolbachia helped to reduce the vector competence of the Zika virus in infected Aedes aegypti released in Medellin, Colombia. Gene drive is a technique for changing wild populations, for instance to combat insects so they cannot transmit diseases (in particular mosquitoes in the cases of malaria and Zika). Another method which been researched aims to render male mosquitoes infertile by nuclear radiation in the hope to reduce populations; this is done with a cobalt-60 gamma cell irradiator. In 2016 the World Health Organization encouraged field trials of transgenic male Aedes aegypti mosquitoes developed by Oxitec to try to halt the spread of the Zika virus. Early in the 2015–16 Zika virus epidemic , research was begun to better understand how Zika virus causes microcephaly and other neurological disorders. However, with the 2019 election of Jair Bolsonaro in Brazil, who cut funding for research, and the emergence of the COVID-19 pandemic in early 2020, most Zika-related research projects were abandoned or reduced. It may involve infection of the primary neural stem cells of the fetal brain, known as neural progenitor cells. The main roles of brain stem cells are to proliferate until the correct number is achieved, and then to produce neurons through the process of neurogenesis . Zika proteins NS4A and NS4B have also been shown to directly suppress neurogenesis. Infection of brain stem cells can cause cell death, which reduces the production of future neurons and leads to a smaller brain. Zika also appears to have an equal tropism for cells of the developing eye, leading to high rates of eye abnormalities as well. In addition to inducing cell death, infection of neural progenitor cells may alter the process of cell proliferation, causing a depletion in the pool of progenitor cells. A large number of cases of microcephaly have been associated with inherited gene mutations, and specifically with mutations that lead to dysfunction of the mitotic spindle . There is some evidence that Zika virus may directly or indirectly interfere with mitotic function, this may play a role in altering cell proliferation. Another line of research considers that Zika, unlike other flaviviruses, may target developing brain cells after it crosses the placenta, and considers the resulting damage likely to be the result of inflammation as a byproduct of the immune response to the infection of those cells. Some experimental methods of prevention include breeding and releasing mosquitoes that have been genetically modified to prevent them from transmitting pathogens, or have been infected with the Wolbachia bacterium, believed to inhibit the spread of viruses. A strain of Wolbachia helped to reduce the vector competence of the Zika virus in infected Aedes aegypti released in Medellin, Colombia. Gene drive is a technique for changing wild populations, for instance to combat insects so they cannot transmit diseases (in particular mosquitoes in the cases of malaria and Zika). Another method which been researched aims to render male mosquitoes infertile by nuclear radiation in the hope to reduce populations; this is done with a cobalt-60 gamma cell irradiator. In 2016 the World Health Organization encouraged field trials of transgenic male Aedes aegypti mosquitoes developed by Oxitec to try to halt the spread of the Zika virus.

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Rift Valley fever

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Nipah virus

Nipah virus is a bat-borne, zoonotic virus that causes Nipah virus infection in humans and other animals, a disease with a very high mortality rate (40-75%). Numerous disease outbreaks caused by Nipah virus have occurred in South East Africa and Southeast Asia. Nipah virus belongs to the genus Henipavirus along with the Hendra virus , which has also caused disease outbreaks. Like other henipaviruses , the Nipah virus genome is a single (non-segmented) negative-sense, single-stranded RNA of over 18 kb, which is substantially longer than that of other paramyxoviruses . The enveloped virus particles are variable in shape, and can be filamentous or spherical; they contain a helical nucleocapsid . Six structural proteins are generated: N (nucleocapsid), P ( phosphoprotein ), M (matrix), F (fusion), G (glycoprotein) and L (RNA polymerase). The P open reading frame also encodes three nonstructural proteins, C, V and W. There are two envelope glycoproteins. The G glycoprotein ectodomain assembles as a homotetramer to form the viral anti-receptor or attachment protein, which binds to the receptor on the host cell. Each strand in the ectodomain consists of four distinct regions: at the N-terminal and connecting to the viral surface is the helical stalk, followed by the beta-sandwich neck domain, the linker region and finally, at the C-terminal, four heads which contain host cell receptor binding domains. Each head consists of a beta-propeller structure with six blades. There are three unique folding patterns of the heads, resulting in a 2-up/2-down configuration where two heads are positioned distal to the virus and two heads are proximal. Due to the folding patterns and subsequent arrangement of the heads, only one of the four heads is positioned with its binding site accessible to associate with the host B2/B3 receptor. The G protein head domain is also highly antigenic, inducing head-specific antibodies in primate models. As such, it is a prime target for vaccine development as well as antibody therapy. One head-specific antibody, m102.4, has been used in compassionate use cases and has completed Phase 1 clinical trials. The F glycoprotein forms a trimer , which mediates membrane fusion. Ephrins B2 and B3 have been identified as the main receptors for Nipah virus. Ephrin sub-types have a complex distribution of expression throughout the body, where the B3 is noted to have particularly high expression in some forebrain sub-regions. Ephrins B2 and B3 have been identified as the main receptors for Nipah virus. Ephrin sub-types have a complex distribution of expression throughout the body, where the B3 is noted to have particularly high expression in some forebrain sub-regions. Nipah virus has been isolated from Lyle's flying fox ( Pteropus lylei ) in Cambodia and viral RNA found in urine and saliva from P. lylei and Horsfield's roundleaf bat ( Hipposideros larvatus ) in Thailand. Ineffective forms of the virus has also been isolated from environmental samples of bat urine and partially eaten fruit in Malaysia. Antibodies to henipaviruses have also been found in fruit bats in Madagascar ( Pteropus rufus , Eidolon dupreanum ) and Ghana ( Eidolon helvum ) indicating a wide geographic distribution of the viruses. No infection of humans or other species have been observed in Cambodia, Thailand or Africa as of May 2018. In September 2023, India reported at least five infections and two deaths. Fever Headache Muscle pain ( myalgia ) Vomiting Sore throat These symptoms can be followed by more serious conditions including: Dizziness Drowsiness Altered consciousness Acute encephalitis Atypical pneumonia Severe respiratory distress Seizures The first cases of Nipah virus infection were identified in 1998, when an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia caused 265 human cases, with 108 deaths. The virus was isolated the following year in 1999. This outbreak resulted in the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The name "Nipah" refers to the place, Sungai Nipah (literally nipah river') in Port Dickson , Negeri Sembilan , the source of the human case from which Nipah virus was first isolated. The outbreak was originally mistaken for Japanese encephalitis , but physicians in the area noted that persons who had been vaccinated against Japanese encephalitis were not protected in the epidemic, and the number of cases among adults was unusual. Although these observations were recorded in the first month of the outbreak, the Ministry of Health failed to take them into account, and launched a nationwide campaign to educate people on the dangers of Japanese encephalitis and its vector, Culex mosquitoes. [ citation needed ] Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. During the 1999 outbreak of Nipah virus, which occurred among pig farmers, the majority of human infections stemmed from direct contact with sick pigs and the unprotected handling of secretions from the pigs. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus ( large flying fox ), and Pteropus hypomelanus ( small flying fox ), both found in Malaysia. The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. In one outbreak, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring, undetected, in Malaysia since 1996. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent . Nipah virus is one of several viruses identified by WHO as a potential cause of future epidemics in a new plan developed after the Ebola epidemic for urgent research and development toward new diagnostic tests, vaccines and medicines. Presently, there are no dedicated drugs or vaccines available for the treatment or prevention of Nipah virus infection. The World Health Organization (WHO) has designated Nipah virus as a priority disease within the WHO Research and Development Blueprint. In cases of severe respiratory and neurological complications resulting from Nipah virus infection, healthcare professionals advise intensive supportive care as the primary treatment approach. In January 2024 a candidate vaccine, ChAdOx1 NipahB, commenced Phase I clinical trials after completing laboratory and animal testing. Nipah virus infection outbreaks have been reported in Malaysia, Singapore, Bangladesh and India. The highest mortality due to Nipah virus infection has occurred in Bangladesh, where outbreaks are typically seen in winter. Nipah virus first appeared in 1998, in peninsular Malaysia in pigs and pig farmers. By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore. In 2001, Nipah virus was reported from Meherpur District , Bangladesh and Siliguri , India. The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District , Manikganj District , Rajbari District , Faridpur District and Tangail District . In Bangladesh there were also outbreaks in subsequent years. In September 2021, Nipah virus resurfaced in Kerala , India claiming the life of a 12-year-old boy. The most recent outbreak of Nipah virus occurred during January and February 2023 in Bangladesh with a total of 11 cases (ten confirmed, one probable) resulting in 8 deaths, a case fatality rate of 73%. This outbreak resulted in the highest number of cases reported since 2015 in Bangladesh, and ten of the 11 cases during the 2023 outbreak had a confirmed history of consuming date palm sap. The first cases of Nipah virus infection were identified in 1998, when an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia caused 265 human cases, with 108 deaths. The virus was isolated the following year in 1999. This outbreak resulted in the culling of one million pigs. In Singapore, 11 cases, including one death, occurred in abattoir workers exposed to pigs imported from the affected Malaysian farms. The name "Nipah" refers to the place, Sungai Nipah (literally nipah river') in Port Dickson , Negeri Sembilan , the source of the human case from which Nipah virus was first isolated. The outbreak was originally mistaken for Japanese encephalitis , but physicians in the area noted that persons who had been vaccinated against Japanese encephalitis were not protected in the epidemic, and the number of cases among adults was unusual. Although these observations were recorded in the first month of the outbreak, the Ministry of Health failed to take them into account, and launched a nationwide campaign to educate people on the dangers of Japanese encephalitis and its vector, Culex mosquitoes. [ citation needed ] Symptoms of infection from the Malaysian outbreak were primarily encephalitic in humans and respiratory in pigs. Later outbreaks have caused respiratory illness in humans, increasing the likelihood of human-to-human transmission and indicating the existence of more dangerous strains of the virus. During the 1999 outbreak of Nipah virus, which occurred among pig farmers, the majority of human infections stemmed from direct contact with sick pigs and the unprotected handling of secretions from the pigs. Based on seroprevalence data and virus isolations, the primary reservoir for Nipah virus was identified as Pteropid fruit bats, including Pteropus vampyrus ( large flying fox ), and Pteropus hypomelanus ( small flying fox ), both found in Malaysia. The transmission of Nipah virus from flying foxes to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. In one outbreak, fruit orchards were in close proximity to the piggery, allowing the spillage of urine, faeces and partially eaten fruit onto the pigs. Retrospective studies demonstrate that viral spillover into pigs may have been occurring, undetected, in Malaysia since 1996. During 1998, viral spread was aided by the transfer of infected pigs to other farms, where new outbreaks occurred. The Nipah virus has been classified by the Centers for Disease Control and Prevention as a Category C agent . Nipah virus is one of several viruses identified by WHO as a potential cause of future epidemics in a new plan developed after the Ebola epidemic for urgent research and development toward new diagnostic tests, vaccines and medicines. Presently, there are no dedicated drugs or vaccines available for the treatment or prevention of Nipah virus infection. The World Health Organization (WHO) has designated Nipah virus as a priority disease within the WHO Research and Development Blueprint. In cases of severe respiratory and neurological complications resulting from Nipah virus infection, healthcare professionals advise intensive supportive care as the primary treatment approach. In January 2024 a candidate vaccine, ChAdOx1 NipahB, commenced Phase I clinical trials after completing laboratory and animal testing. Nipah virus infection outbreaks have been reported in Malaysia, Singapore, Bangladesh and India. The highest mortality due to Nipah virus infection has occurred in Bangladesh, where outbreaks are typically seen in winter. Nipah virus first appeared in 1998, in peninsular Malaysia in pigs and pig farmers. By mid-1999, more than 265 human cases of encephalitis, including 105 deaths, had been reported in Malaysia, and 11 cases of either encephalitis or respiratory illness with one fatality were reported in Singapore. In 2001, Nipah virus was reported from Meherpur District , Bangladesh and Siliguri , India. The outbreak again appeared in 2003, 2004 and 2005 in Naogaon District , Manikganj District , Rajbari District , Faridpur District and Tangail District . In Bangladesh there were also outbreaks in subsequent years. In September 2021, Nipah virus resurfaced in Kerala , India claiming the life of a 12-year-old boy. The most recent outbreak of Nipah virus occurred during January and February 2023 in Bangladesh with a total of 11 cases (ten confirmed, one probable) resulting in 8 deaths, a case fatality rate of 73%. This outbreak resulted in the highest number of cases reported since 2015 in Bangladesh, and ten of the 11 cases during the 2023 outbreak had a confirmed history of consuming date palm sap.

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Rift Valley fever

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Ross River fever

Ross River fever is a mosquito -borne infectious disease caused by infection with the Ross River virus . The illness is typically characterised by flu like symptoms combined with polyarthritis and a rash. The virus is endemic to mainland Australia and Tasmania , the island of New Guinea , Fiji , Samoa , the Cook Islands , New Caledonia and several other islands in the South Pacific. The illness is Queensland's most prolific mosquito-borne disease. Symptoms of the disease vary widely in severity, but major indicators are arthralgia , arthritis , fever , and rash . The incubation period is 7–9 days. About a third of infections are asymptomatic, particularly in children. About 95% of symptomatic cases report joint pain. This is typically symmetrical and with acute onset, affecting the fingers, toes, ankles, wrists, back, knees and elbows. Fatigue occurs in 90% and fever, myalgia and headache occur in 50–60%. A rash occurs in 50% of patients and is widespread and maculopapular . Lymphadenopathy occurs commonly; pharyngitis and rhinorrhea less frequently. Diarrhea is rare. About 50% of people report needing time off work with the acute illness. If the rash is unnoticed, these symptoms are quite easily mistaken for more common illnesses like influenza or the common cold . Recovery from the flu symptoms is expected within a month, but, because the virus currently cannot be removed once infection has occurred secondary symptoms of joint and muscle inflammation, pain and stiffness can last for many years. Less common manifestations include splenomegaly , hematuria and glomerulonephritis . Headache, neck stiffness, and photophobia may occur. There have been three case reports suggesting meningitis or encephalitis. [ citation needed ] Reports from the 1980s and 1990s suggested RRV infection was associated with arthralgia , fatigue and depression lasting for years. More recent prospective studies have reported a steady improvement in symptoms over the first few months, with 15–66% of patients having ongoing arthralgia at 3 months. Arthralgias have resolved in the majority by 5–7 months. The incidence of chronic fatigue is 12% at 6 months and 9% at 12 months, similar to Epstein–Barr virus and Q fever . The only significant predictor of the likelihood of developing chronic symptoms is the severity of the acute illness itself. No other aspects of the patient's medical or psychiatric history have been found to be predictive. However, in those with the most persisting symptoms (12 months or more), comorbid rheumatologic conditions and/or depression are frequently observed. About 95% of symptomatic cases report joint pain. This is typically symmetrical and with acute onset, affecting the fingers, toes, ankles, wrists, back, knees and elbows. Fatigue occurs in 90% and fever, myalgia and headache occur in 50–60%. A rash occurs in 50% of patients and is widespread and maculopapular . Lymphadenopathy occurs commonly; pharyngitis and rhinorrhea less frequently. Diarrhea is rare. About 50% of people report needing time off work with the acute illness. If the rash is unnoticed, these symptoms are quite easily mistaken for more common illnesses like influenza or the common cold . Recovery from the flu symptoms is expected within a month, but, because the virus currently cannot be removed once infection has occurred secondary symptoms of joint and muscle inflammation, pain and stiffness can last for many years. Less common manifestations include splenomegaly , hematuria and glomerulonephritis . Headache, neck stiffness, and photophobia may occur. There have been three case reports suggesting meningitis or encephalitis. [ citation needed ]Reports from the 1980s and 1990s suggested RRV infection was associated with arthralgia , fatigue and depression lasting for years. More recent prospective studies have reported a steady improvement in symptoms over the first few months, with 15–66% of patients having ongoing arthralgia at 3 months. Arthralgias have resolved in the majority by 5–7 months. The incidence of chronic fatigue is 12% at 6 months and 9% at 12 months, similar to Epstein–Barr virus and Q fever . The only significant predictor of the likelihood of developing chronic symptoms is the severity of the acute illness itself. No other aspects of the patient's medical or psychiatric history have been found to be predictive. However, in those with the most persisting symptoms (12 months or more), comorbid rheumatologic conditions and/or depression are frequently observed. The virus can only be spread by mosquitoes . The main reservoir hosts are kangaroos and wallabies , although horses, possums and possibly birds and flying foxes play a role. Over 30 species have been implicated as possible vectors , but the major species for Ross River fever are Culex annulirostris in inland areas, Aedes vigilax in northern coastal regions and Ae. camptorhynchus in southern coastal regions. A blood test is the only way to confirm a case of Ross River fever. Several types of blood tests may be used to examine antibody levels in the blood. Tests may either look for simply elevated antibodies (which indicate some sort of infection), or specific antibodies to the virus. There is currently no vaccine available. The primary method of disease prevention is minimizing mosquito bites, as the disease is only transmitted by mosquitoes. Typical advice includes use of mosquito repellent and mosquito screens, wearing light coloured clothing, and minimising standing water around homes (e.g. removing Bromeliads , plant pots, garden ponds). Staying indoors during dusk/dawn hours when mosquitos are most active may also be effective. Bush camping is a common precipitant of infection so particular care is required. [ citation needed ]Patients are usually managed with simple analgesics , anti-inflammatories , anti-pyretics and rest while the illness runs its course. Pentosan polysulfate has also shown recent promise. Most notifications are from Queensland, tropical Western Australia and the Northern Territory . Geographical risk factors include areas of higher rainfall and higher maximal tides. In the tropics, Ross River fever is more prevalent during the summer/autumn " wet season ", particularly January—March, when mosquito populations numbers are high. In southern parts of Australia, this time period may shift to earlier in the year during spring/summer. Areas noted of common place contraction of the virus include townships and along the River Murray areas. Backwaters and Lagoons are breeding grounds for mosquitos and local medical treating facilities report higher cases than cities away from the river around the riverina areas. Areas near suitable mosquito breeding grounds— marshes , wetlands , waterways and farms with irrigation systems—are high risk areas for outbreaks. As such, the disease is more characteristic of rural and regional areas. Infection is most common in adults aged 25–44 years old, with males and females equally affected. Ross River fever is on the Australian Department of Health and Ageing 's list of notifiable diseases . The first outbreak of RRF was in 1928 in the Hay and Narrandera region in New South Wales , Australia. The virus was first isolated in 1959 from a mosquito trapped along the Ross River in Townsville, Queensland . Since then, outbreaks have occurred in all Australian states, including Tasmania, and metropolitan areas. The largest outbreak occurred in 1979–1980 in the Western Pacific, and affected more than 60,000 people. Before the identification of this infectious agent, the disease was referred to as "epidemic polyarthritis". This term was also used for a similar Australian disease caused by another mosquito -borne virus, Barmah Forest virus . The study of RRF has been recently facilitated by the development of a mouse model . Mice infected with RRV develop hind-limb arthritis/arthralgia which is similar to human disease. The disease in mice is characterized by an inflammatory infiltrate including macrophages which are immunopathogenic and exacerbate disease. Furthermore, mice deficient in the C3 protein do not develop severe disease following infection. This indicates that an aberrant innate immune response is responsible for severe disease following RRV infection.

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Rift Valley fever

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Demographics of Somalia

Demographic features of Somalia 's inhabitants include ethnicity, language, population density, education level, health, economic status, religious affiliations and other aspects of the population. Somalia is believed to be one of the most homogeneous countries in Africa.Child marriages , known to deprive women of opportunities to reach their full potential, have among women aged 20–24, 36 percent of total population. The April 2020 SHDS report further unveils that fertility rates remain very high, the total fertility rate for Somalia is 6.9 children per woman, the highest in the world, which would impact planning for the next years. In addition, 99 percent of women have still been genitally circumcised . According to The Economist , at independence Somalia was "arguably in ethnic terms the most homogeneous country in Africa" however, the publication also notes that "its ethnic homogeneity is misleading. Despite also sharing a single language and religion, it is divided into more than 500 clans and sub-clans". Somalis constitute the largest ethnic group in Somalia, at approximately 98% of the nation's inhabitants. They are organized into clan groupings, which are important social units ; clan membership plays a central part in Somali culture and politics . Clans are patrilineal and are typically divided into sub-clans, sometimes with many sub-divisions. Through the xeer system ( customary law ), the advanced clan structure has served governmental roles in many rural Somali communities. Somali society is traditionally ethnically endogamous . So to extend ties of alliance, marriage is often to another ethnic Somali from a different clan. Thus, for example, a recent study observed that in 89 marriages contracted by men of the Dhulbahante clan, 55 (62%) were with women of Dhulbahante sub-clans other than those of their husbands; 30 (33.7%) were with women of surrounding clans of other clan families ( Isaaq , 28; Gadabuursi , 3); and 3 (4.3%) were with women of other clans of the Darod clan family ( Marehan 2, Ogaden 1). Certain clans are traditionally classed as noble clans, referring to their pastoral lifestyle in contrast to the sedentary "Sab". The four noble clans are the Dir , Darod , Hawiye and Isaaq . Of these, the Dir and Hawiye are regarded as descended from Irir Samaale , the likely source of the ethnonym Somali (soomaali) . Darod have separate agnatic (paternal) traditions of descent from Abdirahman bin Isma'il al-Jabarti (Sheikh Darod). Sheikh Darod is asserted to have married women from the Dir clan, thus establishing matrilateral ties with the Samaale main stem. "Sab" is a term used to refer to minor Somali clans in contrast to "Samaale". Both Samaale and Sab are the children of the father "Hiil" who is the common ancestor of all Somali clans. A few clans in the southern part of Greater Somalia do not belong to the major clans, but came to be associated with them and were eventually adopted into one of the confederations. Gaalje'el in Hirshabelle and elsewhere in central Somalia trace their paternal descent to Gardheere Samaale. The Degoodi clan in the Somali Region and North Eastern Province are related to Gaalje'el as the Saransoor trace patrilineage to Gardheere Samaale; Hawaadle in Hiran belong to the Meyle Samaale; Thus, the Gaalje'el, Garre, Degoodi Ajuraan and Hawaadle are said to have patrilateral ties with the Dir and Hawiye through Samaale to Aqil ibn Abi Talib (a cousin of Muhammad and a brother of Ali ). The Garre clan in the Somali Region and the North Eastern Province is divided into two branches: The Tuuf who claim descent from Garre Gardheere Samaale, and Quranyow, who married Tuuf's daughter, is of the lineage Mahamed Hiniftir Mahe Dir. Ajuraan in the North Eastern Province claim descent from Maqaarre Samaale The Sheekhaal acknowledge descent from Sheikh Abadir Umar Ar-Rida , known as Fiqi Umar . The Sheekhaal clan (Arabic: شيخال), is a Somali clan and a group member of the confederation (Martiile Hiraab) inhabiting Somalia, Ethiopia and with considerable numbers also found in the Northern Frontier District (NFD) in Kenya. The Digil and Mirifle ( Rahanweyn ) are agro - pastoral clans in the areas between the Baay and Bakool. Many do not follow a nomadic lifestyle, live further south, and speak Maay . Although in the past frequently classified as a Somali dialect , more recent research by the linguist Mohamed Diriye Abdullahi suggests that Maay constitutes a separate but closely related Afro-Asiatic language of the Cushitic branch. A third group, the occupational clans, are treated as outcasts. They can only marry among themselves. They live in their settlements among the nomadic populations in the north and performed specialized occupations such as metalworking , tanning and hunting . These minority Somali clans are the Gaboye ( Madhiban ), Tumaal , Yibir , Jaji and Yahar. There is no clear agreement on the clan and sub-clan structures. The divisions and subdivisions as given here are partial and simplified. Many lineages are omitted. Sagaal: Geeladle, Jilible, Gasaargude, Gawaweeyn, Luwaay, Hadame, Yantaar, Hubeer Siyeed: Elaay. Leysaan, Eemid, Diisow, Yalaale, Qoomaal, Maalin Wiing, Harin, Jiron, Reer Dumaal, Garwaale and Haraw Cowrmale known as Coormale Ibraahim Non-Somali ethnic minority groups make up about 5% of the nation's population. They include Arabs , Bantus & Bajunis .Somalis constitute the largest ethnic group in Somalia, at approximately 98% of the nation's inhabitants. They are organized into clan groupings, which are important social units ; clan membership plays a central part in Somali culture and politics . Clans are patrilineal and are typically divided into sub-clans, sometimes with many sub-divisions. Through the xeer system ( customary law ), the advanced clan structure has served governmental roles in many rural Somali communities. Somali society is traditionally ethnically endogamous . So to extend ties of alliance, marriage is often to another ethnic Somali from a different clan. Thus, for example, a recent study observed that in 89 marriages contracted by men of the Dhulbahante clan, 55 (62%) were with women of Dhulbahante sub-clans other than those of their husbands; 30 (33.7%) were with women of surrounding clans of other clan families ( Isaaq , 28; Gadabuursi , 3); and 3 (4.3%) were with women of other clans of the Darod clan family ( Marehan 2, Ogaden 1). Certain clans are traditionally classed as noble clans, referring to their pastoral lifestyle in contrast to the sedentary "Sab". The four noble clans are the Dir , Darod , Hawiye and Isaaq . Of these, the Dir and Hawiye are regarded as descended from Irir Samaale , the likely source of the ethnonym Somali (soomaali) . Darod have separate agnatic (paternal) traditions of descent from Abdirahman bin Isma'il al-Jabarti (Sheikh Darod). Sheikh Darod is asserted to have married women from the Dir clan, thus establishing matrilateral ties with the Samaale main stem. "Sab" is a term used to refer to minor Somali clans in contrast to "Samaale". Both Samaale and Sab are the children of the father "Hiil" who is the common ancestor of all Somali clans. A few clans in the southern part of Greater Somalia do not belong to the major clans, but came to be associated with them and were eventually adopted into one of the confederations. Gaalje'el in Hirshabelle and elsewhere in central Somalia trace their paternal descent to Gardheere Samaale. The Degoodi clan in the Somali Region and North Eastern Province are related to Gaalje'el as the Saransoor trace patrilineage to Gardheere Samaale; Hawaadle in Hiran belong to the Meyle Samaale; Thus, the Gaalje'el, Garre, Degoodi Ajuraan and Hawaadle are said to have patrilateral ties with the Dir and Hawiye through Samaale to Aqil ibn Abi Talib (a cousin of Muhammad and a brother of Ali ). The Garre clan in the Somali Region and the North Eastern Province is divided into two branches: The Tuuf who claim descent from Garre Gardheere Samaale, and Quranyow, who married Tuuf's daughter, is of the lineage Mahamed Hiniftir Mahe Dir. Ajuraan in the North Eastern Province claim descent from Maqaarre Samaale The Sheekhaal acknowledge descent from Sheikh Abadir Umar Ar-Rida , known as Fiqi Umar . The Sheekhaal clan (Arabic: شيخال), is a Somali clan and a group member of the confederation (Martiile Hiraab) inhabiting Somalia, Ethiopia and with considerable numbers also found in the Northern Frontier District (NFD) in Kenya. The Digil and Mirifle ( Rahanweyn ) are agro - pastoral clans in the areas between the Baay and Bakool. Many do not follow a nomadic lifestyle, live further south, and speak Maay . Although in the past frequently classified as a Somali dialect , more recent research by the linguist Mohamed Diriye Abdullahi suggests that Maay constitutes a separate but closely related Afro-Asiatic language of the Cushitic branch. A third group, the occupational clans, are treated as outcasts. They can only marry among themselves. They live in their settlements among the nomadic populations in the north and performed specialized occupations such as metalworking , tanning and hunting . These minority Somali clans are the Gaboye ( Madhiban ), Tumaal , Yibir , Jaji and Yahar. There is no clear agreement on the clan and sub-clan structures. The divisions and subdivisions as given here are partial and simplified. Many lineages are omitted. Sagaal: Geeladle, Jilible, Gasaargude, Gawaweeyn, Luwaay, Hadame, Yantaar, Hubeer Siyeed: Elaay. Leysaan, Eemid, Diisow, Yalaale, Qoomaal, Maalin Wiing, Harin, Jiron, Reer Dumaal, Garwaale and Haraw Cowrmale known as Coormale IbraahimCertain clans are traditionally classed as noble clans, referring to their pastoral lifestyle in contrast to the sedentary "Sab". The four noble clans are the Dir , Darod , Hawiye and Isaaq . Of these, the Dir and Hawiye are regarded as descended from Irir Samaale , the likely source of the ethnonym Somali (soomaali) . Darod have separate agnatic (paternal) traditions of descent from Abdirahman bin Isma'il al-Jabarti (Sheikh Darod). Sheikh Darod is asserted to have married women from the Dir clan, thus establishing matrilateral ties with the Samaale main stem. "Sab" is a term used to refer to minor Somali clans in contrast to "Samaale". Both Samaale and Sab are the children of the father "Hiil" who is the common ancestor of all Somali clans. A few clans in the southern part of Greater Somalia do not belong to the major clans, but came to be associated with them and were eventually adopted into one of the confederations. Gaalje'el in Hirshabelle and elsewhere in central Somalia trace their paternal descent to Gardheere Samaale. The Degoodi clan in the Somali Region and North Eastern Province are related to Gaalje'el as the Saransoor trace patrilineage to Gardheere Samaale; Hawaadle in Hiran belong to the Meyle Samaale; Thus, the Gaalje'el, Garre, Degoodi Ajuraan and Hawaadle are said to have patrilateral ties with the Dir and Hawiye through Samaale to Aqil ibn Abi Talib (a cousin of Muhammad and a brother of Ali ). The Garre clan in the Somali Region and the North Eastern Province is divided into two branches: The Tuuf who claim descent from Garre Gardheere Samaale, and Quranyow, who married Tuuf's daughter, is of the lineage Mahamed Hiniftir Mahe Dir. Ajuraan in the North Eastern Province claim descent from Maqaarre Samaale The Sheekhaal acknowledge descent from Sheikh Abadir Umar Ar-Rida , known as Fiqi Umar . The Sheekhaal clan (Arabic: شيخال), is a Somali clan and a group member of the confederation (Martiile Hiraab) inhabiting Somalia, Ethiopia and with considerable numbers also found in the Northern Frontier District (NFD) in Kenya. The Digil and Mirifle ( Rahanweyn ) are agro - pastoral clans in the areas between the Baay and Bakool. Many do not follow a nomadic lifestyle, live further south, and speak Maay . Although in the past frequently classified as a Somali dialect , more recent research by the linguist Mohamed Diriye Abdullahi suggests that Maay constitutes a separate but closely related Afro-Asiatic language of the Cushitic branch. A third group, the occupational clans, are treated as outcasts. They can only marry among themselves. They live in their settlements among the nomadic populations in the north and performed specialized occupations such as metalworking , tanning and hunting . These minority Somali clans are the Gaboye ( Madhiban ), Tumaal , Yibir , Jaji and Yahar.There is no clear agreement on the clan and sub-clan structures. The divisions and subdivisions as given here are partial and simplified. Many lineages are omitted.Sagaal: Geeladle, Jilible, Gasaargude, Gawaweeyn, Luwaay, Hadame, Yantaar, Hubeer Siyeed: Elaay. Leysaan, Eemid, Diisow, Yalaale, Qoomaal, Maalin Wiing, Harin, Jiron, Reer Dumaal, Garwaale and Haraw Cowrmale known as Coormale IbraahimNon-Somali ethnic minority groups make up about 5% of the nation's population. They include Arabs , Bantus & Bajunis .Somali is the official language of Somalis. The Somali language is the mother tongue of the Somalis, the nation's most populous ethnic group. It is a member of the Cushitic branch of the Afroasiatic family. In addition to Somali, Arabic, which is also an Afroasiatic tongue, is a language in Somalia. Many Somalis speak it due to centuries-old ties with the Arab world , the far-reaching influence of the Arabic media, and religious education. English is widely used and taught. Other minority languages include Bravanese , a variant of the Bantu Swahili language that is spoken along the coast by the Bravanese people , as well as Bajuni , another Swahili dialect that is the mother tongue of the Bajuni ethnic minority group.According to the 2022 revision of the World Population Prospects , the total population was 17,065,581 in 2021 , compared to 2,264,000 in 1950. The proportion of children below the age of 15 in 2010 was 44.9%, 52.3% was between 15 and 65 years of age, while 2.7% was 65 years or older. Registration of vital events in Somalia is incomplete. The Population Department of the United Nations prepared the following estimates: Demographic statistics according to the World Population Review. One birth every 46 seconds One death every 3 minutes One net migrant every 16 minutes Net gain of one person every 1 minutes The following demographic are from the CIA World Factbook unless otherwise indicated. Sunni Muslim (Islam) (official, according to the 2012 Transitional Federal Charter) At birth: 1.03 males/female Under 15 years: 1 male/female 15–64 years: 1.07 males/female 65 years and over: 0.66 males/female Total population: 1.01 males/female (2015 est. ) total population: 55.72 years. Country comparison to the world: 225th male: 53.39 years female: 58.12 years (2022 est.) note: on 21 March 2022, the US Centers for Disease Control and Prevention (CDC) issued a Travel Alert for polio in Africa; Somalia is currently considered a high risk to travelers for circulating vaccine-derived polioviruses (cVDPV); vaccine-derived poliovirus (VDPV) is a strain of the weakened poliovirus that was initially included in oral polio vaccine (OPV) and that has changed over time and behaves more like the wild or naturally occurring virus; this means it can be spread more easily to people who are unvaccinated against polio and who come in contact with the stool or respiratory secretions, such as from a sneeze, of an "infected" person who received oral polio vaccine; the CDC recommends that before any international travel, anyone unvaccinated, incompletely vaccinated, or with an unknown polio vaccination status should complete the routine polio vaccine series; before travel to any high-risk destination, CDC recommends that adults who previously completed the full, routine polio vaccine series receive a single, lifetime booster dose of polio vaccine 0.1% (2017 est.) 11,000 (2017 est.) <1000 (2017 est.) Degree of risk : high Food or waterborne diseases : bacterial and protozoal diarrhea, hepatitis A and E, and typhoid fever Vector-borne diseases : dengue fever, malaria, and Rift Valley fever Water contact disease : schistosomiasis Animal contact disease : rabies (2013) Noun: Somali (singular) or Somali (plural) Adjective: Somali Definition: age 15 and over can read and write Total population: N/A Sunni Muslim (Islam) (official, according to the 2012 Transitional Federal Charter)At birth: 1.03 males/female Under 15 years: 1 male/female 15–64 years: 1.07 males/female 65 years and over: 0.66 males/female Total population: 1.01 males/female (2015 est. )total population: 55.72 years. Country comparison to the world: 225th male: 53.39 years female: 58.12 years (2022 est.)note: on 21 March 2022, the US Centers for Disease Control and Prevention (CDC) issued a Travel Alert for polio in Africa; Somalia is currently considered a high risk to travelers for circulating vaccine-derived polioviruses (cVDPV); vaccine-derived poliovirus (VDPV) is a strain of the weakened poliovirus that was initially included in oral polio vaccine (OPV) and that has changed over time and behaves more like the wild or naturally occurring virus; this means it can be spread more easily to people who are unvaccinated against polio and who come in contact with the stool or respiratory secretions, such as from a sneeze, of an "infected" person who received oral polio vaccine; the CDC recommends that before any international travel, anyone unvaccinated, incompletely vaccinated, or with an unknown polio vaccination status should complete the routine polio vaccine series; before travel to any high-risk destination, CDC recommends that adults who previously completed the full, routine polio vaccine series receive a single, lifetime booster dose of polio vaccine0.1% (2017 est.) 11,000 (2017 est.) <1000 (2017 est.)Degree of risk : high Food or waterborne diseases : bacterial and protozoal diarrhea, hepatitis A and E, and typhoid fever Vector-borne diseases : dengue fever, malaria, and Rift Valley fever Water contact disease : schistosomiasis Animal contact disease : rabies (2013)Noun: Somali (singular) or Somali (plural) Adjective: SomaliDefinition: age 15 and over can read and write Total population: N/A

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Rift Valley fever

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Japanese encephalitis

Japanese encephalitis ( JE ) is an infection of the brain caused by the Japanese encephalitis virus (JEV). While most infections result in little or no symptoms, occasional inflammation of the brain occurs . In these cases, symptoms may include headache, vomiting, fever, confusion and seizures . This occurs about 5 to 15 days after infection. JEV is generally spread by mosquitoes , specifically those of the Culex type. Pigs and wild birds serve as a reservoir for the virus. The disease occurs mostly outside of cities. Diagnosis is based on blood or cerebrospinal fluid testing. Prevention is generally achieved with the Japanese encephalitis vaccine , which is both safe and effective. Other measures include avoiding mosquito bites. Once infected, there is no specific treatment, with care being supportive . This is generally carried out in a hospital. Permanent problems occur in up to half of people who recover from JE. The disease primarily occurs in East and Southeast Asia as well as the Western Pacific . About 3 billion people live in areas where the disease occurs. About 68,000 symptomatic cases occur a year, with about 17,000 deaths. Often, cases occur in outbreaks . The disease was first described in Japan in 1871 . The Japanese encephalitis virus (JEV) has an incubation period of 2 to 26 days. The vast majority of infections are asymptomatic : only 1 in 250 infections develop into encephalitis. Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia , hemiparesis , convulsions and a raised body temperature between 38–41 °C (100.4–105.8 °F) . The mortality rate of the disease is around 25% and is generally higher in children under five, the immuno-suppressed and the elderly. Transplacental spread has been noted. Neurological disorders develop in 40% of those who survive with lifelong neurological defects such as deafness, emotional lability and hemiparesis occurring in those who had central nervous system involvement. Increased microglial activation following Japanese encephalitis infection has been found to influence the outcome of viral pathogenesis. Microglia are the resident immune cells of the central nervous system (CNS) and have a critical role in host defense against invading microorganisms. Activated microglia secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α) , which can cause toxic effects in the brain. Additionally, other soluble factors such as neurotoxins , excitatory neurotransmitters , prostaglandin , reactive oxygen , and nitrogen species are secreted by activated microglia. [ citation needed ] In a murine model of JE, it was found that in the hippocampus and the striatum , the number of activated microglia was more than anywhere else in the brain, closely followed by that in the thalamus . In the cortex, the number of activated microglia was significantly less when compared to other regions of the mouse brain . An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese encephalitis infection was also observed. [ citation needed ] Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as the brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. In animals, key signs include infertility and abortion in pigs, neurological disease in horses, and systemic signs including fever, lethargy and anorexia. It is a disease caused by the mosquito -borne Japanese encephalitis virus (JEV). JEV is a virus from the family Flaviviridae , part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses , and four known to infect humans including West Nile virus . The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase , and NS5 is the viral polymerase . It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins. Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain. The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010. [ citation needed ]JEV is a virus from the family Flaviviridae , part of the Japanese encephalitis serocomplex of 9 genetically and antigenically related viruses, some which are particularly severe in horses , and four known to infect humans including West Nile virus . The enveloped virus is closely related to the West Nile virus and the St. Louis encephalitis virus. The positive sense single-stranded RNA genome is packaged in the capsid which is formed by the capsid protein. The outer envelope is formed by envelope protein and is the protective antigen. It aids in entry of the virus into the cell. The genome also encodes several nonstructural proteins (NS1, NS2a, NS2b, NS3, N4a, NS4b, NS5). NS1 is produced as a secretory form also. NS3 is a putative helicase , and NS5 is the viral polymerase . It has been noted that Japanese encephalitis infects the lumen of the endoplasmic reticulum (ER) and rapidly accumulates substantial amounts of viral proteins. Based on the envelope gene, there are five genotypes (I–V). The Muar strain, isolated from a patient in Malaya in 1952, is the prototype strain of genotype V. Genotype V is the earliest recognized ancestral strain. The first clinical reports date from 1870, but the virus appears to have evolved in the mid-16th century. Over sixty complete genomes of this virus had been sequenced by 2010. [ citation needed ]Japanese encephalitis is diagnosed by commercially available tests detecting JE virus-specific IgM antibodies in serum and/or cerebrospinal fluid , for example by IgM capture ELISA . JE virus IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for 30 to 90 days, but longer persistence has been documented. Therefore, positive IgM antibodies occasionally may reflect a past infection or vaccination. Serum collected within 10 days of illness onset may not have detectable IgM, and the test should be repeated on a convalescent sample. For patients with JE virus IgM antibodies, confirmatory neutralizing antibody testing should be performed. Confirmatory testing in the US is available only at the CDC and a few specialized reference laboratories. In fatal cases, nucleic acid amplification and virus culture of autopsy tissues can be useful. Viral antigen can be shown in tissues by indirect fluorescent antibody staining . Infection with Japanese encephalitis confers lifelong immunity . There are currently three vaccines available: SA14-14-2, IXIARO (IC51, also marketed in Australia, New Zealand as JESPECT and India as JEEV ) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus. [ citation needed ] A formalin -inactivated mouse-brain-derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program. The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there are few adverse effects compared to placebo , the main side effects being headache and myalgia . The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there are no data available regarding the interchangeability of other JE vaccines and IXIARO. [ citation needed ]There is no specific treatment for Japanese encephalitis and treatment is supportive, with assistance given for feeding , breathing or seizure control as required. Raised intracranial pressure may be managed with mannitol . There is no transmission from person to person and therefore patients do not need to be isolated. [ citation needed ] A breakthrough in the field of Japanese encephalitis therapeutics is the identification of macrophage receptor involvement in the disease severity. A recent report of an Indian group demonstrates the involvement of monocyte and macrophage receptor CLEC5A in severe inflammatory response in Japanese encephalitis infection of the brain. This transcriptomic study provides a hypothesis of neuroinflammation and a new lead in development of appropriate therapies for Japanese encephalitis. The effectiveness of intravenous immunoglobulin for the management of encephalitis is unclear due to a lack of evidence. Intravenous immunoglobulin for Japanese encephalitis appeared to have no benefit. Japanese encephalitis (JE) is the leading cause of viral encephalitis in Asia , with up to 70,000 cases reported annually. Case-fatality rates range from 0.3% to 60% and depend on the population and age. Rare outbreaks in U.S. territories in the Western Pacific have also occurred. Residents of rural areas in endemic locations are at highest risk; Japanese encephalitis does not usually occur in urban areas. [ citation needed ] Countries which have had major epidemics in the past, but which have controlled the disease primarily by vaccination, include China , South Korea , Singapore , Japan , Taiwan and Thailand . Other countries that still have periodic epidemics include Vietnam , Cambodia , Myanmar , India , Nepal , and Malaysia . Japanese encephalitis has been reported in the Torres Strait Islands , and two fatal cases were reported in mainland northern Australia in 1998. There were reported cases in Kachin State , Myanmar in 2013. There were 116 deaths reported in Odisha's Malkangiri district of India in 2016. [ citation needed ] In 2022, the notable increase in distribution of the virus in Australia due to climate change became a concern to health officials as the population has limited immunity to the disease and the presence of large numbers of farmed and feral pigs could act as reservoirs for the virus. In February 2022, Japanese encephalitis was detected and confirmed in piggeries in Victoria, Queensland and New South Wales. On 4 March, cases were detected in South Australia. By October 2022, the outbreak in eastern mainland Australia had caused 42 symptomatic human cases of the disease, resulting in seven deaths. Humans, cattle, and horses are dead-end hosts as the disease manifests as fatal encephalitis. Pigs act as an amplifying host and have a very important role in the epidemiology of the disease. Infection in swine is asymptomatic, except in pregnant sows, when abortion and fetal abnormalities are common sequelae. The most important vector is Culex tritaeniorhynchus , which feeds on cattle in preference to humans. The natural hosts of the Japanese encephalitis virus are birds, not humans, and many believe the virus will therefore never be eliminated. In November 2011, the Japanese encephalitis virus was reported in Culex bitaeniorhynchus in South Korea . Recently, whole genome microarray research of neurons infected with the Japanese encephalitis virus has shown that neurons play an important role in their own defense against Japanese encephalitis infection. Although this challenges the long-held belief that neurons are immunologically quiescent, an improved understanding of the proinflammatory effects responsible for immune-mediated control of viral infection and neuronal injury during Japanese encephalitis infection is an essential step for developing strategies for limiting the severity of CNS disease. A number of drugs have been investigated to either reduce viral replication or provide neuroprotection in cell lines or studies upon mice. None are currently advocated in treating human patients.It is theorized that the virus may have originated from an ancestral virus in the mid-1500s in the Malay Archipelago region and evolved there into five different genotypes which spread across Asia. The mean evolutionary rate has been estimated to be 4.35 × 10 −4 (range: 3.49 × 10 −4 to 5.30 × 10 −4 ) nucleotide substitutions per site per year.

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Rift Valley fever

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Kyasanur Forest disease

Kyasanur forest disease ( KFD ) is a tick-borne viral haemorrhagic fever endemic to South-western part of India. The disease is caused by a virus belonging to the family Flaviviridae . KFDV is transmitted to humans through the bite of infected hard ticks ( Haemaphysalis spinigera ) which act as a reservoir of KFDV.The symptoms of the disease include a high fever with frontal headaches, chills, severe muscle pain, vomiting, and other gastrointestinal symptoms. Bleeding problems may occur 3–4 days after initial symptom onset. Patients may experience abnormally low blood pressure, and low platelet, red blood cell, and white blood cell count. After 1–2 weeks of symptoms, some patients recover without complication. However, the illness is biphasic for a subset of patients (10-20%) who experience a second wave of symptoms at the beginning of the third week. These symptoms include fever and signs of neurological manifestations, such as severe headache, mental disturbances, tremors, and vision deficits. The convalescent period is typically very long, lasting several months. Muscle aches and weakness also occur during this period, and the patient is unable to engage in physical activities.Kyasanur Forest virus The KFD virus is a typical flavivirus measuring about 40-60 nm in diameter. The genome of KFDV consists of 10,774 nucleotides of single-stranded, positive-sense RNA encoding a single polyprotein that is cleaved post-translationally into three structural (C, prM/M and E) and seven non-structural (NS1, NS2a, NS2b, NS3, NS4a, NS4b and NS5) proteins. The genome of KFDV is very similar (>92% homologous) to that of Alkhurma Hemorrhagic Fever Virus which is primarily found in Saudi Arabia . These two species both belong to the family Flaviviridae and diverged over 700 years ago and have thus remained geographically separated. A variety of animals are thought to be reservoir hosts for the disease, including porcupines, rats, squirrels, mice, and shrews. Monkeys are the main amplifying hosts for KFD virus and they are also affected by the virus. The surili Presbytis entellus and the bonnet macaque are very susceptible to the KFD virus. They develop tremendous viremia and infect the ticks. The vector for disease transmission is Haemaphysalis spinigera , a forest tick . Humans contract infection from the bite of nymphs of the tick. Man is a terminal host and there no human-to-human transmission because the human domestic environment does not sustain the ticks.Kyasanur Forest virus The KFD virus is a typical flavivirus measuring about 40-60 nm in diameter. The genome of KFDV consists of 10,774 nucleotides of single-stranded, positive-sense RNA encoding a single polyprotein that is cleaved post-translationally into three structural (C, prM/M and E) and seven non-structural (NS1, NS2a, NS2b, NS3, NS4a, NS4b and NS5) proteins. The genome of KFDV is very similar (>92% homologous) to that of Alkhurma Hemorrhagic Fever Virus which is primarily found in Saudi Arabia . These two species both belong to the family Flaviviridae and diverged over 700 years ago and have thus remained geographically separated. A variety of animals are thought to be reservoir hosts for the disease, including porcupines, rats, squirrels, mice, and shrews. Monkeys are the main amplifying hosts for KFD virus and they are also affected by the virus. The surili Presbytis entellus and the bonnet macaque are very susceptible to the KFD virus. They develop tremendous viremia and infect the ticks. The vector for disease transmission is Haemaphysalis spinigera , a forest tick . Humans contract infection from the bite of nymphs of the tick. Man is a terminal host and there no human-to-human transmission because the human domestic environment does not sustain the ticks.The pathogenesis of KFDV is not completely understood . Research using mice models found that KFDV primarily replicated in the brain. Other research has expanded on this by described neurological changes that occurred within infected organisms. This experiment was completed by using KFDV-infected mice and discovered that KFDV caused gliosis , inflammation, and cell death in the brain. They posited that KFDV could be primarily a neuropathic disease and other symptoms are due to this pathogenesis. In earlier days suspected case were confirmed in a laboratory by serum inoculation into suckling mice (Swiss Albino mice) and subsequent death of mice was leveled as KFD Positive case. Other methods of diagnosis included hemagglutination inhibition (HI), complement fixation , neutralization tests . However, new research has introduced more efficient molecular based methods to diagnose KFDV. These methods include: RT-PCR, nested RT-PCR , TaqMan-based real-time RT-PCR , Immunoglobin M antibodies and Immunoglobin G detection by ELISA . The two methods involving RT- PCR are able to function by attaching a primer to the NS-5 gene, which is highly conserved among the genus to which KFDV belongs. PCR positivity is limited to 8–10 days from the onset of symptoms. The ELISA based methods allows for the detections of anti-KFDV antibodies in patients typically from 5th day of onset of symptoms up to 3 months. Prevention is by vaccination, as well as preventive measures such as protective clothing and tick population control. The vaccine for KFDV consists of formalin -inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who receive two doses. For individuals who receive an additional dose, the effectiveness increases to 82.9%. Specific antiviral treatments are not available as of 2022. The spill-over of Kyasanur forest disease happens at the crossroads of the animal-human interaction, especially villages adjoining forest areas and inter-state borders. People who frequently visit the forest areas of the Western Ghats region such as forest guards and officials, range forest officer (RFO), forest watchers, shepherds, firewood collectors, dry leaf collectors, hunters, people who handle dead animal carcasses, travelers who camp in the forest areas, tribal communities living inside the forest areas (Jenu kurubas and Betta kurubas), cashew nut workers especially those who engage in cleaning the dry leaves before the harvest season (seen in Pali and Mauxi outbreaks, North Goa), and areca nut farm workers working in infected tick areas will have a high risk of acquiring KFD infection. People who live in the KFD endemic areas and refuse to take KFD vaccination are at risk in contracting the infection.The disease was first reported from Kattinakere village forest which is in the Kyasanur forest range of Karnataka in India in March 1957. When the officials visited the Kattinakere forest and discovered the diseases they noticed a sign board informing that this was the Kyasanur forest range. Hence the name. The disease first manifested as an epizootic outbreak among monkeys, killing several of them in the year 1957. Hence the disease is also locally known as "monkey disease" or "monkey fever". The similarity with Russian spring-summer encephalitis was noted by the British neurovirologist Hubert Webb and the possibility of migratory birds carrying the disease was raised. Studies began to look for the possible species that acted as reservoirs for the virus and the agents responsible for transmission. Subsequent studies failed to find any involvement of migratory birds, although the possibility of their role in initial establishment was not ruled out. The virus was found to be quite distinctive and not closely related to the Russian virus strains. Antigenic relatedness is, however, close to many other strains including the Omsk hemorrhagic fever (OHF) and birds from Siberia have been found to show an antigenic response to KFD virus. Sequence based studies note the distinctiveness of OHF. Early studies in India were conducted in collaboration with the US Army Medical Research Unit and this led to controversy and conspiracy theories. Subsequent studies based on sequencing found that the Alkhurma virus found in Saudi Arabia is closely related. In 1989 a patient in Nanjianin, China was found with fever symptoms and in 2009 its viral gene sequence was found to exactly match with that of the KFD reference virus of 1957. This has been questioned, though, since the Indian virus shows variations in sequence over time and the exact match with the virus sequence of 1957 and the Chinese virus of 1989 is not expected. This study also found using immune response tests that birds and humans in the region appeared to have been exposed to the virus. Another study has suggested that the virus is recent in origin dating the nearest common ancestor of it and related viruses to around 1942, based on the estimated rate of sequence substitutions. The study also raises the possibility of bird involvement in long-distance transfer. It appears that these viruses diverged 700 years ago. A recent outbreak in 2020, claimed two lives in Siddapura , Karnataka. The peak season for this disease in Malnad is from March till May but has been observed to peak earlier in the year as well. There were a total of 55 reported cases in Shivamogga district, Karntaka. The disease initially reported from Shimoga district of Karnataka which is a primitive sylvan territory in Western Ghats of India. The disease spread out to other districts of Karnataka involving districts of Chikkamagalore, Uttara Kannada, Dakshina Kannada, Udupi, Chamarajanagar (2012), Belagavi (2016). In 2013, KFDV was detected in monkey autopsies from Nilgiris district of Tamil Nadu state. Monkey deaths and human cases have now been reported from three neighbouring states bordering Karnataka, i.e., Wayanad (2013) and Malappuram districts of Kerala (2014), North Goa district of Goa state (2015), and Sindhudurg district of Maharashtra (2016). There are reported serological evidence for KFD detected in humans in other parts of India, namely Kutch and Saurashtra regions of Gujarat state, Kingaon and Parbatpur of West Bengal state. A seroprevalence study in Andaman and Nicobar islands in 2002 revealed a high prevalence of hemagglutination inhibition (HI) antibodies against KFDV. The disease has a fatality rate of 3-10%, and it affects 400-500 people annually. The disease was first noted at Kyasanur village near Sagar in Shivamogga district of Karnataka. The virus has been detected in monkeys in parts of Bandipur National Park (Chamarajnagar) and parts of the Nilgiris. Human infection occurred in Bandipur through handling of dead monkeys that were infected. A human carrier was also detected in Wayanad (Kerala). The disease has shown its presence in the adjacent states of Karnataka including Kerala, Maharashtra, Goa, Tamil Nadu and Gujarat.

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Rift Valley fever

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Michael J. Ryan (doctor)

Michael Joseph Ryan (born 1965) is an Irish epidemiologist and former trauma surgeon, specialising in infectious disease and public health. He is executive director of the World Health Organization 's Health Emergencies Programme, leading the team responsible for the international containment and treatment of COVID-19 . Ryan has held leadership positions and has worked on various outbreak response teams in the field to eradicate the spread of diseases including bacillary dysentery , cholera , Crimean–Congo hemorrhagic fever , Ebola , Marburg virus disease , measles , meningitis , relapsing fever , Rift Valley fever , SARS , and Shigellosis . Mike Ryan is from the townland of Curry, near Tubbercurry , in County Sligo , Ireland . He grew up in the town of Charlestown in County Mayo . His father worked as a merchant sailor. Ryan trained in medicine at the National University of Ireland in Galway . He received training in orthopaedics in Scotland. Ryan has a Masters of Public Health (1992) from University College Dublin . He later completed specialist training in communicable disease control, public health and infectious disease at the Health Protection Agency in London. Ryan also completed the European Programme for Intervention Epidemiology Training (EPIET). In 2021, Ryan was awarded UCD Alumnus of the Year in Health and Agriculture Sciences. In July 1990, Ryan moved to Iraq with his girlfriend, later his wife, to train Iraqi doctors. Very shortly after his arrival the Invasion of Kuwait happened, which suspended his work and meant he and his wife were made to work as doctors under captivity, often working under duress. A military convoy ran a vehicle Ryan was in off the road, crushing multiple vertebrae. Eventually Ryan and his wife were allowed to leave Iraq due to their injuries. Ryan's severe back injury prohibited him from working as a surgeon. He made a shift into the fields of public health and infectious disease. Ryan worked with the Bill & Melinda Gates Foundation on their efforts to stamp out infectious diseases in Africa. In 1996, Ryan joined the World Health Organization to work in a newly opened unit that focused on epidemics and infectious diseases under the direction of the infectious disease expert, David L. Heymann . He developed measles outbreak response guidelines as part of the Expanded Programme on Immunization (EPI) team who implemented surveillance for acute flaccid paralysis , which is how polio is eradicated. From 2000 to 2003, Ryan was coordinator of Epidemic Response at the WHO. In 2001, he was based in Uganda where he was head of a team of international experts involved in the containment of the Ebola epidemic . During this time, he was in areas of conflict like the Democratic Republic of the Congo , where aid workers were often attacked and murdered. In 2003, he also worked as an Operational Coordinator on the SARS outbreak . From 2005 to 2011, Ryan was Director of Global Alert and Response Operations for the WHO. During this time he worked on the development of the WHO's Strategic Health Operations Centre and Event Management System. He worked on the implementation of the International Health Regulations (IHR), among other duties to do with infectious disease and emergency responses to pathogens and epidemics. In 2011, Ryan left the WHO and returned to Galway , Ireland, to work on the Global Polio Eradication Initiative (GPEI) in Pakistan, Afghanistan, and the Middle East, where he worked until 2017 and re-joined the WHO. In the early days of the Ebola crisis, Ryan was a field epidemiologist, field coordinator, operational coordinator or director during the majority of the reported Ebola outbreaks in Africa. From 2014 to 2015, he served as a senior advisor to the UN Mission for Ebola Emergency Response (UNMEER) in West Africa . He worked in the field in Guinea , Liberia and Sierra Leone . From 2013 to 2017, Ryan worked in the Middle East as Senior Advisor on Polio Eradication and Emergencies for the World Health Organization's Global Polio Eradication Initiative (GPEI). The goal was to eradicate polio from Pakistan and Afghanistan . He coordinated operational and technical support to polio outbreak response activities in the region which included Syria and Iraq. In 2014, Director General Margaret Chan appointed Ryan to the WHO Advisory Group on the Ebola Virus Disease Response, which was co-chaired by Sam Zaramba and David L. Heymann . During this time he was based in Islamabad , Pakistan at the National Emergency Operations Centre (NEOC), where he liaised with the Government of Pakistan . From 2017 to 2019, Ryan served as Assistant Director-General for Emergency Preparedness and Response in WHO's Health Emergencies Programme . In 2019, he was part of the leadership that created the Global Preparedness Report for the Global Preparedness Monitoring Board (GPMB). In 2019, Ryan became Executive Director of the World Health Organization's Health Emergencies Programme replacing Peter Salama in an internal reshuffle. He delivered remarks via pre-recorded video to participants of Event 201 , a pandemic preparedness exercise held in October 2019 by the Johns Hopkins Center for Health Security , the Bill & Melinda Gates Foundation and the World Economic Forum . As part of his work with the World Health Organization, Ryan appears in regular press conferences by the WHO regarding the COVID-19 pandemic . Ryan has provided answers to common questions about strategies to combat the COVID-19 pandemic and find a vaccine. Based on his experience in the Democratic Republic of the Congo with Ebola , Ryan has said that while physical distancing, lock-downs, and movement restrictions will stop the spread of COVID-19, eradicating the virus will require large scale public health interventions with a focus on the central tenets of containment: community-based surveillance, contact tracing , isolation, and quarantine. Since 2022, Ryan has been chairing the Technical Advisory Panel of the joint World Bank /WHO Pandemic Fund. In addition to his activities at WHO, Ryan has worked as a Professor of International Health at University College Dublin . He has taught and lectured on medicine and public health on the undergraduate and post graduate level. In July 1990, Ryan moved to Iraq with his girlfriend, later his wife, to train Iraqi doctors. Very shortly after his arrival the Invasion of Kuwait happened, which suspended his work and meant he and his wife were made to work as doctors under captivity, often working under duress. A military convoy ran a vehicle Ryan was in off the road, crushing multiple vertebrae. Eventually Ryan and his wife were allowed to leave Iraq due to their injuries. Ryan's severe back injury prohibited him from working as a surgeon. He made a shift into the fields of public health and infectious disease. Ryan worked with the Bill & Melinda Gates Foundation on their efforts to stamp out infectious diseases in Africa. In 1996, Ryan joined the World Health Organization to work in a newly opened unit that focused on epidemics and infectious diseases under the direction of the infectious disease expert, David L. Heymann . He developed measles outbreak response guidelines as part of the Expanded Programme on Immunization (EPI) team who implemented surveillance for acute flaccid paralysis , which is how polio is eradicated. From 2000 to 2003, Ryan was coordinator of Epidemic Response at the WHO. In 2001, he was based in Uganda where he was head of a team of international experts involved in the containment of the Ebola epidemic . During this time, he was in areas of conflict like the Democratic Republic of the Congo , where aid workers were often attacked and murdered. In 2003, he also worked as an Operational Coordinator on the SARS outbreak . From 2005 to 2011, Ryan was Director of Global Alert and Response Operations for the WHO. During this time he worked on the development of the WHO's Strategic Health Operations Centre and Event Management System. He worked on the implementation of the International Health Regulations (IHR), among other duties to do with infectious disease and emergency responses to pathogens and epidemics. In 2011, Ryan left the WHO and returned to Galway , Ireland, to work on the Global Polio Eradication Initiative (GPEI) in Pakistan, Afghanistan, and the Middle East, where he worked until 2017 and re-joined the WHO. In the early days of the Ebola crisis, Ryan was a field epidemiologist, field coordinator, operational coordinator or director during the majority of the reported Ebola outbreaks in Africa. From 2014 to 2015, he served as a senior advisor to the UN Mission for Ebola Emergency Response (UNMEER) in West Africa . He worked in the field in Guinea , Liberia and Sierra Leone . From 2013 to 2017, Ryan worked in the Middle East as Senior Advisor on Polio Eradication and Emergencies for the World Health Organization's Global Polio Eradication Initiative (GPEI). The goal was to eradicate polio from Pakistan and Afghanistan . He coordinated operational and technical support to polio outbreak response activities in the region which included Syria and Iraq. In 2014, Director General Margaret Chan appointed Ryan to the WHO Advisory Group on the Ebola Virus Disease Response, which was co-chaired by Sam Zaramba and David L. Heymann . During this time he was based in Islamabad , Pakistan at the National Emergency Operations Centre (NEOC), where he liaised with the Government of Pakistan . From 2017 to 2019, Ryan served as Assistant Director-General for Emergency Preparedness and Response in WHO's Health Emergencies Programme . In 2019, he was part of the leadership that created the Global Preparedness Report for the Global Preparedness Monitoring Board (GPMB). In 2019, Ryan became Executive Director of the World Health Organization's Health Emergencies Programme replacing Peter Salama in an internal reshuffle. He delivered remarks via pre-recorded video to participants of Event 201 , a pandemic preparedness exercise held in October 2019 by the Johns Hopkins Center for Health Security , the Bill & Melinda Gates Foundation and the World Economic Forum . As part of his work with the World Health Organization, Ryan appears in regular press conferences by the WHO regarding the COVID-19 pandemic . Ryan has provided answers to common questions about strategies to combat the COVID-19 pandemic and find a vaccine. Based on his experience in the Democratic Republic of the Congo with Ebola , Ryan has said that while physical distancing, lock-downs, and movement restrictions will stop the spread of COVID-19, eradicating the virus will require large scale public health interventions with a focus on the central tenets of containment: community-based surveillance, contact tracing , isolation, and quarantine. Since 2022, Ryan has been chairing the Technical Advisory Panel of the joint World Bank /WHO Pandemic Fund. In addition to his activities at WHO, Ryan has worked as a Professor of International Health at University College Dublin . He has taught and lectured on medicine and public health on the undergraduate and post graduate level. On 5 January 2022, Ryan received an award from Irish President Michael D. Higgins at Áras an Uachtaráin in recognition of his "enormous service to global public health over the course of a number of decades." In 1988, Ryan met his wife, Máire Connolly, in medical school in Galway. They were married in 1997. Connolly is also a doctor and author who has specialized in infectious disease by training and also worked at the World Health Organization . She is a professor of health security and infectious disease at National University of Ireland Galway . They have three children. Ryan is based in Geneva , Switzerland.

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Rift Valley fever

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One Health

One Health is an approach calling for "the collaborative efforts of multiple disciplines working locally, nationally, and globally, to attain optimal health for people, animals and our environment", as defined by the One Health Initiative Task Force (OHITF). It developed in response to evidence of the spreading of zoonotic diseases between species and increasing awareness of "the interdependence of human and animal health and ecological change". : 205 In this viewpoint, public health is no longer seen in purely human terms. Due to a shared environment and highly conserved physiology, animals and humans not only suffer from the same zoonotic diseases but can also be treated by either structurally related or identical drugs. For this reason, special care must be taken to avoid unnecessary or over-treatment of zoonotic diseases, particularly in the context of drug resistance in infectious microbes. A number of organizations throughout the world support the objectives of "One Health" including the One Health Commission (OHC), One Health Initiative, One Health Platform, CDC One Health Office, and the Quadripartite Organizations. The Quadripartite Organizations are: In particular, the One Health High Level Expert Panel, an independent advisory group to the Quadripartite Organizations, provided a comprehensive definition of One Health, whereby: "One Health is an integrated, unifying approach that aims to sustainably balance and optimize the health of humans, animals, plants and ecosystems. It recognizes the health of humans, domestic and wild animals, plants and the wider environment (including ecosystems) are closely linked and interdependent. The approach mobilizes multiple sectors, disciplines and communities at varying levels of society to work together to foster well-being and tackle threats to health and ecosystems, while addressing the collective need for clean water, energy and air, safe and nutritious food, taking action on climate change, and contributing to sustainable development." Calvin Schwabe , a veterinarian trained in public health, coined the term "One Medicine" in a veterinary medical textbook in 1964 to reflect the similarities between animal and human medicine and stress the importance of collaboration between veterinarians and physicians to help solve global health problems . He established a department at the University of California, Davis , to jointly address issues in the animal and human health sciences. In 2004, The Wildlife Conservation Society held a conference called "One World, One Health" at Rockefeller University in New York. Out of that conference the twelve Manhattan Principles were created to describe a unified approach to preventing epidemic diseases. These principles emphasized links between humans, animals, and the environment, their importance in understanding disease dynamics, and the need for interdisciplinary approaches to prevention, education, investment, and policy development. Due to global scares surrounding the H5N1 influenza outbreaks of the early-mid 2000s, the American Veterinary Medical Association established a One Health Initiative Task Force in 2006, the American Medical Association passed a One Health resolution to promote partnering between veterinary and human medical organizations in 2007, and a One Health approach was recommended for responses to global disease outbreaks in 2007. Building on these initiatives, the Food and Agriculture Organization (FAO), World Organization for Animal Health (OIE), and World Health Organization (WHO) came together with the United Nations Children's Fund ( UNICEF ), United Nations System Influenza Coordination, and the World Bank to develop a framework entitled Contributing to One World, One Health-A Strategic Framework for Reducing Risks of Infectious Diseases at the Animal-Human-Ecosystems Interface in 2008, reiterating recommendations for a One Health approach to global health. This framework was expanded and implementable policies were developed at Stone Mountain, Georgia in May 2010. International meetings on One Health were held in 2011 in Africa and Australia. In 2012, Barbara Natterson-Horowitz , a physician, and Kathryn Bowers, a science journalist, published the book Zoobiquity , coining the term as they drew parallels between animal and human health through vivid case studies. They called for the biomedical scientific and clinical communities to rediscover comparative medicine and reexamine human and animal health in terms of evolution and the environment. A New York Times bestseller, the book has been described as "easy to read and entertaining" in its presentation of ideas similar to the "One Health" concept, but also criticized as lacking depth and failing to recognize the extent to which animals and humans have differently evolved as complex systems. In 2016, The One Health Commission, One Health Platform, and One Health Initiative Team deemed International One Health Day to be November 3. In 2019, Senator Tina Smith and Representative Kurt Schrader introduced the Advancing Emergency Preparedness Through One Health Act into the United States Senate and House of Representatives , respectively. This bi-partisan piece of legislation would require that the Department of Health and Human Services , Department of Agriculture , and other federal agencies develop a coordinated plan to create a One Health Framework to help prepare responses to zoonotic disease and prevent disease outbreaks. The bill was re-introduced by Tina Smith and Todd Young on March 18, 2021. In 2007, Roger K. Mahr from the American Veterinary Medical Association , Jay H. Glasser from the American Public Health Association , and Ronald M. Davis from the American Medical Association came together as liaisons with other health science professionals, academics, students, government workers, and industry scientists to create a task force and have teleconferences to discuss One Health. This One Health Initiative Task Force created a report in 2008 which outlined recommendations to: Create a joint steering committee, Implement improved communications efforts, Plan national One Health studies, Develop a One Health Commission, Create advisory teams, Establish national meetings, and engage medical, veterinary, and public health students. The One Health Commission (OHC) was chartered in Washington, D.C. in 2009 as a 501(c)3 non-profit organization. Its mission is to connect individuals and create relationships across human, animal, and environmental health sectors, as well as to educate the public about these issues with the intent to improve global health. Roger Mahr was the founding CEO. A request for proposal for an institutional partner was put forth in 2010, and Iowa State University was selected to be the main site for operations. In 2013, Roger Mahr retired from the commission and the operations site moved to the Research Triangle of North Carolina, where it currently resides. The current executive director is Cheryl Stroud, a veterinarian, who has held the position since 2013. The One Health Commission began in 2014 compiling a Who's Who in One Health, a Directory of organizations around the world that are actively working to further the One Health paradigm shift. The OHC also oversees a Global One Health Community listserv. In addition the commission has a webpage known as the One Health Library with many types of resources available on the topic of or connected to One Health. The One Health Initiative is an interdisciplinary movement to create collaborations between animal, human, and environmental health organizations including the American Veterinary Medical Association , American Medical Association , Centers for Disease Control and Prevention , United States Department of Agriculture , Vétérinaires sans Frontières/ Tierärzte ohne Grenzen and the United States National Environmental Health Association, among others. Such collaboration, which often remains very limited, could lead to more quick and profound exchange of knowledge and insights between disciplines and professionals, which is important to better and more rapidly respond to outbreaks and newly emerging zoonoses and diseases. The One Health Platform is a scientific reference network to unite researchers and experts to better understand and prepare for zoonotic disease outbreaks from animals to humans, and antimicrobial resistance , including a better understanding of environmental factors that impact disease dynamics. The management board is made up of Ab Osterhaus , John Mackenzie, and Chris Vanlangendonck. The organization has nine objectives, which include: Disseminating research results at biennial meetings, Identifying knowledge gaps in the field, Engaging policy makers, Establishing a Bio Threats Scanning Group to connect One Health and global health security, Share data, Serve as a reference network to the government, Foster collaborations, Implement policies, and increase awareness during One Health Day. The One Health Platform was responsible for organizing the World One Health Congress meeting each year 2015 - 2020. The next World One Health Congress scheduled for 2022 continued in Singapore hosted by SingHealth Duke-NUS Global Health Institute. FAO works closely with WOAH (formerly OIE) and WHO, referred to all together as the Tripartite organizations. WHO was a partner in the 2008 establishment of a strategic One Health framework for approaching global health problems. In September 2017, a feature page for One Health was included on the WHO website, defining One Health and highlighting important topic areas such as food safety, zoonotic disease , and antimicrobial resistance . WOAH (headquartered in Paris, France ) was also a partner in establishing a strategic One Health framework in 2008. WOAH works to maintain transparency surrounding global animal disease, collect and distribute veterinary information, publish international trade standards for animals/ animal products, improve veterinary services globally, and to promote animal welfare and food safety. FAO put forth in 2011 a strategic action plan for One Health, which had the objective to strengthen food security by improving animal production systems and veterinary services and called for action in improving collaborations between animal, human, and environmental health sectors. FAO, WOAH and WHO published a new guide to approaching zoonotic disease with a One Health framework in 2019. In February 2021, acknowledging the importance of the environment for the One Health approach, the three partner organizations invited UNEP to join the Tripartite. In March of the same year, the Tripartite and UNEP agreed to work together on a strategy to apply the One Health approach in the prevention of future pandemics. One year later, in March 2022, the Twenty-eighth Tripartite Annual Executive Meeting saw the signing of a memorandum of understanding by all organizations involved to mark the change from a Tripartite to a Quadripartite partnership. The Centers for Disease Control and Prevention (CDC) , created a One Health Office in 2009, becoming the first United States federal agency to have an office dedicated to this field. This office works alongside other animal, human, and environmental health organizations both within the United States and across the world in order to increase the awareness of One Health and develop tools to help strengthen One Health movements. The CDC One Health Office is involved in multiple initiatives, including working to implement a Zoonotic Disease Prioritization process, creating Global Health Security Agenda Action Packages, overseeing the Zoonoses Education Coalition, developing guidelines with the National Association of State Public Health Veterinarians , and helping educate youth involved with agriculture about influenza . Additionally, the CDC One Health Office hosts webinars to educate audiences about One Health issues such as food safety, antimicrobial resistance, and recent disease outbreaks. The One Health Zoonotic Disease Prioritization process is led by the CDC. It involves holding workshops internationally to prioritize which zoonotic diseases are of the most concern and helping countries develop action plans to address those diseases. The process involves 3-6 facilitators representing human, animal, and environmental health sectors, up to 12 voting members which represent human health/public health, agriculture/livestock, wildlife/fisheries, the environment and other relevant government sectors, and 10-15 advisors from international organizations (such as the WHO, FAO or OIE), academic partners or NGOs not directly involved in zoonotic diseases. The CDC One Health Office trains facilitators and it takes months to prepare for a workshop to acquire the necessary resources, identify participants, review zoonotic information and confirm logistics. Completed workshops have been held in a variety of countries including Pakistan , Tanzania , Thailand , Uzbekistan and China . Diseases most commonly prioritized include rabies , brucellosis , influenza , Ebola virus , and Rift Valley fever . In 2007, Roger K. Mahr from the American Veterinary Medical Association , Jay H. Glasser from the American Public Health Association , and Ronald M. Davis from the American Medical Association came together as liaisons with other health science professionals, academics, students, government workers, and industry scientists to create a task force and have teleconferences to discuss One Health. This One Health Initiative Task Force created a report in 2008 which outlined recommendations to: Create a joint steering committee, Implement improved communications efforts, Plan national One Health studies, Develop a One Health Commission, Create advisory teams, Establish national meetings, and engage medical, veterinary, and public health students. The One Health Commission (OHC) was chartered in Washington, D.C. in 2009 as a 501(c)3 non-profit organization. Its mission is to connect individuals and create relationships across human, animal, and environmental health sectors, as well as to educate the public about these issues with the intent to improve global health. Roger Mahr was the founding CEO. A request for proposal for an institutional partner was put forth in 2010, and Iowa State University was selected to be the main site for operations. In 2013, Roger Mahr retired from the commission and the operations site moved to the Research Triangle of North Carolina, where it currently resides. The current executive director is Cheryl Stroud, a veterinarian, who has held the position since 2013. The One Health Commission began in 2014 compiling a Who's Who in One Health, a Directory of organizations around the world that are actively working to further the One Health paradigm shift. The OHC also oversees a Global One Health Community listserv. In addition the commission has a webpage known as the One Health Library with many types of resources available on the topic of or connected to One Health. The One Health Initiative is an interdisciplinary movement to create collaborations between animal, human, and environmental health organizations including the American Veterinary Medical Association , American Medical Association , Centers for Disease Control and Prevention , United States Department of Agriculture , Vétérinaires sans Frontières/ Tierärzte ohne Grenzen and the United States National Environmental Health Association, among others. Such collaboration, which often remains very limited, could lead to more quick and profound exchange of knowledge and insights between disciplines and professionals, which is important to better and more rapidly respond to outbreaks and newly emerging zoonoses and diseases. The One Health Platform is a scientific reference network to unite researchers and experts to better understand and prepare for zoonotic disease outbreaks from animals to humans, and antimicrobial resistance , including a better understanding of environmental factors that impact disease dynamics. The management board is made up of Ab Osterhaus , John Mackenzie, and Chris Vanlangendonck. The organization has nine objectives, which include: Disseminating research results at biennial meetings, Identifying knowledge gaps in the field, Engaging policy makers, Establishing a Bio Threats Scanning Group to connect One Health and global health security, Share data, Serve as a reference network to the government, Foster collaborations, Implement policies, and increase awareness during One Health Day. The One Health Platform was responsible for organizing the World One Health Congress meeting each year 2015 - 2020. The next World One Health Congress scheduled for 2022 continued in Singapore hosted by SingHealth Duke-NUS Global Health Institute. FAO works closely with WOAH (formerly OIE) and WHO, referred to all together as the Tripartite organizations. WHO was a partner in the 2008 establishment of a strategic One Health framework for approaching global health problems. In September 2017, a feature page for One Health was included on the WHO website, defining One Health and highlighting important topic areas such as food safety, zoonotic disease , and antimicrobial resistance . WOAH (headquartered in Paris, France ) was also a partner in establishing a strategic One Health framework in 2008. WOAH works to maintain transparency surrounding global animal disease, collect and distribute veterinary information, publish international trade standards for animals/ animal products, improve veterinary services globally, and to promote animal welfare and food safety. FAO put forth in 2011 a strategic action plan for One Health, which had the objective to strengthen food security by improving animal production systems and veterinary services and called for action in improving collaborations between animal, human, and environmental health sectors. FAO, WOAH and WHO published a new guide to approaching zoonotic disease with a One Health framework in 2019. In February 2021, acknowledging the importance of the environment for the One Health approach, the three partner organizations invited UNEP to join the Tripartite. In March of the same year, the Tripartite and UNEP agreed to work together on a strategy to apply the One Health approach in the prevention of future pandemics. One year later, in March 2022, the Twenty-eighth Tripartite Annual Executive Meeting saw the signing of a memorandum of understanding by all organizations involved to mark the change from a Tripartite to a Quadripartite partnership. The Centers for Disease Control and Prevention (CDC) , created a One Health Office in 2009, becoming the first United States federal agency to have an office dedicated to this field. This office works alongside other animal, human, and environmental health organizations both within the United States and across the world in order to increase the awareness of One Health and develop tools to help strengthen One Health movements. The CDC One Health Office is involved in multiple initiatives, including working to implement a Zoonotic Disease Prioritization process, creating Global Health Security Agenda Action Packages, overseeing the Zoonoses Education Coalition, developing guidelines with the National Association of State Public Health Veterinarians , and helping educate youth involved with agriculture about influenza . Additionally, the CDC One Health Office hosts webinars to educate audiences about One Health issues such as food safety, antimicrobial resistance, and recent disease outbreaks. The One Health Zoonotic Disease Prioritization process is led by the CDC. It involves holding workshops internationally to prioritize which zoonotic diseases are of the most concern and helping countries develop action plans to address those diseases. The process involves 3-6 facilitators representing human, animal, and environmental health sectors, up to 12 voting members which represent human health/public health, agriculture/livestock, wildlife/fisheries, the environment and other relevant government sectors, and 10-15 advisors from international organizations (such as the WHO, FAO or OIE), academic partners or NGOs not directly involved in zoonotic diseases. The CDC One Health Office trains facilitators and it takes months to prepare for a workshop to acquire the necessary resources, identify participants, review zoonotic information and confirm logistics. Completed workshops have been held in a variety of countries including Pakistan , Tanzania , Thailand , Uzbekistan and China . Diseases most commonly prioritized include rabies , brucellosis , influenza , Ebola virus , and Rift Valley fever . To ensure fair and community-oriented investment in One Health initiatives that involve multiple institutional and international partners, it is crucial to strengthen their governance foundations. The global One Health community can learn three important lessons to make One Health more inclusive. Firstly, One Health Networks should promote collaboration and cooperation among stakeholders through appropriate governance arrangements and management strategies, as demonstrated by GARC and DANMAP. Secondly, power should be balanced and calibrated to ensure that country leadership and ownership of activities are prioritized. Investment in One Health Networks should be based on local needs and priorities, rather than donor priorities. Lastly, community stakeholders should be included in partnership structures and governance arrangements of One Health Networks to engage meaningfully with local realities and establish action priorities. In 2017, a case study was undertaken by a team of researchers to explore the health implications linked to the land application of biosolids within the framework of One Health. This investigation encompassed the One Health study design across all three health domains, revealing certain limitations encountered when applying One Health research in practical settings. These obstacles encompass, among others, the necessity for enhanced collaborations spanning different fields and administrative hurdles, the enhancement of science-driven risk management strategies, and the augmentation of workforce and research infrastructure capabilities, particularly in developing nations. Moreover, notable impediments to the execution of One Health research may continue if funding agencies fail to establish effective mechanisms to bolster interdisciplinary One Health research.

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Rift Valley fever

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Kenya Medical Research Institute

The Kenya Medical Research Institute (KEMRI) is a state corporation established through the Science and Technology (Amendment) Act of 1979, (since amended to the Sciences, Technology and Innovation Act 2013), during the tenure of Nicholas Biwott as Minister of State, as the national body responsible for carrying out health research in Kenya. KEMRI is the medical research arm of the Kenya Government providing advice on various aspects of healthcare and delivery, including national diseases surveillance and rapid re https://www.kemri.org/ sponse capacity for major disease outbreaks such as HIV, Cholera, Chikungunya Virus, H1N1 Flu, Yellow Fever, Rift Valley Fever, Ebola, Aflatoxicosis and COVID-19. KEMRI is mandated to carry out research in human health; to cooperate with other research organizations and institutions of higher learning on matters of relevant research and training; to work with other research bodies within and outside Kenya carrying out similar research; to cooperate with the Ministry of Public Health and Sanitation, the Ministry of Medical Services, the National Council of Science and Technology (NSCT) and the Medical Science Advisory Research Committee in matters pertaining to research policies and priorities. KEMRI has grown over the last 40 years to become a regional leader in human health research. The institute currently ranks as one of the leading Centres of excellence in health research both in Africa and globally. KEMRI Research includes the following centers: [ citation needed ] Centre for Biotechnology Research and Development (CBRD):Mandate is to develop biotechnological innovations such as diagnostic kits, vaccines and associated delivery technology Centre for Clinical Research (CCR) Centre for Geographic Medicine Research-Coast (CGMR-C) Centre for Global Health Research (CGHR) Centre for Infectious and Parasitic Diseases Control Research (CIPDCR) Centre for Microbiology Research (CMR) Centre for Public Health Research (CPHR) Centre for Respiratory Diseases Research (CRDR) Centre for Traditional Medicine and Drug Research (CTMDR) Centre for Virus Research (CVR) The Eastern and Southern Africa Centre of International Parasite Control (ESACIPAC) KEMRI Graduate School of Health Sciences Health Safety and Environment Production CentreKEMRI has links with a number of international, regional and local partners. INTERNATIONAL PARTNERS The Wellcome (Trust) ,  a global charitable foundation dedicated to improving health and research. The US Centre for Disease Control and Prevention (CDC). The Japan International Cooperation Agency (JICA). The United States Army Medical Research Directorate – Kenya. The World Health Organization . The US Agency for International Developmen t (USAID). The British Medical Research Council . KIT Royal Tropical Institute (Amsterdam). The World Association of Industrial and Technological Research Organization (WAITRO). REGIONAL PARTNERS Ghana National Institute of Medical Research . Ethiopia Health and Nutrition Research Institute . Ethiopia Virus Research Institute. Makere University Medical School. University of Zambia Medical School . LOCAL PARTNERSHIPS Jomo Kenyatta University of Agriculture and Technology . University of Nairobi . Maseno University .

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Rift Valley fever

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Rhabdoviridae

See text Rhabdoviridae is a family of negative-strand RNA viruses in the order Mononegavirales . Vertebrates (including mammals and humans), invertebrates , plants , fungi and protozoans serve as natural hosts. Diseases associated with member viruses include rabies encephalitis caused by the rabies virus , and flu-like symptoms in humans caused by vesiculoviruses . The name is derived from Ancient Greek rhabdos , meaning rod, referring to the shape of the viral particles. The family has 40 genera, most assigned to three subfamilies. The individual virus particles (virions) of rhabdoviruses are composed of RNA, protein, carbohydrate and lipid. They have complex bacilliform or bullet-like shapes. All these viruses have structural similarities and have been classified as a single family. The virions are about 75 nm wide and 180 nm long. Rhabdoviruses are enveloped and have helical nucleocapsids and their genomes are linear, around 11–15 kb in length. Rhabdoviruses carry their genetic material in the form of negative-sense single-stranded RNA . They typically carry genes for five proteins: large protein (L), glycoprotein (G), nucleoprotein (N), phosphoprotein (P), and matrix protein (M). The sequence of these protein genes from the 3 'end to the 5' end in the genome is N–P–M–G–L. Every rhabdoviruses encode these five proteins in their genomes. In addition to these proteins, many rhabdoviruses encode one or more proteins. The first four genes encode major structural proteins that participate in the structure of the virion envelope. The matrix protein (M) constitutes a layer between the virion envelope and the nucleocapsid core of the rhabdovirus. In addition to the functions about virus assembly, morphogenesis and budding off enveloped from the host plasma membrane, additional functions such as the regulation of RNA synthesis, affecting the balance of replication and transcription products was found, making reverse genetics experiments with rabies virus, a member of the family Rhabdoviridae. The large (L) protein has several enzymatic functions in viral RNA synthesis and processing. The L gene encodes this L protein, which contains multiple domains. In addition to RNA synthesis, it is thought to be involved in methyl capping and polyadenylation activity. P protein plays important and multiple roles during transcription and replication of the RNA genome. The multifunctional P protein is encoded by the P gene. P protein acts as a non-catalytic cofactor of large protein polymerase. It is binding to N and L protein. P protein has two independent binding regions. By forming N-P complexes, it can keep the N protein in the form suitable for specific encapsulation. P protein interferes with the host's innate immune system through inhibition of the activities of interferon regulatory factor 3 (IRF3) and signal transducer and activator of transcription 1 (STAT1), thus eliminating the cellular type 1 interferon pathway. Also, P protein acts as an antagonist against antiviral PML function. Rhabdoviruses that infect vertebrates (especially mammals and fishes), plants, and insects are usually bullet-shaped. However, in contrast to paramyxoviruses , rhabdoviruses do not have hemagglutinating and neuraminidase activities. Transcriptase of rhabdovirus is composed of 1 L and 3 P proteins. Transcriptase components are always present in the complete virion to permit rhabdoviruses to begin transcription immediately after entry. [ citation needed ] The rhabdovirus transcriptase proceeds in a 3' to 5' direction on the genome and the transcription terminates randomly at the end of protein sequences. For example, if a transcription finishes at the end of M sequence; leader RNA and N, P and M mRNAs are formed separately from each other. [ citation needed ] Also, mRNAs accumulate according to the order of protein sequences on the genome, solving the logistics problem in the cell. For example, N protein is necessary in high quantities for the virus, as it coats the outside of the replicated genomes completely. Since the N protein sequence is located at the beginning of the genome (3' end) after the leader RNA sequence, mRNAs for N protein can always be produced and accumulate in high amounts with every termination of transcription. After the transcription processes, all of the mRNAs are capped at the 5' end and polyadenylated at the 3' end by L protein. This transcription mechanism thus provides mRNAs according to the need of the viruses. : 173–184The virus proteins translated on free ribosomes but G protein is translated by the rough endoplasmic reticulum. This means G protein has a signal peptide on its mRNA's starting codes. Phosphoproteins (P) and glycoprotein (G) undergo post-translational modification. Trimers of P protein are formed after phosphorylation by kinase activity of L protein. The G protein is glycosylated in the rough endoplasmic reticulum and the Golgi complex. : 180Viral replication is cytoplasmic. The replication cycle is the same for most rhabdoviruses. All components required for early transcription and the nucleocapsid are released to the cytoplasm of the infected cell after the first steps of binding, penetration and uncoating take place. Entry into the host cell is achieved by attachment of the viral G glycoproteins to host receptors, which mediates clathrin-mediated endocytosis. Replication follows the negative stranded RNA virus replication model. Negative stranded RNA virus transcription, using polymerase stuttering is the method of transcription. The virus exits the host cell by budding, and tubule-guided viral movement. Transmission routes are zoonosis and bite. Replication of many rhabdoviruses occurs in the cytoplasm , although several of the plant infecting viruses replicate in the nucleus. The rhabdovirus matrix (M) protein is very small (~20–25 kDa) however plays a number of important roles during the replication cycle of the virus. These proteins of rhabdoviruses constitute major structural components of the virus and they are multifunctional proteins and required for virus maturation and viral budding process that also regulate the balance of virus RNA synthesis by shifting synthesis from transcription to replication. In order for replication, both the L and P protein must be expressed to regulate transcription . Phosphoprotein (P) also plays a crucial role during replication, as N-P complexes, rather than N alone, are necessary for appropriate and selective encapsidation of viral RNA. Therefore, replication is not possible after infection until the primary transcription and translation produce enough N protein. The L protein has a lot of enzymatic activity such as RNA replication, capping mRNAs phosphorylation of P. L protein gives feature in about replication in cytoplasm. Transcription results in five monocistronic mRNAs being produced because the intergenic sequences act as both termination and promoter sequences for adjacent genes . This type of transcription mechanism is explained by stop-start model (stuttering transcription). Owing to stop-start model, the large amounts of the structural proteins are produced. According to this model, the virus-associated RNA polymerase starts firstly the synthesis of leader RNA and then the five mRNA which will produce N, P, M, G, L proteins, respectively. After the leader RNA was produced, the polymerase enzyme reinitiates virion transcription on N gene and proceeds its synthesis until it ends 3′ end of the chain. Then, the synthesis of P mRNAs are made by same enzyme with new starter sinyal. These steps continue until the enzyme arrives the end of the L gene. During transcription process, the polymerase enzyme may leave the template at any point and then bound just at the 3′ end of the genome RNA to start mRNA synthesis again. This process will results concentration gradient of the amount of mRNA based on its place and its range from the 3′ end. In the circumstances, the amounts of mRNA species change and will be produced N>P>M>G>L proteins. During their synthesis the mRNAs are processed to introduce a 5' cap and a 3' polyadenylated tail to each of the molecules. This structure is homologous to cellular mRNAs and can thus be translated by cellular ribosomes to produce both structural and non-structural proteins. Genomic replication requires a source of newly synthesized N protein to encapsidate the RNA. This occurs during its synthesis and results in the production of a full-length anti-genomic copy. This in turn is used to produce more negative-sense genomic RNA. The viral polymerase is required for this process, but how the polymerase engages in both mRNA synthesis and genomic replication is not well understood. Replication characteristically occurs in an inclusion body within the cytoplasm, from where they bud through various cytoplasmic membranes and the outer membrane of the cell. This process results in the acquisition of the M + G proteins, responsible for the characteristic bullet- shaped morphology of the virus .These viruses fall into four groups based on the RNA polymerase gene. The basal clade appears to be novirhabdoviruses , which infect fish. Cytorhabdoviruses and the nucleorhabdoviruses , which infect plants, are sister clades. Lyssaviruses form a clade of their own which is more closely related to the land vertebrate and insect clades than to the plant viruses. The remaining viruses form a number of highly branched clades and infect arthropods and land vertebrates. A 2015 analysis of 99 species of animal rhabdoviruses found that they fell into 17 taxonomic groupings, eight – Lyssavirus , Vesiculovirus , Perhabdovirus , Sigmavirus , Ephemerovirus , Tibrovirus , Tupavirus and Sprivivirus – which were previously recognized. The authors proposed seven new taxa on the basis of their findings: "Almendravirus", "Bahiavirus", "Curiovirus", "Hapavirus", "Ledantevirus", "Sawgravirus" and "Sripuvirus". Seven species did not group with the others suggesting the need for additional taxa. An unofficial supergroup – "Dimarhabdovirus" – refers to the genera Ephemerovirus and Vesiculovirus . A number of other viruses that have not been classified into genera also belong to this taxon. This supergroup contains the genera with species that replicate in both vertebrate and invertebrate hosts and have biological cycles that involve transmission by haematophagous dipterans (bloodsucking flies). The prototypical and best studied rhabdovirus is vesicular stomatitis Indiana virus . It is a preferred model system to study the biology of rhabdoviruses, and mononegaviruses in general. The mammalian disease rabies is caused by lyssaviruses, of which several have been identified. Rhabdoviruses are important pathogens of animals and plants. Rhabdoviruses are transmitted to hosts by arthropods, such as aphids, planthoppers, leafhoppers, black flies, sandflies, and mosquitoes. In September 2012, researchers writing in the journal PLOS Pathogens described a novel species of rhabdovirus, called Bas-Congo virus (BASV), which was discovered in a blood sample from a patient who survived an illness that resembled hemorrhagic fever. No cases of BASV have been reported since its discovery and it is uncertain if BASV was the actual cause of the patient's illness. In 2015 two novel rhabdoviruses, Ekpoma virus 1 and Ekpoma virus 2, were discovered in samples of blood from two healthy women in southwestern Nigeria. Ekpoma virus 1 and Ekpoma virus 2 appear to replicate well in humans (viral load ranged from ~45,000 - ~4.5 million RNA copies/mL plasma) but did not cause any observable symptoms of disease. Exposure to Ekpoma virus 2 appears to be widespread in certain parts of Nigeria where seroprevalence rates are close to 50%. These viruses fall into four groups based on the RNA polymerase gene. The basal clade appears to be novirhabdoviruses , which infect fish. Cytorhabdoviruses and the nucleorhabdoviruses , which infect plants, are sister clades. Lyssaviruses form a clade of their own which is more closely related to the land vertebrate and insect clades than to the plant viruses. The remaining viruses form a number of highly branched clades and infect arthropods and land vertebrates. A 2015 analysis of 99 species of animal rhabdoviruses found that they fell into 17 taxonomic groupings, eight – Lyssavirus , Vesiculovirus , Perhabdovirus , Sigmavirus , Ephemerovirus , Tibrovirus , Tupavirus and Sprivivirus – which were previously recognized. The authors proposed seven new taxa on the basis of their findings: "Almendravirus", "Bahiavirus", "Curiovirus", "Hapavirus", "Ledantevirus", "Sawgravirus" and "Sripuvirus". Seven species did not group with the others suggesting the need for additional taxa.An unofficial supergroup – "Dimarhabdovirus" – refers to the genera Ephemerovirus and Vesiculovirus . A number of other viruses that have not been classified into genera also belong to this taxon. This supergroup contains the genera with species that replicate in both vertebrate and invertebrate hosts and have biological cycles that involve transmission by haematophagous dipterans (bloodsucking flies).The prototypical and best studied rhabdovirus is vesicular stomatitis Indiana virus . It is a preferred model system to study the biology of rhabdoviruses, and mononegaviruses in general. The mammalian disease rabies is caused by lyssaviruses, of which several have been identified. Rhabdoviruses are important pathogens of animals and plants. Rhabdoviruses are transmitted to hosts by arthropods, such as aphids, planthoppers, leafhoppers, black flies, sandflies, and mosquitoes. In September 2012, researchers writing in the journal PLOS Pathogens described a novel species of rhabdovirus, called Bas-Congo virus (BASV), which was discovered in a blood sample from a patient who survived an illness that resembled hemorrhagic fever. No cases of BASV have been reported since its discovery and it is uncertain if BASV was the actual cause of the patient's illness. In 2015 two novel rhabdoviruses, Ekpoma virus 1 and Ekpoma virus 2, were discovered in samples of blood from two healthy women in southwestern Nigeria. Ekpoma virus 1 and Ekpoma virus 2 appear to replicate well in humans (viral load ranged from ~45,000 - ~4.5 million RNA copies/mL plasma) but did not cause any observable symptoms of disease. Exposure to Ekpoma virus 2 appears to be widespread in certain parts of Nigeria where seroprevalence rates are close to 50%. In the Alpharhabdovirinae subfamily, the following genera are recognized: The genera of the other subfamilies are as follows: The following genera are unassigned to the a subfamily: In addition to the above, there are a large number of rhabdo-like viruses that have not yet been officially classified by the ICTV .

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Rift Valley fever

https://api.wikimedia.org/core/v1/wikipedia/en/page/Arthropod_bites_and_stings/html

Arthropod bites and stings

Many species of arthropods (insects, arachnids, millipedes and centipedes) can bite or sting human beings. These bites and stings generally occur as a defense mechanism or during normal arthropod feeding. While most cases cause self-limited irritation, medically relevant complications include envenomation , allergic reactions , and transmission of vector-borne diseases . Most arthropod bites and stings cause self-limited redness, itchiness and/or pain around the site. Less commonly (around 10% of Hymenoptera sting reactions), a large local reaction occurs when the area of swelling is greater than 10 centimetres (4 in) . Rarely (1-3% of Hymenoptera sting reactions), systemic reactions can affect multiple organs and pose a medical emergency, as in the case of anaphylactic shock . Many arthropods bite or sting in order to immobilize their prey or deter potential predators as a defense mechanism. Stings containing venom are more likely to be painful. Less frequently, venomous spider bites are also associated with morbidity and mortality in humans. Most arthropod stings involve Hymenoptera (ants, wasps, and bees). While the majority of Hymenoptera stings are locally painful, their associated venom rarely cause toxic reactions unless victims receive many stings at once. The low mortality (around 60 deaths per year in the US out of unreported millions of stings nationwide) associated with Hymenoptera is mostly due to anaphylaxis from venom hypersensitivity . Most scorpion stings also cause self-limited pain or paresthesias . Only certain species (from family Buthidae ) inject neurotoxic venom, responsible for most morbidity and mortality. Severe toxic reactions can occur resulting in progressive hemodynamic instability, neuromuscular dysfunction, cardiogenic shock , pulmonary edema , multi-organ failure, and death. Although robust epidemiological data is unavailable, global estimates of scorpion stings exceed 1.2 million resulting in more than 3000 deaths annually. Spider bites most often cause minor symptoms and resolve without intervention. Medically significant spider bites involve substantial envenomation from only certain species such as widow spiders and recluse spiders . Symptoms of latrodectism (from widow spiders) may include pain at the bite or involve the chest and abdomen, sweating, muscle cramps and vomiting among others. By comparison, loxoscelism (from recluse spiders) can present with local necrosis of the surrounding skin and widespread breakdown of red blood cells . Headaches, vomiting and a mild fever may also occur. Feeding bites have characteristic patterns and symptoms that reflect feeding habits of the offending pest and the chemistry of its saliva. Feeding bites are less likely to be felt at the time of the bite, although there are some exceptions. Since feeding requires longer attachment to prey than envenomation, feeding bites are more often associated with vector transmission of disease. Many arthropods bite or sting in order to immobilize their prey or deter potential predators as a defense mechanism. Stings containing venom are more likely to be painful. Less frequently, venomous spider bites are also associated with morbidity and mortality in humans. Most arthropod stings involve Hymenoptera (ants, wasps, and bees). While the majority of Hymenoptera stings are locally painful, their associated venom rarely cause toxic reactions unless victims receive many stings at once. The low mortality (around 60 deaths per year in the US out of unreported millions of stings nationwide) associated with Hymenoptera is mostly due to anaphylaxis from venom hypersensitivity . Most scorpion stings also cause self-limited pain or paresthesias . Only certain species (from family Buthidae ) inject neurotoxic venom, responsible for most morbidity and mortality. Severe toxic reactions can occur resulting in progressive hemodynamic instability, neuromuscular dysfunction, cardiogenic shock , pulmonary edema , multi-organ failure, and death. Although robust epidemiological data is unavailable, global estimates of scorpion stings exceed 1.2 million resulting in more than 3000 deaths annually. Spider bites most often cause minor symptoms and resolve without intervention. Medically significant spider bites involve substantial envenomation from only certain species such as widow spiders and recluse spiders . Symptoms of latrodectism (from widow spiders) may include pain at the bite or involve the chest and abdomen, sweating, muscle cramps and vomiting among others. By comparison, loxoscelism (from recluse spiders) can present with local necrosis of the surrounding skin and widespread breakdown of red blood cells . Headaches, vomiting and a mild fever may also occur. Feeding bites have characteristic patterns and symptoms that reflect feeding habits of the offending pest and the chemistry of its saliva. Feeding bites are less likely to be felt at the time of the bite, although there are some exceptions. Since feeding requires longer attachment to prey than envenomation, feeding bites are more often associated with vector transmission of disease. In addition to stings and bites causing discomfort in of themselves, bites can also spread secondary infections if the arthropod is carrying a virus, bacteria, or parasite. The World Health Organization (WHO) estimates that 17% of all infectious diseases worldwide were transmitted by arthropod vectors, resulting in over 700,000 deaths annually. The table below lists common arthropod vectors and their associated diseases. The figure below represents endemic areas of common vector-borne diseases . ( Culicidae ) Protozoa ( Plasmodia ) Nematode ( Wuchereria bancrofti ) Malaria Lymphatic filariasis ( Simuliidae ) ( Reduviidae ) ( Phlebotominae ) ( Ixodidae ) Bacteria ( Rickettsia , Anaplasma , Ehrlichia , Borrelia burgdorferi , Coxiella burnetti ) Protozoa ( Babesia ) Rocky Mountain spotted fever , anaplasmosis , ehrlichiosis , Lyme disease , Q fever Babesiosis ( Glossinidae ) ( Tabanidae ) ( Siphonaptera , Pulicidae ) ( Phthiraptera , Pediculidae ) * Estimated global number of cases annually according to WHO in 2017. If a vector transmits multiple diseases, aggregate case numbers are listed. Rough estimates are only meant to provide a sense of scale. Unknown disease burden is listed as NA for not available.Most arthropod bites and stings do not require a specific diagnosis since they typically improve with supportive management alone. Certain bites and stings present with characteristic appearances and distributions. In general, however, dermoscopic findings of bitten or stung skin rarely aid in diagnosis. Rather, patient history (recent travel to endemic areas, outdoor activities, and other risk factors) primarily guides the diagnostic approach, which can raise clinical suspicion for more serious complications like vector-borne diseases. Skin biopsies are not indicated for bites or stings, since the histomorphologic appearance is non-specific . Bites and stings as well as other conditions (e.g. drug reactions, urticarial reactions , and early bullous pemphigoid ) can cause microscopic changes such as a wedge -shaped superficial dermal perivascular infiltrate consisting of abundant lymphocytes and scattered eosinophils , as shown in the adjacent figure: Skin biopsies are not indicated for bites or stings, since the histomorphologic appearance is non-specific . Bites and stings as well as other conditions (e.g. drug reactions, urticarial reactions , and early bullous pemphigoid ) can cause microscopic changes such as a wedge -shaped superficial dermal perivascular infiltrate consisting of abundant lymphocytes and scattered eosinophils , as shown in the adjacent figure: Prevention strategies against arthropod bites and stings comprise measures for personal protection, travel advisories, public health and environmental concerns. Travelers should seek to minimize outdoor activity during peak activity times and avoid high risk areas such as regions with known outbreaks or epidemics . Standing water and dense vegetation also commonly attract arthropods. Clothes covering most exposed skin can also provide a measure of physical protection, which may be augmented when the fabric is treated with pesticides such as Permethrin . Topical repellants such as N,N-diethyl-m-toluamide ( DEET ) is supported by a large body of evidence. Vaccines may also help prevent vector-borne diseases for eligible patients. For example, Japanese encephalitis , Yellow fever , and Dengue fever have FDA-approved vaccines available. Since they are relatively new vaccines, however, they are not standard of care as of 2023. Additionally, patients traveling to Malaria endemic regions are routinely prescribed Malaria chemoprophylaxis . Patients with a history of venom hypersensitivity may benefit from venom immunotherapy (VIT). Patients eligibile for VIT include those with a prior anaphylactic reaction to a venomous sting and who have IgE to venom allergens. VIT can help prevent future severe systemic reactions in select patients. International organizations such as WHO aim to reduce disease burdens of neglected tropical diseases, many of which are vector borne. Such campaigns must incorporate multipronged approaches to consider global inequality, access to resources, and climate change.Travelers should seek to minimize outdoor activity during peak activity times and avoid high risk areas such as regions with known outbreaks or epidemics . Standing water and dense vegetation also commonly attract arthropods. Clothes covering most exposed skin can also provide a measure of physical protection, which may be augmented when the fabric is treated with pesticides such as Permethrin . Topical repellants such as N,N-diethyl-m-toluamide ( DEET ) is supported by a large body of evidence. Vaccines may also help prevent vector-borne diseases for eligible patients. For example, Japanese encephalitis , Yellow fever , and Dengue fever have FDA-approved vaccines available. Since they are relatively new vaccines, however, they are not standard of care as of 2023. Additionally, patients traveling to Malaria endemic regions are routinely prescribed Malaria chemoprophylaxis . Patients with a history of venom hypersensitivity may benefit from venom immunotherapy (VIT). Patients eligibile for VIT include those with a prior anaphylactic reaction to a venomous sting and who have IgE to venom allergens. VIT can help prevent future severe systemic reactions in select patients. International organizations such as WHO aim to reduce disease burdens of neglected tropical diseases, many of which are vector borne. Such campaigns must incorporate multipronged approaches to consider global inequality, access to resources, and climate change.Most arthropod bites and stings require only supportive care. However, complications such as envenomation and severe allergic reactions can present as medical emergencies. Local reactions to bites and stings are treated symptomatically. If a stinger is still embedded, manual removal can reduce further irritation. Washing the affected area with soap and water can help reduce risk of contamination. Oral antihistamines , calamine lotion, topical corticosteroids and cold compresses are common over the counter remedies to reduce itchiness and local inflammation. In more severe cases, such as large local reactions, systemic glucocorticoids are sometimes prescribed, although limited evidence supports their effectiveness. There are limited data to support one treatment over another. Systemic reactions from venom hypersensitivity can rapidly progress to a medical emergency. The mainstay of anaphylactic shock management is intramuscularly injected epinephrine . The patient should be stabilized and transferred to an intensive care unit. Toxic reactions to envenomation are similarly managed with medical stabilization and symptomatic treatment. Tetanus prophylaxis should be up to date but antibiotics are typically unnecessary unless a bacterial superinfection is suspected. Antivenom drugs have been created for certain species such as Centruroides scorpion stings, but these drugs are not yet widely available and so typically reserved for severe systemic toxicity. Several vector-borne diseases can present emergently. After confirmation of diagnosis, antimicrobials are prescribed according to standard of care.Local reactions to bites and stings are treated symptomatically. If a stinger is still embedded, manual removal can reduce further irritation. Washing the affected area with soap and water can help reduce risk of contamination. Oral antihistamines , calamine lotion, topical corticosteroids and cold compresses are common over the counter remedies to reduce itchiness and local inflammation. In more severe cases, such as large local reactions, systemic glucocorticoids are sometimes prescribed, although limited evidence supports their effectiveness. There are limited data to support one treatment over another. Systemic reactions from venom hypersensitivity can rapidly progress to a medical emergency. The mainstay of anaphylactic shock management is intramuscularly injected epinephrine . The patient should be stabilized and transferred to an intensive care unit. Toxic reactions to envenomation are similarly managed with medical stabilization and symptomatic treatment. Tetanus prophylaxis should be up to date but antibiotics are typically unnecessary unless a bacterial superinfection is suspected. Antivenom drugs have been created for certain species such as Centruroides scorpion stings, but these drugs are not yet widely available and so typically reserved for severe systemic toxicity. Several vector-borne diseases can present emergently.After confirmation of diagnosis, antimicrobials are prescribed according to standard of care.A bite is defined as coming from the mouthparts of the arthropod . The bite consists of both the bite wound and the saliva . The saliva of the arthropod may contain anticoagulants , as in insects and arachnids which feed from blood. Feeding bites may also contain anaesthetic , to prevent the bite from being felt. Feeding bites may also contain digestive enzymes , as in spiders ; spider bites have primarily evolved to paralyse and then digest prey. A sting comes from the abdomen; in most insects (which are all largely hymenopterans ), the stinger is a modified ovipositor , which protrudes from the abdomen. The sting consists of an insertion wound, and venom. The venom is evolved to cause pain to a predator, paralyse a prey item, or both. Because insect stingers evolved from ovipositors, in most hymenopterans only the female can sting. However, there are a few orders of wasp where the male has evolved a "pseudo sting" - the male genitalia has evolved two sharp protrusions which can deliver an insertion wound. However, they do not contain venom, so they are not considered a true sting. In ants that bite instead of sting, such as the Formicinae , the bite causes the wound, but during the bite the abdomen bends forward to spray formic acid into the wound, causing additional pain. In arachnids that sting (all largely scorpions ), the stinger is not a modified ovipositor, but instead a metasoma that bears a telson. (Scorpians lack an ovipositor entirely and give birth to live young .) All species stingAll species stingAll species sting

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Favipiravir

In general: ℞ (Prescription only) 6-fluoro-3-hydroxypyrazine-2-carboxamide C1=C(N=C(C(=O)N1)C(=O)N)F InChI=1S/C5H4FN3O2/c6-2-1-8-5(11)3(9-2)4(7)10/h1H,(H2,7,10)(H,8,11) Key:ZCGNOVWYSGBHAU-UHFFFAOYSA-N Favipiravir , sold under the brand name Avigan among others, is an antiviral medication used to treat influenza in Japan. It is also being studied to treat a number of other viral infections, including SARS-CoV-2 . Like the experimental antiviral drugs T-1105 and T-1106, it is a pyrazinecarboxamide derivative. It is being developed and manufactured by Toyama Chemical (a subsidiary of Fujifilm ) and was approved for medical use in Japan in 2014. In 2016, Fujifilm licensed it to Zhejiang Hisun Pharmaceutical Co. It became a generic drug in 2019. [ citation needed ]Favipiravir has been approved to treat influenza in Japan. It is, however, only indicated for novel influenza (strains that cause more severe disease) rather than seasonal influenza . As of 2020, the probability of resistance developing appears low. There is evidence that use during pregnancy may result in harm to the baby . Teratogenic and embryotoxic effects were shown on four animal species. In one case report, a 6-month old infant developed benign bright blue discolouration of the cornea after treatment with favipiravir which resolved after treatment cessation. The mechanism of its actions is thought to be related to the selective inhibition of viral RNA-dependent RNA polymerase . [ medical citation needed ] Favipiravir is a prodrug that is metabolized to its active form, favipiravir-ribofuranosyl-5'-triphosphate (favipiravir-RTP), available in both oral and intravenous formulations. In 2014, favipiravir was approved in Japan for stockpiling against influenza pandemics . However, favipiravir has not been shown to be effective in primary human airway cells, casting doubt on its efficacy in influenza treatment. Favipiravir-RTP is a nucleoside analogue . It mimics both guanosine and adenosine for the viral RdRP. Incorporating two such bases in a row stops primer extension, although it is unclear how as of 2013. The US Department of Defense developed favipiravir in partnership with MediVector, Inc. as a broad-spectrum antiviral and sponsored it through FDA Phase II and Phase III clinical trials, where it demonstrated safety in humans and efficacy against the influenza virus. favipiravir remains unapproved in the UK and the USA. In 2014, Japan approved favipiravir for treating influenza strains unresponsive to current antivirals. Toyama Chemical initially hoped that favipiravir would become a new influenza medication that could replace oseltamivir (brand name Tamiflu). However, animal experiments show the potential for teratogenic effects, and the approval of production by The Ministry of Health, Labor and Welfare was greatly delayed and the production condition is limited only in an emergency in Japan. Despite limited data on efficacy, as of March 2021 favipiravir is widely prescribed for outpatient treatment of mild to moderate COVID-19 in Egypt, Hungary and Serbia. Patients are required to sign a consent form before obtaining the drug. [ citation needed ] Favipiravir is sold under the brand names Avigan ( アビガン , Abigan ) , Avifavir, Avipiravir, Areplivir, FabiFlu, Favipira, Reeqonus, and Qifenda. Coronavir is the brand name of favipiravir used in Russia , where it is approved for the treatment of COVID-19 . It is produced and sold by R-Pharm . Coronavir was approved for use in Russia in hospitals in July 2020, and in September 2020 it received approval for prescription sales for outpatient use. The US Department of Defense developed favipiravir in partnership with MediVector, Inc. as a broad-spectrum antiviral and sponsored it through FDA Phase II and Phase III clinical trials, where it demonstrated safety in humans and efficacy against the influenza virus. favipiravir remains unapproved in the UK and the USA. In 2014, Japan approved favipiravir for treating influenza strains unresponsive to current antivirals. Toyama Chemical initially hoped that favipiravir would become a new influenza medication that could replace oseltamivir (brand name Tamiflu). However, animal experiments show the potential for teratogenic effects, and the approval of production by The Ministry of Health, Labor and Welfare was greatly delayed and the production condition is limited only in an emergency in Japan. Despite limited data on efficacy, as of March 2021 favipiravir is widely prescribed for outpatient treatment of mild to moderate COVID-19 in Egypt, Hungary and Serbia. Patients are required to sign a consent form before obtaining the drug. [ citation needed ]Favipiravir is sold under the brand names Avigan ( アビガン , Abigan ) , Avifavir, Avipiravir, Areplivir, FabiFlu, Favipira, Reeqonus, and Qifenda.Coronavir is the brand name of favipiravir used in Russia , where it is approved for the treatment of COVID-19 . It is produced and sold by R-Pharm . Coronavir was approved for use in Russia in hospitals in July 2020, and in September 2020 it received approval for prescription sales for outpatient use. Favipiravir, as an antiviral drug, has been authorized for treating COVID-19 in several countries including Japan, Russia, Serbia, Turkey, India, and Thailand, under emergency provisions. A rapid meta-review in September 2020 (analyzing four studies) noted that the drug led to clinical and radiological improvements; however, no reduction in mortality or differences in oxygen-support requirement were observed and more rigorous studies were sought. A Cochrane Systematic review published in Feb 2024, noted that there is actually no real benefit with Favipiravir in treating Covid-19 in terms of mortality benefits, or admission to mechanical ventillation, or hospitalisation, and it may not make any difference in adverse effects or serious adverse effects. As of May 2021 [ update ] , large-cohort clinical trials are underway. Research in 2014, suggested that favipiravir may have efficacy against Ebola based on studies in mouse models ; efficacy in humans was unaddressed. During the 2014 West Africa Ebola virus outbreak , a French nurse who contracted Ebola while volunteering for Médecins Sans Frontières (MSF) in Liberia reportedly recovered after receiving a course of favipiravir. A clinical trial investigating the use of favipiravir against Ebola virus disease began in Guéckédou , Guinea, in December 2014. Preliminary results presented in 2016 at the Conference on Retroviruses and Opportunistic Infections (CROI), later published, showed a decrease in mortality in patients with low-to-moderate levels of virus in blood, but no effect on patients with high levels (the group at a higher risk of death). The trial design was concomitantly criticised for using only historical controls. Nipah virus is a causative agent of outbreaks of encephalitis with pneumonia and has a high case fatality rate . The first outbreak occurred in Malaysia-Singapore, related to contact with pigs in slaughterhouses and an outbreak in Philippines related to slaughter of horses, most other outbreaks have affected India and Bangladesh. in Bangladesh outbreaks are often associated with consumption of raw date palm sap contaminated by saliva and urine of fruit bats. In a study published in the Scientific Reports, Syrian hamster model for Nipah virus infection was used, which closely mirrors most aspects of human disease, such as widespread vasculitis, pneumonia, and encephalitis. The hamsters were infected with a lethal dose of 10 4 PFU NiV-M via the intraperitoneal (i.p.) route similar to previous studies and treatment was initiated immediately after infection. Favipiravir was administered twice daily via the peroral (p.o.) route for 14 days. The treated hamsters displayed 100% survival and no obvious morbidity after lethal NiV challenge, whereas all the control cases died of severe disease. In experiments in animals favipiravir has shown activity against West Nile virus , yellow fever virus , foot-and-mouth disease virus as well as other flaviviruses , arenaviruses , bunyaviruses and alphaviruses . Activity against enteroviruses and Rift Valley fever virus has also been demonstrated. Favipiravir has showed limited efficacy against Zika virus in animal studies, but was less effective than other antivirals such as MK-608 . The agent has also shown some efficacy against rabies , and has been used experimentally in some humans infected with the virus. The possible tautomerism of favipiravir has been investigated computationally and experimentally. It was found that the enol-like form was substantially more stable in organic solvents than the keto-like form, meaning that Favipiravir likely exists almost exclusively in the enol-like form. In aqueous solution the keto-like tautomer is substantially stabilized due to the specific interaction with the water molecules. Upon protonation the keto form is switched on. [ citation needed ]Favipiravir, as an antiviral drug, has been authorized for treating COVID-19 in several countries including Japan, Russia, Serbia, Turkey, India, and Thailand, under emergency provisions. A rapid meta-review in September 2020 (analyzing four studies) noted that the drug led to clinical and radiological improvements; however, no reduction in mortality or differences in oxygen-support requirement were observed and more rigorous studies were sought. A Cochrane Systematic review published in Feb 2024, noted that there is actually no real benefit with Favipiravir in treating Covid-19 in terms of mortality benefits, or admission to mechanical ventillation, or hospitalisation, and it may not make any difference in adverse effects or serious adverse effects. As of May 2021 [ update ] , large-cohort clinical trials are underway. Research in 2014, suggested that favipiravir may have efficacy against Ebola based on studies in mouse models ; efficacy in humans was unaddressed. During the 2014 West Africa Ebola virus outbreak , a French nurse who contracted Ebola while volunteering for Médecins Sans Frontières (MSF) in Liberia reportedly recovered after receiving a course of favipiravir. A clinical trial investigating the use of favipiravir against Ebola virus disease began in Guéckédou , Guinea, in December 2014. Preliminary results presented in 2016 at the Conference on Retroviruses and Opportunistic Infections (CROI), later published, showed a decrease in mortality in patients with low-to-moderate levels of virus in blood, but no effect on patients with high levels (the group at a higher risk of death). The trial design was concomitantly criticised for using only historical controls. Nipah virus is a causative agent of outbreaks of encephalitis with pneumonia and has a high case fatality rate . The first outbreak occurred in Malaysia-Singapore, related to contact with pigs in slaughterhouses and an outbreak in Philippines related to slaughter of horses, most other outbreaks have affected India and Bangladesh. in Bangladesh outbreaks are often associated with consumption of raw date palm sap contaminated by saliva and urine of fruit bats. In a study published in the Scientific Reports, Syrian hamster model for Nipah virus infection was used, which closely mirrors most aspects of human disease, such as widespread vasculitis, pneumonia, and encephalitis. The hamsters were infected with a lethal dose of 10 4 PFU NiV-M via the intraperitoneal (i.p.) route similar to previous studies and treatment was initiated immediately after infection. Favipiravir was administered twice daily via the peroral (p.o.) route for 14 days. The treated hamsters displayed 100% survival and no obvious morbidity after lethal NiV challenge, whereas all the control cases died of severe disease. In experiments in animals favipiravir has shown activity against West Nile virus , yellow fever virus , foot-and-mouth disease virus as well as other flaviviruses , arenaviruses , bunyaviruses and alphaviruses . Activity against enteroviruses and Rift Valley fever virus has also been demonstrated. Favipiravir has showed limited efficacy against Zika virus in animal studies, but was less effective than other antivirals such as MK-608 . The agent has also shown some efficacy against rabies , and has been used experimentally in some humans infected with the virus. The possible tautomerism of favipiravir has been investigated computationally and experimentally. It was found that the enol-like form was substantially more stable in organic solvents than the keto-like form, meaning that Favipiravir likely exists almost exclusively in the enol-like form. In aqueous solution the keto-like tautomer is substantially stabilized due to the specific interaction with the water molecules. Upon protonation the keto form is switched on. [ citation needed ]

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Medical entomology

The discipline of medical entomology , or public health entomology , and also veterinary entomology is focused upon insects and arthropods that impact human health. Veterinary entomology is included in this category, because many animal diseases can "jump species" and become a human health threat, for example, bovine encephalitis. Medical entomology also includes scientific research on the behavior, ecology, and epidemiology of arthropod disease vectors , and involves a tremendous outreach to the public, including local and state officials and other stake holders in the interest of public safety. Public health entomology has seen a huge surge in interest since 2005, due to the resurgence of the bed bug, Cimex lectularius.There are many insects (and other arthropods) that affect human health. These arthropods include Diptera , Hemiptera , Thysanoptera , Phthiraptera , and Siphonaptera . They can parasitize, bite, sting, cause allergic reactions, and/or vector disease to humans. insects are good for it can be impossible to know the full impact that insects and other arthropods have on human health. Medical entomologists worldwide are working to combat the known effects in order to improve public health.Personal pests such as lice , fleas , bedbugs , ticks , scabies mites , may vector pathogens. They are hematophagous , meaning they feed on the blood of their host. Nearly all personal pests can be transmitted to an uninfected host with prolonged exposure to an infected host. Lice, fleas, bedbugs, and ticks are known as ectoparasites . Ectoparasites live on the skin of their host. They have adaptations that allow them to access the nutrients inside of the host, such as methods to penetrate skin, insert digestive enzymes and a gut microbiome that can digest the nutrients received from the host. While these ectoparasites feed, the transfer of fluids may transmit diseases such as typhus, plague, and Lyme disease. It is also suspected that bedbugs may also be vectors of hepatitis B. Scabies mites cannot be classified as ectoparasites. The mite that causes scabies, Sarcoptes scabiei also known as the itch mite, burrows into the skin of its host making it an endoparasite . The act of S. scabiei living in the skin and the allergic response to the parasite is the condition known as scabies .The housefly is a very common and cosmopolitan species which transmits diseases to man. The organisms of both amoebic and bacillary dysenteries are picked up by flies from the faeces of infected people and transferred to clean food either on the fly's hairs or by the fly vomiting during feeding. Typhoid germs may be deposited on food with the fly's faeces. The house fly cause the spread of yaws germs by carrying them from a yaws ulcer to an ordinary sore. Houseflies also transmit poliomyelitis by carrying the virus from infected faeces to food or drink. Cholera and hepatitis are sometimes fly-borne. Other diseases carried by houseflies are Salmonella , tuberculosis , anthrax , and some forms of ophthalmia . They carry over 100 pathogens and transmit some parasitic worms. The flies in poorer and lower-hygiene areas usually carry more pathogens. Some strains have become immune to most common insecticides.Cockroaches carry disease-causing organisms (typically gastroenteritis ) as they forage. Cockroach excrement and cast skins also contain a number of allergens causing responses such as, watery eyes, rashes, congestion of nasal passages and asthma.There are many insects that bite including mosquitoes , biting midges , sandflies , black flies , Horse-flies , and stable flies . Through feeding, insects or other arthropod vectors can transmit diseases to humans. Medical entomologists and other medical professionals have helped to develop vaccines that can prevent humans from contracting some of those diseases. They have also developed ways to prevent the arthropods from biting humans. According to a study by the Centers for Disease Control and Prevention published in May 2018, illnesses caused by insect bites have tripled from 2004 to 2016.

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Human T-lymphotropic virus 1

Human T-cell lymphotropic virus type 1 or human T-lymphotropic virus ( HTLV-I ), also called the adult T-cell lymphoma virus type 1 , is a retrovirus of the human T-lymphotropic virus (HTLV) family. Most people with HTLV-1 infection do not appear to develop health conditions that can be directly linked to the infection. However, there is a subgroup of people who experience severe complications. The most well characterized are adult T-cell lymphoma (ATL) and HTLV-I-associated myelopathy / Tropical spastic paraparesis (HAM/TSP), both of which are only diagnosed in individuals testing positive to HTLV-1 infection. The estimated lifetime risk of ATL among people with HTLV-1 infection is approximately 5%, while that of HAM/TSP is approximately 2%. In 1977, Adult T-cell lymphoma (ATL) was first described in a case series of individuals from Japan. The symptoms of ATL were different from other lymphomas known at the time. The common birthplace shared amongst most of the ATL patients was suggestive of an infectious cause, referred to as ATLV. Strikingly, ATLV had the transforming activity in vitro. These studies established that HTLV-1 was the causitive agent of ATL. The retrovirus is now generally called HTLV-I because later studies proved that ATLV is the same as the firstly identified human retrovirus called HTLV discovered by Bernard Poiesz and Francis Ruscetti and their co-workers in the laboratory of Robert C. Gallo at the National Cancer Institute . Persistent lifelong infection is established when HTLV-1 integrates into the host genome as a provirus. A patient infected with HTLV-1 can be diagnosed when antibodies against HTLV-1 are detected in the serum . HTLV-1 is a retrovirus belonging to the family retroviridae and the genus deltaretrovirus . It has a positive-sense RNA genome that is reverse transcribed into DNA and then integrated into the cellular DNA. Once integrated, HTLV-1 continues to exist only as a provirus which can spread from cell to cell through a viral synapse . Few, if any, free virions are produced and there is usually no detectable virus in the blood plasma though the virus is present in genital secretions. Like HIV , HTLV-1 predominantly infects CD4+ T cells . The viral RNA is packed into the icosahedral capsid which is contained inside the protein inner envelope. The lipid outer envelope is of host cell origin but contains viral transmembrane and surface proteins. The virion is spherical in shape with a diameter of about 100 nm. HTLV-1 is genetically classified into seven subtypes, each defined by a unique geographic distribution influenced by population migration. The most globally widespread is the cosmopolitan subtype A, which further branches into several subgroups: transcontinental, Japanese, West African, North African, Senegalese, and Afro-Peruvian. While subtypes B, D, E, F, and G are localized to distinct regions in Africa, subtype C is predominant in Australia and Oceania. HTLV-1 is believed to have originated from the simian T-lymphotropic virus type 1 (STLV-1), a retrovirus prevalent among numerous nonhuman primates in intertropical Africa. This theory is supported by the significant genetic diversity of HTLV-1 subtypes in Africa, potentially arising from repeated zoonotic transmissions during human interactions with STLV-1 endemic nonhuman primates. This correlation is further reinforced by the observation that individuals bitten by nonhuman primates exhibit HTLV-1 strains with sequences remarkably homologous to the STLV-1 found in local primate species. The global distribution of HTLV-I is highly heterogeneous, with focal occurrence in diverse regions. Within areas where HTLV-I is found, its occurrence varies considerably, with endemic clusters often situated near populations with lower prevalence. This pattern might be influenced by the founder effect, suggesting prolonged viral transmission within isolated groups, but this theory warrants further investigation. Consistent findings reveal that HTLV-1 prevalence increases with age and is usually higher in adult females than males. Areas broadly regarded as having endemic regions include Japan, Iran, the Americas, the Caribbean, Melanesia, Central and West Africa, and Australia. Globally, there remains a lack of robust data from populous countries like India and Nigeria and most of North and East Africa. As such, current global prevalence estimates, which are based on known endemic regions, likely underestimate the true global prevalence. In Australia, HTLV-I has notably high prevalence among Aboriginal communities in Central Australia. Community-based cross-sectional studies from Central Australia report HTLV-1 prevalences exceeding 30%, representing the highest reported prevalence for any population worldwide. In Taiwan, in Iran, and in Fujian (a Chinese province near Taiwan) the prevalence is 0.1–1%. The infection rate is about 1% in Papua New Guinea , the Solomon Islands , and Vanuatu , where the genotype C predominates. In Europe HTLV-1 is uncommon, although it is present in some populations, generally people who have migrated from known endemic regions. In the Americas HTLV-1 is found in some Indigenous populations and descendants of African ancestry from where it is thought to have originated. Prevalence ranges from 0.1 to 1%. In Africa the prevalence is not well known, but it is about 1% in some countries {{ Citation needed }}. HTLV-I infection in the United States appears to be about half as prevalent among IV drug users and about one-tenth as prevalent in the population at large as HIV infection {{ Citation needed }}. Although little serologic data exist, the prevalence of infection is thought to be highest among blacks living in the Southeast {{ Citation needed }}. A prevalence rate of 30% has been found among black intravenous drug users in New Jersey , and a rate of 49% has been found in a similar group in New Orleans . {{Citation needed|reason=Prevalence is not a rate. Additionally, the citation references an old study that did not discriminate between HTLV-1 or HTLV-2, which has substantially different pathologic, and transmission characteristics. |date=October 2023}} It is also high among the Inuit of Northern Canada, in Japan, northeastern Iran. Peru, the Pacific coast of Colombia and Ecuador, and the Caribbean. [ citation needed ]HTLV-1 has three main routes of transmission. Vertical transmission is most common, through which an infected mother transmits the virus to her child {{Citation needed|reason= Sexual transmission is the most common, hence increasing prevalence with age |date=October 2023}}. Interestingly, the risk to a fetus while inside the womb is minimal, given the virtual absence of viral particles in human plasma. Most vertical infection occurs through breastfeeding. About 25% of infants who are breastfed by infected mothers are infected, while less than 5% of children born to but not breastfed by infected mothers are infected. Sexual transmission is second-most common, whereby an individual infects another through exchange of bodily fluids. Some evidence has suggested that male-to-female transmission is more efficient than female-to-male transmission. For example, one study in Japan found a 61% transmission rate for males to females vs. a less than 1% rate for females to males. Least common is parenteral transmission through blood transfusion, with an infection rate of 44-63% estimated in one study, and needle sharing among intravenous drug users. With proper prophylaxis (e.g. breastfeeding counseling for mothers, condom use, and donor blood screening), rates of transmission can be effectively reduced. The importance of the various routes of transmission is believed to vary geographically. The research in discordant couples showed that probability of sexual transmission is about 0.9 per 100 person-years. The term viral tropism refers to which cell types HTLV-I infects. Although HTLV-1 is primarily found in CD4+ T cells, other cell types in the peripheral blood of infected individuals have been found to contain HTLV-1, including CD8+ T cells, dendritic cells and B cells. HTLV-I entry is mediated through interaction of the surface unit of the virion envelope glycoprotein (SU) with its cellular receptor GLUT1 , a glucose transporter, on target cells. HTLV-1 is also associated with adult T-cell leukemia/lymphoma and has been quite well studied in Japan. The time between infection and onset of cancer also varies geographically. It is believed to be about sixty years in Japan and less than forty years in the Caribbean. The cancer is thought to be due to the pro-oncogenic effect of viral RNA incorporated into host lymphocyte DNA. Chronic stimulation of the lymphocytes at the cytokine level may play a role in the development of the malignancy. The lymphoma ranges from a very indolent and slowly progressive type to a very aggressive and nearly uniformly lethal proliferative type. [ citation needed ] There is some evidence that HTLV-1 is a causative agent of cutaneous T-cell lymphoma . HTLV-1 is also associated with a progressive demyelinating upper motor neuron disease known as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), characterized by sensory and motor deficits, particularly of the lower extremities, incontinence and impotence. Only 0.3 to 4% of infected individuals develop HAM/TSP, but this will vary from one geographic location to another. Signs and symptoms of HTLV myelopathy include: Other neurologic findings that may be found in HTLV include: HTLV-1 is associated with a rheumatoid-like arthropathy , although the evidence is contradictory. In these cases patients have a negative rheumatoid factor . Studies from Japan demonstrated that HTLV-1 infection may be associated with an intermediate uveitis . At onset the patients present with blurred vision and floaters. The prognosis is favorable—the condition usually resolves within weeks. Individuals infected with HTLV-1 are at risk for opportunistic infections —diseases not caused by the virus itself, but by alterations in the host's immune functions. HTLV-1, unlike the distantly related retrovirus HIV, has an immunostimulating effect which actually becomes immunosuppressive. The virus activates a subset of T-helper cells called Th1 cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-γ and TNF-α ). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (mainly IL-4 , IL-5 , IL-10 and IL-13 ). The result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependent response (these include parasitic infections and production of mucosal and humoral antibodies). [ citation needed ] In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis . It is also particularly associated with bronchiectasis , a chronic lung condition predisposing to recurrent pneumonia . It is also associated with chronic infected dermatitis , often superinfected with Staphylococcus aureus and a severe form of Strongyloides stercoralis infection called hyper-infestation which may lead to death from polymicrobial sepsis. HTLV-1 infection has also been associated with Tuberculosis . HTLV-1 is also associated with adult T-cell leukemia/lymphoma and has been quite well studied in Japan. The time between infection and onset of cancer also varies geographically. It is believed to be about sixty years in Japan and less than forty years in the Caribbean. The cancer is thought to be due to the pro-oncogenic effect of viral RNA incorporated into host lymphocyte DNA. Chronic stimulation of the lymphocytes at the cytokine level may play a role in the development of the malignancy. The lymphoma ranges from a very indolent and slowly progressive type to a very aggressive and nearly uniformly lethal proliferative type. [ citation needed ] There is some evidence that HTLV-1 is a causative agent of cutaneous T-cell lymphoma . HTLV-1 is also associated with adult T-cell leukemia/lymphoma and has been quite well studied in Japan. The time between infection and onset of cancer also varies geographically. It is believed to be about sixty years in Japan and less than forty years in the Caribbean. The cancer is thought to be due to the pro-oncogenic effect of viral RNA incorporated into host lymphocyte DNA. Chronic stimulation of the lymphocytes at the cytokine level may play a role in the development of the malignancy. The lymphoma ranges from a very indolent and slowly progressive type to a very aggressive and nearly uniformly lethal proliferative type. [ citation needed ]There is some evidence that HTLV-1 is a causative agent of cutaneous T-cell lymphoma . HTLV-1 is also associated with a progressive demyelinating upper motor neuron disease known as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), characterized by sensory and motor deficits, particularly of the lower extremities, incontinence and impotence. Only 0.3 to 4% of infected individuals develop HAM/TSP, but this will vary from one geographic location to another. Signs and symptoms of HTLV myelopathy include: Other neurologic findings that may be found in HTLV include: HTLV-1 is associated with a rheumatoid-like arthropathy , although the evidence is contradictory. In these cases patients have a negative rheumatoid factor . Studies from Japan demonstrated that HTLV-1 infection may be associated with an intermediate uveitis . At onset the patients present with blurred vision and floaters. The prognosis is favorable—the condition usually resolves within weeks. HTLV-1 is also associated with a progressive demyelinating upper motor neuron disease known as HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP), characterized by sensory and motor deficits, particularly of the lower extremities, incontinence and impotence. Only 0.3 to 4% of infected individuals develop HAM/TSP, but this will vary from one geographic location to another. Signs and symptoms of HTLV myelopathy include: Other neurologic findings that may be found in HTLV include:HTLV-1 is associated with a rheumatoid-like arthropathy , although the evidence is contradictory. In these cases patients have a negative rheumatoid factor . Studies from Japan demonstrated that HTLV-1 infection may be associated with an intermediate uveitis . At onset the patients present with blurred vision and floaters. The prognosis is favorable—the condition usually resolves within weeks. Individuals infected with HTLV-1 are at risk for opportunistic infections —diseases not caused by the virus itself, but by alterations in the host's immune functions. HTLV-1, unlike the distantly related retrovirus HIV, has an immunostimulating effect which actually becomes immunosuppressive. The virus activates a subset of T-helper cells called Th1 cells. The result is a proliferation of Th1 cells and overproduction of Th1 related cytokines (mainly IFN-γ and TNF-α ). Feedback mechanisms of these cytokines cause a suppression of the Th2 lymphocytes and a reduction of Th2 cytokine production (mainly IL-4 , IL-5 , IL-10 and IL-13 ). The result is a reduction in the ability of the infected host to mount an adequate immune response to invading organisms that require a predominantly Th2 dependent response (these include parasitic infections and production of mucosal and humoral antibodies). [ citation needed ] In the central Australian Aboriginal population, HTLV-1 is thought to be related to their extremely high rate of death from sepsis . It is also particularly associated with bronchiectasis , a chronic lung condition predisposing to recurrent pneumonia . It is also associated with chronic infected dermatitis , often superinfected with Staphylococcus aureus and a severe form of Strongyloides stercoralis infection called hyper-infestation which may lead to death from polymicrobial sepsis. HTLV-1 infection has also been associated with Tuberculosis . Treatment of opportunistic infections varies depending on the type of disease and ranges from careful observation to aggressive chemotherapy and antiretroviral agents. [ citation needed ] Adult T cell lymphoma is a common complication of HTLV infection and requires aggressive chemotherapy, typically R-CHOP . Other treatments for ATL in HTLV infected patients include interferon alpha, zidovudine with interferon alpha and CHOP with arsenic trioxide . Treatments for HTLV myelopathy are even more limited and focus mainly on symptomatic therapy. Therapies studied include corticosteroids , plasmapheresis , cyclophosphamide , and interferon , which may produce a temporary symptomatic improvement in myelopathy symptoms. Valproic acid has been studied to determine if it might slow the progression of HTLV disease by reducing viral load. Although in one human study it was effective in reducing viral load, there did not appear to be a clinical benefit. Recently however, a study of valproic acid combined with zidovudine showed a major decrease in the viral load of baboons infected with HTLV-1. It is important to monitor HTLV patients for opportunistic infections such as cytomegalovirus , histoplasmosis , scabies , pneumocystis pneumonia , and staphylococcal infections . HIV testing should also be performed, as some patients may be co-infected with both viruses. [ citation needed ] Allogenic bone marrow transplantation has been investigated in the treatment of HTLV-1 disease with varied results. One case report describes an HTLV-1 infected woman who developed chronic refractory eczema, corneal injury and adult T cell leukemia. She was subsequently treated with allogenic stem cell transplantation and had complete resolution of symptoms. One year post-transplant, she has had no recurrence of any symptoms, and furthermore has had a decrease in her proviral load. [ citation needed ]

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Rift Valley fever

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Disease X

Disease X is a placeholder name that was adopted by the World Health Organization (WHO) in February 2018 on their shortlist of blueprint priority diseases to represent a hypothetical, unknown pathogen that could cause a future epidemic . The WHO adopted the placeholder name to ensure that their planning was sufficiently flexible to adapt to an unknown pathogen (e.g., broader vaccines and manufacturing facilities). Director of the US National Institute of Allergy and Infectious Diseases Anthony Fauci stated that the concept of Disease X would encourage WHO projects to focus their research efforts on entire classes of viruses (e.g., flaviviruses ), instead of just individual strains (e.g., zika virus ), thus improving WHO capability to respond to unforeseen strains. In 2020, experts, including some of the WHO's own expert advisors, speculated that COVID-19 , caused by the SARS-CoV-2 virus strain, met the requirements to be the first Disease X. In May 2015, in pandemic preparations prior to the COVID-19 pandemic , the WHO was asked by member organizations to create an "R&D Blueprint for Action to Prevent Epidemics" to generate ideas that would reduce the time lag between the identification of viral outbreaks and the approval of vaccines/treatments, to stop the outbreaks from turning into a "public health emergency". The focus was to be on the most serious emerging infectious diseases (EIDs) for which few preventive options were available. A group of global experts, the "R&D Blueprint Scientific Advisory Group", was assembled by the WHO to draft a shortlist of less than ten "blueprint priority diseases". Since 2015, the shortlist of EIDs has been reviewed annually and originally included widely known diseases such as Ebola and Zika which have historically caused epidemics, as well as lesser known diseases which have potential for serious outbreaks, such as SARS , Lassa fever , Marburg virus , Rift Valley fever , and Nipah virus . Since then, COVID-19 has been added to the list. In February 2018, after the "2018 R&D Blueprint" meeting in Geneva , the WHO added Disease X to the shortlist as a placeholder for a " knowable unknown " pathogen. The Disease X placeholder acknowledged the potential for a future epidemic that could be caused by an unknown pathogen, and by its inclusion, challenged the WHO to ensure their planning and capabilities were flexible enough to adapt to such an event. At the 2018 announcement of the updated shortlist of blueprint priority diseases, the WHO said: "Disease X represents the knowledge that a serious international epidemic could be caused by a pathogen currently unknown to cause human disease". John-Arne Røttingen , of the R&D Blueprint Special Advisory Group, said: "History tells us that it is likely the next big outbreak will be something we have not seen before", and "It may seem strange to be adding an 'X' but the point is to make sure we prepare and plan flexibly in terms of vaccines and diagnostic tests. We want to see 'plug and play' platforms developed which will work for any or a wide number of diseases; systems that will allow us to create countermeasures at speed". US expert Anthony Fauci said: "WHO recognizes it must 'nimbly move' and this involves creating platform technologies", and that to develop such platforms, WHO would have to research entire classes of viruses, highlighting flaviviruses . He added: "If you develop an understanding of the commonalities of those, you can respond more rapidly". Jonathan D. Quick , the author of End of Epidemics , described the WHO's act of naming Disease X as "wise in terms of communicating risk", saying "panic and complacency are the hallmarks of the world's response to infectious diseases, with complacency currently in the ascendance". Women's Health wrote that the establishment of the term "might seem like an uncool move designed to incite panic" but that the whole purpose of including it on the list was to "get it on people's radars". Richard Hatchett of the Coalition for Epidemic Preparedness Innovations (CEPI), wrote "It might sound like science fiction, but Disease X is something we must prepare for", noting that despite the success in controlling the 2014 Western African Ebola virus epidemic , strains of the disease had returned in 2018. In February 2019, CEPI announced funding of US$34 million to the German-based CureVac biopharmaceutical company to develop an "RNA Printer prototype", that CEPI said could "prepare for rapid response to unknown pathogens (i.e., Disease X)". Parallels were drawn with the efforts by the United States Agency for International Development (USAID) and their PREDICT program, which was designed to act as an early warning pandemic system, by sourcing and researching animal viruses in particular "hot spots" of animal-human interaction. In September 2019, The Daily Telegraph reported on how Public Health England (PHE) had launched its own investigation for a potential Disease X in the United Kingdom from the diverse range of diseases reported in their health system; they noted that 12 novel diseases and/or viruses had been recorded by PHE in the last decade. In October 2019 in New York, the WHO's Health Emergencies Program ran a "Disease X dummy run" to simulate a global pandemic by Disease X, for its 150 participants from various world health agencies and public health systems to better prepare and share ideas and observations for combatting such an eventuality. In March 2020, The Lancet Infectious Diseases published a paper titled "Disease X: accelerating the development of medical countermeasures for the next pandemic", which expanded the term to include Pathogen X (the pathogen that leads to Disease X), and identified areas of product development and international coordination that would help in combatting any future Disease X. In April 2020, The Daily Telegraph described remdesivir , a drug being trialed to combat COVID-19, as an anti-viral that Gilead Sciences started working on a decade previously to treat a future Disease X. In August 2023, the UK Government announced the creation of a new research center, located on the Porton Down campus, which is tasked at researching pathogens with the potential to emerge as Disease X. Live viruses will be kept in specialist containment facilities in order to develop tests and potential vaccines within 100 days in case a new threat is identified. In January 2024, during the World Economic Forum 's annual meeting, Disease X was once again discussed as being a potential threat following the COVID-19 pandemic. A paper published in 2022 listed the following strategies in preparation for Disease X: On the addition of Disease X in 2018, the WHO said it could come from many sources citing hemorrhagic fevers and the more recent non-polio enterovirus . However, Røttingen speculated that Disease X would be more likely to come from zoonotic transmission (an animal virus that jumps to humans), saying: "It's a natural process and it is vital that we are aware and prepare. It is probably the greatest risk". WHO special advisor Professor Marion Koopmans, also noted that the rate at which zoonotic diseases were appearing was accelerating, saying: "The intensity of animal and human contact is becoming much greater as the world develops. This makes it more likely new diseases will emerge but also modern travel and trade make it much more likely they will spread". From the outset of the COVID-19 pandemic , experts have speculated whether COVID-19 met the criteria to be Disease X. In early February 2020, Chinese virologist Shi Zhengli from the Wuhan Institute of Virology wrote that the first Disease X is from a coronavirus. Later that month, Marion Koopmans , Head of Viroscience at Erasmus University Medical Center in Rotterdam , and a member of the WHO's R&D Blueprint Special Advisory Group, wrote in the scientific journal Cell , "Whether it will be contained or not, this outbreak is rapidly becoming the first true pandemic challenge that fits the disease X category". At the same time, Peter Daszak , also a member of the WHO's R&D Blueprint, wrote in an opinion piece in The New York Times saying: "In a nutshell, Covid-19 is Disease X". At the 2018 announcement of the updated shortlist of blueprint priority diseases, the media speculated that a future Disease X could be created intentionally as a biological weapon . In 2018, WHO R&D Blueprint Special Advisor Group member Røttingen was questioned about the potential of Disease X to come from the ability of gene-editing technology to produce synthetic viruses (e.g., the 2017 synthesis of Orthopoxvirus in Canada was cited), which could be released through an accident or even an act of terror . Røttingen said it was unlikely that a future Disease X would originate from a synthetic virus or a bio-weapon. However, he noted the seriousness of such an event, saying, "Synthetic biology allows for the creation of deadly new viruses. It is also the case that where you have a new disease there is no resistance in the population and that means it can spread fast". In September 2019, Public Health England (PHE) reported that the increasing antibiotic resistance of bacteria, even to "last-resort" antibiotics such as carbapenems and colistin , could also turn into a potential Disease X, citing the antibiotic resistance in gonorrhea as an example. On the addition of Disease X in 2018, the WHO said it could come from many sources citing hemorrhagic fevers and the more recent non-polio enterovirus . However, Røttingen speculated that Disease X would be more likely to come from zoonotic transmission (an animal virus that jumps to humans), saying: "It's a natural process and it is vital that we are aware and prepare. It is probably the greatest risk". WHO special advisor Professor Marion Koopmans, also noted that the rate at which zoonotic diseases were appearing was accelerating, saying: "The intensity of animal and human contact is becoming much greater as the world develops. This makes it more likely new diseases will emerge but also modern travel and trade make it much more likely they will spread". From the outset of the COVID-19 pandemic , experts have speculated whether COVID-19 met the criteria to be Disease X. In early February 2020, Chinese virologist Shi Zhengli from the Wuhan Institute of Virology wrote that the first Disease X is from a coronavirus. Later that month, Marion Koopmans , Head of Viroscience at Erasmus University Medical Center in Rotterdam , and a member of the WHO's R&D Blueprint Special Advisory Group, wrote in the scientific journal Cell , "Whether it will be contained or not, this outbreak is rapidly becoming the first true pandemic challenge that fits the disease X category". At the same time, Peter Daszak , also a member of the WHO's R&D Blueprint, wrote in an opinion piece in The New York Times saying: "In a nutshell, Covid-19 is Disease X". From the outset of the COVID-19 pandemic , experts have speculated whether COVID-19 met the criteria to be Disease X. In early February 2020, Chinese virologist Shi Zhengli from the Wuhan Institute of Virology wrote that the first Disease X is from a coronavirus. Later that month, Marion Koopmans , Head of Viroscience at Erasmus University Medical Center in Rotterdam , and a member of the WHO's R&D Blueprint Special Advisory Group, wrote in the scientific journal Cell , "Whether it will be contained or not, this outbreak is rapidly becoming the first true pandemic challenge that fits the disease X category". At the same time, Peter Daszak , also a member of the WHO's R&D Blueprint, wrote in an opinion piece in The New York Times saying: "In a nutshell, Covid-19 is Disease X". At the 2018 announcement of the updated shortlist of blueprint priority diseases, the media speculated that a future Disease X could be created intentionally as a biological weapon . In 2018, WHO R&D Blueprint Special Advisor Group member Røttingen was questioned about the potential of Disease X to come from the ability of gene-editing technology to produce synthetic viruses (e.g., the 2017 synthesis of Orthopoxvirus in Canada was cited), which could be released through an accident or even an act of terror . Røttingen said it was unlikely that a future Disease X would originate from a synthetic virus or a bio-weapon. However, he noted the seriousness of such an event, saying, "Synthetic biology allows for the creation of deadly new viruses. It is also the case that where you have a new disease there is no resistance in the population and that means it can spread fast". In September 2019, Public Health England (PHE) reported that the increasing antibiotic resistance of bacteria, even to "last-resort" antibiotics such as carbapenems and colistin , could also turn into a potential Disease X, citing the antibiotic resistance in gonorrhea as an example. In 2018, the Museum of London ran an exhibition titled "Disease X: London's next epidemic?", hosted for the centenary of the Spanish flu epidemic from 1918. The term features in the title of several fiction books that involve global pandemic diseases, such as Disease (2020), and Disease X: The Outbreak (2019). Disease X has become the subject of several conspiracy theories , claiming that it may be a real disease, or conceived as a biological weapon, or engineered to create a planned epidemic.

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Rift Valley fever

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Biological hazard

A biological hazard , or biohazard , is a biological substance that poses a threat (or is a hazard ) to the health of living organisms , primarily humans. This could include a sample of a microorganism , virus or toxin that can adversely affect human health . A biohazard could also be a substance harmful to other living beings. [lower-alpha 1] The term and its associated symbol are generally used as a warning, so that those potentially exposed to the substances will know to take precautions. The biohazard symbol was developed in 1966 by Charles Baldwin, an environmental-health engineer working for the Dow Chemical Company on their containment products. It is used in the labeling of biological materials that carry a significant health risk, including viral samples and used hypodermic needles . In Unicode , the biohazard symbol is U+2623 ( ☣ ).Biohazardous safety issues are identified with specified labels, [lower-alpha 2] signs and paragraphs established by the American National Standards Institute (ANSI). Today, ANSI Z535 standards for biohazards are used worldwide and should always be used appropriately within ANSI Z535 Hazardous Communications (HazCom) signage, labeling and paragraphs. The goal is to help workers rapidly identify the severity of a biohazard from a distance and through colour and design standardization. [ citation needed ] Biological hazard symbol design: A red on white or white-coloured background is used behind a black biohazard symbol when integrated with a DANGER sign, label or paragraph. An orange on black or white-coloured background is used behind a black biohazard symbol when integrated with a WARNING sign, label or paragraph. A yellow on black or white-coloured background is used behind a black biohazard symbol when integrated with a CAUTION sign, label or paragraph. A green on white or white-coloured background is used behind a black biohazard symbol when integrated with a NOTICE sign, label or paragraph. DANGER is used to identify a biohazard that will cause death. WARNING is used to identify a biohazard that may cause death. CAUTION is used to identify a biohazard that will cause injury, but not death. NOTICE is used to identify a non-injury biohazard message (e.g. hygiene, cleanup or general lab policies). OSHA requires the use of proper ANSI HazCom where applicable in American workplaces. States and local governments also use these standards as codes and laws within their own jurisdictions. Proper use of ANSI Z535 signs, labels and paragraphs are written into many of OSHA's standards for HazCom and crafted to integrate with ISO symbols. Reference ANSI Z535 for a complete description on how to use DANGER, WARNING, CAUTION and NOTICE signs, labels or paragraphs.Biohazardous agents are classified for transportation by UN number : Category A, UN 2814 – Infectious substance, affecting humans: An infectious substance in a form capable of causing permanent disability or life-threatening or fatal disease in otherwise healthy humans or animals when exposure to it occurs. Category A, UN 2900 – Infectious substance, affecting animals (only): An infectious substance that is not in a form generally capable of causing permanent disability or life-threatening or fatal disease in otherwise healthy humans and animals when exposure to themselves occurs. Category B, UN 3373 – Biological substance transported for diagnostic or investigative purposes. Regulated Medical Waste, UN 3291 – Waste or reusable material derived from medical treatment of an animal or human, or from biomedical research, which includes the production and testing. The United States Centers for Disease Control and Prevention (CDC) categorizes various diseases in levels of biohazard, Level 1 being minimum risk and Level 4 being extreme risk. Laboratories and other facilities are categorized as BSL ( Biosafety Level ) 1–4 or as P1 through P4 for short (Pathogen or Protection Level). [ citation needed ]

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Rift Valley fever

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United States biological defense program

The United States Biological Defense Program —in recent years also called the National Biodefense Strategy —refers to the collective effort by all levels of government, along with private enterprise and other stakeholders, in the United States to carry out biodefense activities. Biodefense is a system of planned actions to counter and reduce the risk of biological threats and to prepare, respond to, and recover from them if they happen. The National Defense Authorization Act (NDAA) of 2016 required high-level officials across the federal government to create a national biodefense strategy together. As a result, in 2018 the National Biodefense Strategy was released by President Donald J. Trump. In essence, the strategy comprises the U.S. biological defense program in that it is the official framework that provides a "single coordinated effort" to coordinate all biodefense activities across the federal government. To execute the strategy, the White House issued a Presidential Memorandum on the Support for National Biodefense, which puts the specific directives and rules in place for carrying out the plans written in the strategy. It is worth noting that the National Biodefense Strategy elevated natural outbreaks as a vital component of the U.S. biological defense program for the first time, mostly because of the significant risk that natural outbreaks pose to civilian, animal and agricultural populations across the country. The U.S. Biological Defense Program began as a small defensive effort that parallels the country's offensive biological weapons development and production program , active since 1943. Organizationally, the medical defense research effort was pursued first (1956-1969) by the U.S. Army Medical Unit (USAMU) and later, after publicly known discontinuation of the offensive program, by the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID). Both of these units were located at Fort Detrick , Maryland , where the U.S. Army Biological Warfare Laboratories were headquartered. The current mission is multi-agency, not exclusively military, and is purely to develop defensive measures against bio-agents , as opposed to the former bio-weapons development program. In 1951, due to biological warfare concerns arising from the Korean War , the US Centers for Disease Control and Prevention (CDC) created the Epidemic Intelligence Service (EIS), a hands-on two-year postgraduate training program in epidemiology, with a focus on field work. Since the 2001 anthrax attacks , and the consequent expansion of federal bio-defense expenditures, USAMRIID has been joined at Fort Detrick by sister bio-defense agencies of the U.S. Department of Health and Human Services ( NIAID 's Integrated Research Facility ) and the U.S. Department of Homeland Security (the National Biodefense Analysis and Countermeasures Center and the National Bioforensic Analysis Center ). These—along with the much older Foreign Disease Weed Science Research Unit of the U.S. Department of Agriculture —now constitute the National Interagency Confederation for Biological Research (NICBR). Broadly defined, the "United States Biological Defense Program" now also encompasses all federal-level programs and efforts to monitor, prevent, and contain naturally occurring infectious disease outbreaks of widespread public health concern. These include efforts to forestall large-scale disasters such as flu pandemics and other " emerging infections " such as novel pathogens or those imported from other countries.Biological agents have been used in warfare for centuries to produce death or disease in humans, animals, or plants. The United States officially began its biological warfare offensive program in 1941. During the next 28 years, the U.S. initiative evolved into an effective, military-driven research and acquisition program, shrouded in secrecy and, later, controversy. Most research and development was done at Fort Detrick , Maryland , while production and testing of bio-weapons occurred at Pine Bluff, Arkansas , and Dugway Proving Ground (DPG), Utah . Field testing was done secretly and successfully with simulants and actual agents disseminated over wide areas. A small defensive effort always paralleled the weapons development and production program. With the presidential decision in 1969 to halt offensive biological weapons production—and the agreement in 1972 at the international BWC never to develop, produce, stockpile, or retain biological agents or toxins—the program became entirely defensive, with medical and non-medical components. The U.S. biological defense research program exists today, conducting research to develop physical and medical countermeasures to protect service members and civilians from the threat of modern biological warfare. Both the U.S. bio-weapons ban and the BWC restricted any work in the area of biological warfare to defensive in nature. In reality, this gives BWC member-states wide latitude to conduct biological weapons research because the BWC contains no provisions for monitoring of enforcement. The treaty, essentially, is a gentlemen's agreement amongst members backed by the long-prevailing thought that biological warfare should not be used in battle. In recent years certain critics have claimed the U.S. stance on biological warfare and the use of biological agents has differed from historical interpretations of the BWC. For example, it is said that the U.S. now maintains that the Article I of the BWC (which explicitly bans bio-weapons), does not apply to "non-lethal" biological agents. Previous interpretation was stated to be in line with a definition laid out in Public Law 101-298, the Biological Weapons Anti-Terrorism Act of 1989 . That law defined a biological agent as: any micro-organism, virus, infectious substance, or biological product that may be engineered as a result of biotechnology, or any naturally occurring or bio-engineered component of any such microorganism, virus, infectious substance, or biological product, capable of causing death, disease, or other biological malfunction in a human, an animal, a plant, or another living organism; deterioration of food, water, equipment, supplies, or material of any kind ... According to the Federation of American Scientists , U.S. work on non-lethal agents exceeds limitations in the BWC. After World War II , and with the onset of Cold War tensions, the US continued its clandestine wartime bio-weapons program. The Korean War (1950–53) added justification for continuing the program, when the possible entry of the Soviet Union into the war was feared. Concerns over the Soviet Union were justified, for the Soviet Union would pronounce in 1956 that chemical and biological weapons would, indeed, be used for mass destruction in future wars. In October 1950, the US Secretary of Defense approved continuation of the program, based largely on the Soviet threat and a belief that the North Korean and Chinese communists would use biological weapons. With expansion of the biological warfare retaliatory program, the scope of the defensive program was nearly doubled. Data were obtained on personnel protection, decontamination, and immunization. Early detection research produced prototype alarms for use on the battlefield, but progress was slow, apparently limited by technology. The U.S. Army Medical Unit, under the direction of The U.S. Army Surgeon General, began formal operations in 1956. One of the Unit's first missions was to manage all aspects of Project CD-22, the exposure of volunteers to aerosols containing a pathogenic strain of Coxiella burnetii , the etiologic agent of Q fever . The volunteers were closely monitored and antibiotic therapy was administered when appropriate. All volunteers recovered from Q fever with no adverse aftereffects. One year later, the Unit submitted to the U.S. Food and Drug Administration an Investigational New Drug application for a Q fever vaccine. In the following decade, the US accumulated significant data on personnel protection, decontamination, and immunization; and, in the offensive program, on the potential for mosquitoes to be used as biological vectors. A new Department of Defense (DoD) Biological and Chemical Defense Planning Board was created in 1960 to establish program priorities and objectives. Preventive approaches toward infections of all kinds were funded under the auspices of biological warfare. As concern increased over the biological warfare threat during the Cold War, so did the budget for the program: to $38 million by fiscal year 1966. The U.S. Army Chemical Corps was given the responsibility to conduct biological warfare research for all of the services. In 1962, the responsibility for the testing of promising biological warfare agents was given to a separate Testing and Evaluation Command (TEC). Depending on the particular program, different test centers were used, such as the Deseret Test Center at Fort Douglas, Utah , the headquarters for the new biological and chemical warfare testing organization. In response to increasing concerns over public safety and the environment, the TEC implemented a complex system of approval of its research programs that included the U.S. Army Chief of Staff , the Joint Chiefs of Staff , the Secretary of Defense, and the President of the United States. During the last 10 years of the offensive research and development program (1959–69), many scientific advances were made that proved that biological warfare was clearly feasible, although dependent on careful planning, especially with regard to meteorological conditions. Large-scale fermentation, purification, concentration, stabilization, drying, and weaponization of pathogenic microorganisms could be done safely. Furthermore, modern principles of biosafety and containment were established at the Fort Detrick laboratories which have greatly facilitated biomedical research in general; still today, these are followed throughout the world. Arnold G. Wedum , M.D., Ph.D., a civilian scientist who was Director of Industrial Health and Safety at Fort Detrick, was the leader in the development of containment facilities. During the 1960s, the US program underwent a philosophical change, and attention was now directed more towards biological agents that could incapacitate, but not kill. In 1964, research programs involved staphylococcal enterotoxins capable of causing food poisoning . Research initiatives also included new therapy and prophylaxis. Pathogens studied included the agents causing anthrax , glanders , brucellosis , melioidosis , plague , psittacosis , Venezuelan equine encephalitis , Q fever , coccidioidomycosis , and a variety of plant and animal pathogens Particular attention was directed at chemical and biological detectors during the 1960s. The first devices were primitive field alarms to detect chemicals. Although the development of sensitive biological warfare agent detectors was at a standstill, two systems were, nonetheless, investigated. The first was a monitor that detected increases in the number of particles sized 1 to 5 µm in diameter, based on the assumption that a biological agent attack would include airborne particles of this size. The second system involved the selective staining of particles collected from the air. Both systems lacked enough specificity and sensitivity to be of any practical use. But in 1966, a research effort directed at detecting the presence of adenosine triphosphate (a chemical found only in living organisms) was begun. By using a fluorescent material found in fireflies , preliminary studies indicated that it was possible to detect the presence of a biological agent in the atmosphere. The important effort to find a satisfactory detection system continues today, for timely detection of a biological attack would allow the attacked force to use its protective masks effectively, and identification of the agent would allow any pre-treatment regimens to be instituted. The US Army also experimented with and developed highly effective barrier protective measures against both chemical and biological agents. Special impervious tents and personal protective equipment were developed, including individual gas masks even for military dogs. During the late 1960s, funding for the biological warfare program decreased temporarily, to accommodate the accelerating costs of the Vietnam War . The budget for fiscal year 1969 was $31 million, decreasing to $11.8 million by fiscal year 1973. Although the offensive program had been stopped in 1969, both offensive and defensive programs continued to be defended. John S. Foster, Jr , Director of Defense Research and Engineering, responded to a query by Congressman Richard D. McCarthy : It is the policy of the U.S. to develop and maintain a defensive chemical-biological (CB) capability so that our military forces could operate for some period of time in a toxic environment, if necessary; to develop and maintain a limited offensive capability in order to deter all use of CB weapons by the threat of retaliation in kind; and to continue a program of research and development in this area to minimize the possibility of technological surprise. On 25 November 1969, President Richard Nixon visited Fort Detrick to announce a new policy on biological warfare. In two National Security Memoranda, the U.S. government renounced all development, production, and stockpiling of biological weapons and declared its intent to maintain only small research quantities of biological agents, such as are necessary for the development of vaccines, drugs, and diagnostics. Ground was broken in 1967 for the construction of a new, modern laboratory building at Fort Detrick. The building would open in phases during 1971 and 1972. With the disestablishment of the biological warfare laboratories, the name of the U.S. Army Medical Unit, which was to have been housed in the new laboratories, was formally changed to U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) in 1969. The institute's new mission was stated in General Order 137, 10 November 1971 (since superseded): Conducts studies related to medical defensive aspects of biological agents of military importance and develops appropriate biological protective measures, diagnostic procedures and therapeutic methods. The emphasis now shifted away from offensive weapons to the development of vaccines, diagnostic systems, personal protection, chemoprophylaxis, and rapid detection systems. After Nixon declared an end to the U.S. bio-weapons program, debate in the Army centered around whether or not toxin weapons were included in the president's declaration. Following Nixon's November 1969 order, scientists at Fort Detrick worked on one toxin, Staphylococcus enterotoxin type B (SEB), for several more months. Nixon ended the debate when he added toxins to the bio-weapons ban in February 1970 In response to Nixon's 1969 decision, all antipersonnel biological warfare stocks were destroyed between 10 May 1971 and 1 May 1972. The laboratory at Pine Bluff Arsenal, Arkansas, was converted to a toxicological research laboratory, and was no longer under the direction or control of the DoD. Biological anticrop agents were destroyed by February 1973. Biological warfare demilitarization continued through the 1970s, with input provided by the U.S. Department of Health, Education and Welfare ; U.S. Department of the Interior ; U.S. Department of Agriculture ; and the Environmental Protection Agency . Fort Detrick and other installations involved in the biological warfare program took on new identities, and their missions were changed to biological defense and the development of medical countermeasures. The necessary containment capability, Biosafety Levels 3 and 4 (BSL-3 and BSL-4) continued to be maintained at USAMRIID. In 1984, the DoD requested funds for the construction of another biological aerosol test facility in Utah. The proposal submitted by the army called for BSL-4 containment, although maintaining that the BSL-4 inclusion was based on a possible need in the future and not on a current research effort. The proposal was not well received in Utah, where many citizens and government officials still recalled the secretive projects of the military: the areas on DPG still contaminated with anthrax spores, and the well-publicized accidental chemical poisoning of a flock of sheep in Skull Valley, Utah , in March 1968. Questions arose over the safety of the employees and the surrounding communities, and a suggestion was even made to shift all biological defense research to a civilian agency, such as the National Institutes of Health . The plan for a new facility was revised to utilize a BSL-3 facility, but not before the US Congress had instituted more surveillance, reporting, and control measures on the army to ensure compliance with the BWC. In the 1990s, the US medical biological defense research effort (part of the U.S. Army's Biological Defense Research Program [BDRP]) was concentrated at USAMRIID at Fort Detrick. The army maintained state-of-the-art containment laboratory facilities there, with more than 10,000 ft2 of BSL-4 and 50,000 ft2 of BSL-3 laboratory space. BSL-4, the highest containment level, included laboratory suites that are isolated by internal walls and protected by rigorous entry restrictions, air-locks, negative-pressure air-handling systems, and filtration of all out-flow air through high-efficiency particulate air (HEPA) filters. Workers in BSL-4 laboratories also wore filtered positive-pressure total body suits , which isolated the workers from the internal air of the laboratory. BSL-3 laboratories had a similar design, but do not require that personnel wear positive-pressure suits. Workers in BSL-3 suites were protected immunologically by vaccines. U.S. governmental standards provided guidance as to which organisms might be handled under various containment levels in laboratories such as USAMRIID. The unique facilities available at USAMRIID also included a 16-bed clinical research ward capable of BSL-3 containment, and a 2-bed patient care isolation suite—the Medical Containment Suite (MCS), known as "The Slammer"—where ICU-level care could be provided under BSL-4 containment. Here, healthcare personnel wore the same positive-pressure suits as are worn in BSL-4 research laboratories. The level of patient isolation required depended on the infecting organism and the risk to healthcare providers. Patient care can be provided at BSL-4. There were no patient-care category analogous to BSL-3; humans who are ill as a result of exposure to BSL-3 agents were to be cared for in an ordinary hospital room with barrier nursing procedures. USAMRIID guidelines were prepared to determine which level of containment would be employed for individual patients who required BSL-4 isolation or barrier nursing care. Staff augmentation for BSL-4 critical care expertise came from the Walter Reed Army Medical Center (WRAMC), Washington, D.C., in accordance with a memorandum of agreement between the two institutions. Patients could be brought directly into the BSL-4 suite from the outside through specialized ports with unique patient-isolation equipment. (The MCS was decommissioned and discontinued in December 2010.) Additionally, starting in the 1970s USAMRIID maintained a unique evacuation capability known as the Aeromedical Isolation Team (AIT). Led by a physician and a registered nurse, each of the two teams consisted of eight volunteers who trained intensively to provide an evacuation capability for casualties suspected of being infected with highly transmissible, life-threatening BSL-4 infectious diseases (e.g., hemorrhagic fever viruses). The unit used special adult-sized Vickers isolation units (Vickers Medical Containment Stretcher Transit Isolator). These units were aircraft transportable and isolated a patient placed inside from the external environment. The AIT could transport two patients simultaneously; obviously, this was not designed for a mass casualty situation. During the 1995 outbreak of Ebola fever in Zaire , the AIT remained on alert to evacuate any US citizens who might have become ill while working to control the disease in that country. During this period, some biological defense research also continued at the U.S. Army Medical Research Institute of Chemical Defense , Edgewood Arsenal , Maryland, and the Walter Reed Army Institute of Research (WRAIR), Washington, D.C. USAMRIID and these sister laboratories conducted basic research in support of the medical component of the US biological defense research program, which developed strategies, products, information, procedures, and training for medical defense against biological warfare agents. The products included diagnostic reagents and procedures, drugs, vaccines, toxoids, and antitoxins. Emphasis is placed on protecting personnel before any potential exposure to the biological agent occurs. In 1997, United States law formally defined weaponizable bio-agents as "Biological Select Agents or Toxins" (BSATs) — or simply Select Agents for short — which fall under the oversight of either the U.S. Department of Health and Human Services or the U.S. Department of Agriculture (or both) and which have the "potential to pose a severe threat to public health and safety". In 1998, several DoD organizations consolidated to create the Defense Threat Reduction Agency (DTRA), headquartered in Fort Belvoir, Virginia . This agency is DOD's official Combat Support Agency for countering weapons of mass destruction , including bio-agents. DTRA's main functions are threat reduction, threat control, combat support, and technology development. In the US national interest, DTRA supports projects at more than 14 locations around the world, including Russia, Kazakhstan, Azerbaijan, Uzbekistan, Georgia, and Ukraine. In 1999, a "National Pharmaceutical Stockpile" — renamed Strategic National Stockpile in 2002 — was created under the oversight of DHHS. In the same year, the Laboratory Response Network — a collaborative effort within the US federal government involving the Association of Public Health Laboratories and the Centers for Disease Control and Prevention — was established to facilitate the confirmatory diagnosis and typing of possible bio-agents. Also in 1999, President Bill Clinton issued Executive Order 13139 , which provided for experimental anti-WMD drugs to be given to service members at the discretion of the Secretary of Defense only under informed consent ; only the President may waive the necessity for informed consent. Three secret DoD projects involving countermeasures against anthrax – code named Project Bacchus , Project Clear Vision and Project Jefferson – were publicly disclosed by The New York Times in 2001. (The projects were undertaken between 1997 and 2000 and focused on the concern that the old Soviet BW program was secretly continuing and had developed a genetically modified anthrax weapon.) Since the September 11 attacks and the 2001 anthrax attacks , the US government has allocated nearly $50 billion to address the threat of biological weapons. Funding for bioweapons-related activities focuses primarily on research for and acquisition of medicines for defense. Biodefense funding also goes toward stockpiling protective equipment, increased surveillance and detection of bio-agents, and improving state and hospital preparedness. Significant funding goes to BARDA ( Biomedical Advanced Research and Development Authority ), part of DHHS. Funding for activities aimed at prevention has more than doubled since 2007 and is distributed among 11 federal agencies. Efforts toward cooperative international action are part of the project. A "Select Agent Program" (SAP) was established to satisfy requirements of the USA PATRIOT Act of 2001 and the Public Health Security and Bioterrorism Preparedness and Response Act of 2002 . The Centers for Disease Control and Prevention administers the SAP, which regulates the laboratories that may possess, use, or transfer Select Agents within the United States. The Project Bioshield Act was passed by Congress in 2004 calling for $5 billion for purchasing vaccines that would be used in the event of a bioterrorist attack. According to President George W. Bush : Project BioShield will transform our ability to defend the nation in three essential ways. First, Project BioShield authorizes $5.6 billion over 10 years for the government to purchase and stockpile vaccines and drugs to fight anthrax, smallpox and other potential agents of bioterror. The DHHS has already taken steps to purchase 75 million doses of an improved anthrax vaccine for the Strategic National Stockpile . Under Project BioShield, HHS is moving forward with plans to acquire a safer, second generation smallpox vaccine, an antidote to botulinum toxin, and better treatments for exposure to chemical and radiological weapons. This was a ten-year program to acquire medical countermeasures to biological, chemical, radiological and nuclear agents for civilian use. A key element of the Act was to allow stockpiling and distribution of vaccines that had not been tested for safety or efficacy in humans , due to ethical concerns. Efficacy of these agents cannot be directly tested in humans without also exposing humans to the chemical, biological, or radioactive threat being treated. In these cases efficacy testing follows the US Food and Drug Administration Animal Rule for pivotal animal efficacy. Since 2007, USAMRIID has been joined at Fort Detrick by sister bio-defense agencies of the U.S. Department of Health and Human Services (NIAID's Integrated Research Facility) and the U.S. Department of Homeland Security (the National Biodefense Analysis and Countermeasures Center and the National Bioforensic Analysis Center ). These—along with the much older Foreign Disease Weed Science Research Unit of the U.S. Department of Agriculture—now constitute the National Interagency Confederation for Biological Research (NICBR). In July 2012, the White House issued its guiding document on the National Biosurveillance Strategy . In December 2019, Congress moved forward with a spending package that provided increases for several key U.S. biological defense programs, including the Strategic National Stockpile. The Centers for Disease Control and Prevention was slated to receive $8 billion, a $636 million increase over 2019, with a mandate written in the bill for CDC "to maintain a strong and central role in the medical countermeasures enterprise." Within the CDC budget, the Public Health and Social Services Emergency Fund , which prepares for "all public health emergencies" including bioterrorism and federal efforts against infectious diseases, was funded at $2.74 billion. Another change was a specific item in the budget for the Strategic National Stockpile, which directed $535 million for vaccines, medicines and diagnostic tools to fight Ebola, which has become an emerging threat. After World War II , and with the onset of Cold War tensions, the US continued its clandestine wartime bio-weapons program. The Korean War (1950–53) added justification for continuing the program, when the possible entry of the Soviet Union into the war was feared. Concerns over the Soviet Union were justified, for the Soviet Union would pronounce in 1956 that chemical and biological weapons would, indeed, be used for mass destruction in future wars. In October 1950, the US Secretary of Defense approved continuation of the program, based largely on the Soviet threat and a belief that the North Korean and Chinese communists would use biological weapons. With expansion of the biological warfare retaliatory program, the scope of the defensive program was nearly doubled. Data were obtained on personnel protection, decontamination, and immunization. Early detection research produced prototype alarms for use on the battlefield, but progress was slow, apparently limited by technology. The U.S. Army Medical Unit, under the direction of The U.S. Army Surgeon General, began formal operations in 1956. One of the Unit's first missions was to manage all aspects of Project CD-22, the exposure of volunteers to aerosols containing a pathogenic strain of Coxiella burnetii , the etiologic agent of Q fever . The volunteers were closely monitored and antibiotic therapy was administered when appropriate. All volunteers recovered from Q fever with no adverse aftereffects. One year later, the Unit submitted to the U.S. Food and Drug Administration an Investigational New Drug application for a Q fever vaccine.In the following decade, the US accumulated significant data on personnel protection, decontamination, and immunization; and, in the offensive program, on the potential for mosquitoes to be used as biological vectors. A new Department of Defense (DoD) Biological and Chemical Defense Planning Board was created in 1960 to establish program priorities and objectives. Preventive approaches toward infections of all kinds were funded under the auspices of biological warfare. As concern increased over the biological warfare threat during the Cold War, so did the budget for the program: to $38 million by fiscal year 1966. The U.S. Army Chemical Corps was given the responsibility to conduct biological warfare research for all of the services. In 1962, the responsibility for the testing of promising biological warfare agents was given to a separate Testing and Evaluation Command (TEC). Depending on the particular program, different test centers were used, such as the Deseret Test Center at Fort Douglas, Utah , the headquarters for the new biological and chemical warfare testing organization. In response to increasing concerns over public safety and the environment, the TEC implemented a complex system of approval of its research programs that included the U.S. Army Chief of Staff , the Joint Chiefs of Staff , the Secretary of Defense, and the President of the United States. During the last 10 years of the offensive research and development program (1959–69), many scientific advances were made that proved that biological warfare was clearly feasible, although dependent on careful planning, especially with regard to meteorological conditions. Large-scale fermentation, purification, concentration, stabilization, drying, and weaponization of pathogenic microorganisms could be done safely. Furthermore, modern principles of biosafety and containment were established at the Fort Detrick laboratories which have greatly facilitated biomedical research in general; still today, these are followed throughout the world. Arnold G. Wedum , M.D., Ph.D., a civilian scientist who was Director of Industrial Health and Safety at Fort Detrick, was the leader in the development of containment facilities. During the 1960s, the US program underwent a philosophical change, and attention was now directed more towards biological agents that could incapacitate, but not kill. In 1964, research programs involved staphylococcal enterotoxins capable of causing food poisoning . Research initiatives also included new therapy and prophylaxis. Pathogens studied included the agents causing anthrax , glanders , brucellosis , melioidosis , plague , psittacosis , Venezuelan equine encephalitis , Q fever , coccidioidomycosis , and a variety of plant and animal pathogens Particular attention was directed at chemical and biological detectors during the 1960s. The first devices were primitive field alarms to detect chemicals. Although the development of sensitive biological warfare agent detectors was at a standstill, two systems were, nonetheless, investigated. The first was a monitor that detected increases in the number of particles sized 1 to 5 µm in diameter, based on the assumption that a biological agent attack would include airborne particles of this size. The second system involved the selective staining of particles collected from the air. Both systems lacked enough specificity and sensitivity to be of any practical use. But in 1966, a research effort directed at detecting the presence of adenosine triphosphate (a chemical found only in living organisms) was begun. By using a fluorescent material found in fireflies , preliminary studies indicated that it was possible to detect the presence of a biological agent in the atmosphere. The important effort to find a satisfactory detection system continues today, for timely detection of a biological attack would allow the attacked force to use its protective masks effectively, and identification of the agent would allow any pre-treatment regimens to be instituted. The US Army also experimented with and developed highly effective barrier protective measures against both chemical and biological agents. Special impervious tents and personal protective equipment were developed, including individual gas masks even for military dogs. During the late 1960s, funding for the biological warfare program decreased temporarily, to accommodate the accelerating costs of the Vietnam War . The budget for fiscal year 1969 was $31 million, decreasing to $11.8 million by fiscal year 1973. Although the offensive program had been stopped in 1969, both offensive and defensive programs continued to be defended. John S. Foster, Jr , Director of Defense Research and Engineering, responded to a query by Congressman Richard D. McCarthy : It is the policy of the U.S. to develop and maintain a defensive chemical-biological (CB) capability so that our military forces could operate for some period of time in a toxic environment, if necessary; to develop and maintain a limited offensive capability in order to deter all use of CB weapons by the threat of retaliation in kind; and to continue a program of research and development in this area to minimize the possibility of technological surprise. On 25 November 1969, President Richard Nixon visited Fort Detrick to announce a new policy on biological warfare. In two National Security Memoranda, the U.S. government renounced all development, production, and stockpiling of biological weapons and declared its intent to maintain only small research quantities of biological agents, such as are necessary for the development of vaccines, drugs, and diagnostics. Ground was broken in 1967 for the construction of a new, modern laboratory building at Fort Detrick. The building would open in phases during 1971 and 1972. With the disestablishment of the biological warfare laboratories, the name of the U.S. Army Medical Unit, which was to have been housed in the new laboratories, was formally changed to U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) in 1969. The institute's new mission was stated in General Order 137, 10 November 1971 (since superseded): Conducts studies related to medical defensive aspects of biological agents of military importance and develops appropriate biological protective measures, diagnostic procedures and therapeutic methods. The emphasis now shifted away from offensive weapons to the development of vaccines, diagnostic systems, personal protection, chemoprophylaxis, and rapid detection systems.After Nixon declared an end to the U.S. bio-weapons program, debate in the Army centered around whether or not toxin weapons were included in the president's declaration. Following Nixon's November 1969 order, scientists at Fort Detrick worked on one toxin, Staphylococcus enterotoxin type B (SEB), for several more months. Nixon ended the debate when he added toxins to the bio-weapons ban in February 1970 In response to Nixon's 1969 decision, all antipersonnel biological warfare stocks were destroyed between 10 May 1971 and 1 May 1972. The laboratory at Pine Bluff Arsenal, Arkansas, was converted to a toxicological research laboratory, and was no longer under the direction or control of the DoD. Biological anticrop agents were destroyed by February 1973. Biological warfare demilitarization continued through the 1970s, with input provided by the U.S. Department of Health, Education and Welfare ; U.S. Department of the Interior ; U.S. Department of Agriculture ; and the Environmental Protection Agency . Fort Detrick and other installations involved in the biological warfare program took on new identities, and their missions were changed to biological defense and the development of medical countermeasures. The necessary containment capability, Biosafety Levels 3 and 4 (BSL-3 and BSL-4) continued to be maintained at USAMRIID. In 1984, the DoD requested funds for the construction of another biological aerosol test facility in Utah. The proposal submitted by the army called for BSL-4 containment, although maintaining that the BSL-4 inclusion was based on a possible need in the future and not on a current research effort. The proposal was not well received in Utah, where many citizens and government officials still recalled the secretive projects of the military: the areas on DPG still contaminated with anthrax spores, and the well-publicized accidental chemical poisoning of a flock of sheep in Skull Valley, Utah , in March 1968. Questions arose over the safety of the employees and the surrounding communities, and a suggestion was even made to shift all biological defense research to a civilian agency, such as the National Institutes of Health . The plan for a new facility was revised to utilize a BSL-3 facility, but not before the US Congress had instituted more surveillance, reporting, and control measures on the army to ensure compliance with the BWC. In the 1990s, the US medical biological defense research effort (part of the U.S. Army's Biological Defense Research Program [BDRP]) was concentrated at USAMRIID at Fort Detrick. The army maintained state-of-the-art containment laboratory facilities there, with more than 10,000 ft2 of BSL-4 and 50,000 ft2 of BSL-3 laboratory space. BSL-4, the highest containment level, included laboratory suites that are isolated by internal walls and protected by rigorous entry restrictions, air-locks, negative-pressure air-handling systems, and filtration of all out-flow air through high-efficiency particulate air (HEPA) filters. Workers in BSL-4 laboratories also wore filtered positive-pressure total body suits , which isolated the workers from the internal air of the laboratory. BSL-3 laboratories had a similar design, but do not require that personnel wear positive-pressure suits. Workers in BSL-3 suites were protected immunologically by vaccines. U.S. governmental standards provided guidance as to which organisms might be handled under various containment levels in laboratories such as USAMRIID. The unique facilities available at USAMRIID also included a 16-bed clinical research ward capable of BSL-3 containment, and a 2-bed patient care isolation suite—the Medical Containment Suite (MCS), known as "The Slammer"—where ICU-level care could be provided under BSL-4 containment. Here, healthcare personnel wore the same positive-pressure suits as are worn in BSL-4 research laboratories. The level of patient isolation required depended on the infecting organism and the risk to healthcare providers. Patient care can be provided at BSL-4. There were no patient-care category analogous to BSL-3; humans who are ill as a result of exposure to BSL-3 agents were to be cared for in an ordinary hospital room with barrier nursing procedures. USAMRIID guidelines were prepared to determine which level of containment would be employed for individual patients who required BSL-4 isolation or barrier nursing care. Staff augmentation for BSL-4 critical care expertise came from the Walter Reed Army Medical Center (WRAMC), Washington, D.C., in accordance with a memorandum of agreement between the two institutions. Patients could be brought directly into the BSL-4 suite from the outside through specialized ports with unique patient-isolation equipment. (The MCS was decommissioned and discontinued in December 2010.) Additionally, starting in the 1970s USAMRIID maintained a unique evacuation capability known as the Aeromedical Isolation Team (AIT). Led by a physician and a registered nurse, each of the two teams consisted of eight volunteers who trained intensively to provide an evacuation capability for casualties suspected of being infected with highly transmissible, life-threatening BSL-4 infectious diseases (e.g., hemorrhagic fever viruses). The unit used special adult-sized Vickers isolation units (Vickers Medical Containment Stretcher Transit Isolator). These units were aircraft transportable and isolated a patient placed inside from the external environment. The AIT could transport two patients simultaneously; obviously, this was not designed for a mass casualty situation. During the 1995 outbreak of Ebola fever in Zaire , the AIT remained on alert to evacuate any US citizens who might have become ill while working to control the disease in that country. During this period, some biological defense research also continued at the U.S. Army Medical Research Institute of Chemical Defense , Edgewood Arsenal , Maryland, and the Walter Reed Army Institute of Research (WRAIR), Washington, D.C. USAMRIID and these sister laboratories conducted basic research in support of the medical component of the US biological defense research program, which developed strategies, products, information, procedures, and training for medical defense against biological warfare agents. The products included diagnostic reagents and procedures, drugs, vaccines, toxoids, and antitoxins. Emphasis is placed on protecting personnel before any potential exposure to the biological agent occurs. In 1997, United States law formally defined weaponizable bio-agents as "Biological Select Agents or Toxins" (BSATs) — or simply Select Agents for short — which fall under the oversight of either the U.S. Department of Health and Human Services or the U.S. Department of Agriculture (or both) and which have the "potential to pose a severe threat to public health and safety". In 1998, several DoD organizations consolidated to create the Defense Threat Reduction Agency (DTRA), headquartered in Fort Belvoir, Virginia . This agency is DOD's official Combat Support Agency for countering weapons of mass destruction , including bio-agents. DTRA's main functions are threat reduction, threat control, combat support, and technology development. In the US national interest, DTRA supports projects at more than 14 locations around the world, including Russia, Kazakhstan, Azerbaijan, Uzbekistan, Georgia, and Ukraine. In 1999, a "National Pharmaceutical Stockpile" — renamed Strategic National Stockpile in 2002 — was created under the oversight of DHHS. In the same year, the Laboratory Response Network — a collaborative effort within the US federal government involving the Association of Public Health Laboratories and the Centers for Disease Control and Prevention — was established to facilitate the confirmatory diagnosis and typing of possible bio-agents. Also in 1999, President Bill Clinton issued Executive Order 13139 , which provided for experimental anti-WMD drugs to be given to service members at the discretion of the Secretary of Defense only under informed consent ; only the President may waive the necessity for informed consent.Three secret DoD projects involving countermeasures against anthrax – code named Project Bacchus , Project Clear Vision and Project Jefferson – were publicly disclosed by The New York Times in 2001. (The projects were undertaken between 1997 and 2000 and focused on the concern that the old Soviet BW program was secretly continuing and had developed a genetically modified anthrax weapon.) Since the September 11 attacks and the 2001 anthrax attacks , the US government has allocated nearly $50 billion to address the threat of biological weapons. Funding for bioweapons-related activities focuses primarily on research for and acquisition of medicines for defense. Biodefense funding also goes toward stockpiling protective equipment, increased surveillance and detection of bio-agents, and improving state and hospital preparedness. Significant funding goes to BARDA ( Biomedical Advanced Research and Development Authority ), part of DHHS. Funding for activities aimed at prevention has more than doubled since 2007 and is distributed among 11 federal agencies. Efforts toward cooperative international action are part of the project. A "Select Agent Program" (SAP) was established to satisfy requirements of the USA PATRIOT Act of 2001 and the Public Health Security and Bioterrorism Preparedness and Response Act of 2002 . The Centers for Disease Control and Prevention administers the SAP, which regulates the laboratories that may possess, use, or transfer Select Agents within the United States. The Project Bioshield Act was passed by Congress in 2004 calling for $5 billion for purchasing vaccines that would be used in the event of a bioterrorist attack. According to President George W. Bush : Project BioShield will transform our ability to defend the nation in three essential ways. First, Project BioShield authorizes $5.6 billion over 10 years for the government to purchase and stockpile vaccines and drugs to fight anthrax, smallpox and other potential agents of bioterror. The DHHS has already taken steps to purchase 75 million doses of an improved anthrax vaccine for the Strategic National Stockpile . Under Project BioShield, HHS is moving forward with plans to acquire a safer, second generation smallpox vaccine, an antidote to botulinum toxin, and better treatments for exposure to chemical and radiological weapons. This was a ten-year program to acquire medical countermeasures to biological, chemical, radiological and nuclear agents for civilian use. A key element of the Act was to allow stockpiling and distribution of vaccines that had not been tested for safety or efficacy in humans , due to ethical concerns. Efficacy of these agents cannot be directly tested in humans without also exposing humans to the chemical, biological, or radioactive threat being treated. In these cases efficacy testing follows the US Food and Drug Administration Animal Rule for pivotal animal efficacy. Since 2007, USAMRIID has been joined at Fort Detrick by sister bio-defense agencies of the U.S. Department of Health and Human Services (NIAID's Integrated Research Facility) and the U.S. Department of Homeland Security (the National Biodefense Analysis and Countermeasures Center and the National Bioforensic Analysis Center ). These—along with the much older Foreign Disease Weed Science Research Unit of the U.S. Department of Agriculture—now constitute the National Interagency Confederation for Biological Research (NICBR).In July 2012, the White House issued its guiding document on the National Biosurveillance Strategy .In December 2019, Congress moved forward with a spending package that provided increases for several key U.S. biological defense programs, including the Strategic National Stockpile. The Centers for Disease Control and Prevention was slated to receive $8 billion, a $636 million increase over 2019, with a mandate written in the bill for CDC "to maintain a strong and central role in the medical countermeasures enterprise." Within the CDC budget, the Public Health and Social Services Emergency Fund , which prepares for "all public health emergencies" including bioterrorism and federal efforts against infectious diseases, was funded at $2.74 billion. Another change was a specific item in the budget for the Strategic National Stockpile, which directed $535 million for vaccines, medicines and diagnostic tools to fight Ebola, which has become an emerging threat. In August 2019, the U.S. Government Accountability Office (GAO) issued a report that identified specific challenges that the United States faces in protecting the nation against biological events. The report focused on four specific vulnerabilities: assessment of "enterprise-wide threats", situational awareness and data integration, biodetection technologies, and lab safety and security. Products currently being produced or under development through military research include: Some vaccines also have applicability for diseases of domestic animals (e.g., Rift Valley fever and Venezuelan equine encephalitis). In addition, vaccines are provided to persons who may be occupationally exposed to such agents (e.g., laboratory workers, entomologists , and veterinary personnel) throughout government, industry, and academe. USAMRIID also provides diagnostic and epidemiological support to federal, state, and local agencies and foreign governments. Examples of assistance rendered to civilian health efforts by the U.S. Army Medical Research and Materiel Command (USAMRMC) include: The current [ when? ] research effort combines new technological advances, such as genetic engineering and molecular modeling , applying them toward development of prevention and treatment of diseases of military significance. The program is conducted in compliance with requirements set forth by the U.S. Food and Drug Administration (FDA), U.S. Public Health Service , Nuclear Regulatory Commission , U.S. Department of Agriculture , Occupational Safety and Health Administration , and Biological Weapons Convention .

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Rift Valley fever

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Madras Red sheep

Sheep Ovis aries The Madras Red Sheep is an indigenous breed of sheep native to the northeastern parts of Tamil Nadu . The breed is characterized by medium size, reddish brown in colour with white markings on the leg and forehead. They are hardy and drought tolerant. Males are horned and ewes are polled. Wattles are found in about 73% females and 69% males. They feed on grass and a variety of tree leaves including those of Albizzia , Ficus , Leucaena , Gliricidia , Erythrina , Inga dulce and Thespesia . The breed is maintained mostly for meat and is one of five hairy breeds from Tamil Nadu. The breed has been traditionally developed and maintained in the Kancheepuram and Thiruvallur district by Naicker and Pillai communities. In an outbreak of sheep pox there was a mortality of up to 10% among adults, while the mortality was about 37% in adults of Mechery sheep. A virus similar to that causing Rift Valley Fever has also been noted to affect the sheep in an outbreak 1994. They breed during July to September.

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Rift Valley fever

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Biosafety level

A biosafety level ( BSL ), or pathogen/protection level , is a set of biocontainment precautions required to isolate dangerous biological agents in an enclosed laboratory facility. The levels of containment range from the lowest biosafety level 1 (BSL-1) to the highest at level 4 (BSL-4). In the United States, the Centers for Disease Control and Prevention (CDC) have specified these levels in a publication referred to as BMBL. In the European Union , the same biosafety levels are defined in a directive . In Canada the four levels are known as Containment Levels. Facilities with these designations are also sometimes given as P1 through P4 (for pathogen or protection level), as in the term P3 laboratory . At the lowest level of biosafety, precautions may consist of regular hand-washing and minimal protective equipment. At higher biosafety levels, precautions may include airflow systems, multiple containment rooms, sealed containers, positive pressure personnel suits , established protocols for all procedures, extensive personnel training, and high levels of security to control access to the facility. Health Canada reports that world-wide until 1999 there were recorded over 5,000 cases of accidental laboratory infections and 190 deaths. The first prototype Class III (maximum containment) biosafety cabinet was fashioned in 1943 by Hubert Kaempf Jr., then a U.S. Army soldier, under the direction of Arnold G. Wedum, Director (1944–1969) of Industrial Health and Safety at the United States Army Biological Warfare Laboratories , Camp Detrick , Maryland . Kaempf was tired of his MP duties at Detrick and was able to transfer to the sheet metal department working with the contractor, the H.K. Ferguson Co. On 18 April 1955, fourteen representatives met at Camp Detrick in Frederick, Maryland. The meeting was to share knowledge and experiences regarding biosafety , chemical, radiological, and industrial safety issues that were common to the operations at the three principal biological warfare (BW) laboratories of the U.S. Army. Because of the potential implication of the work conducted at biological warfare laboratories, the conferences were restricted to top level security clearances . Beginning in 1957, these conferences were planned to include non-classified sessions as well as classified sessions to enable broader sharing of biological safety information. It was not until 1964, however, that conferences were held in a government installation not associated with a biological warfare program. Over the next ten years, the biological safety conferences grew to include representatives from all federal agencies that sponsored or conducted research with pathogenic microorganisms. By 1966, it began to include representatives from universities, private laboratories, hospitals, and industrial complexes. Throughout the 1970s, participation in the conferences continued to expand and by 1983 discussions began regarding the creation of a formal organization. The American Biological Safety Association (ABSA) was officially established in 1984 and a constitution and bylaws were drafted the same year. As of 2008, ABSA includes some 1,600 members in its professional association. In 1977, Jim Peacock of the Australian Academy of Science asked Bill Snowdon, then chief of the CSIRO 's Australian Animal Health Laboratory (AAHL) if he could have the newly released United States' National Institutes of Health and the British equivalent requirements for the development of infrastructure for bio-containment reviewed by AAHL personnel with a view to recommending the adoption of one of them by Australian authorities. The review was carried out by CSIRO AAHL Project Manager Bill Curnow and CSIRO Engineer Arthur Jenkins. They drafted outcomes for each of the levels of security. AAHL was notionally classified as "substantially beyond P4". These were adopted by the Australian Academy of Science and became the basis for Australian legislation. It opened in 1985 costing AU$185 million, built on Corio Oval . The Australian Animal Health Laboratory is a Class 4/ P4 Laboratory. In 2003, the Chinese Academy of Sciences approved the construction of mainland China's first BSL-4 laboratory at the Wuhan Institute of Virology (WIV). In 2014, the WIV's National Bio-safety Laboratory was built at a cost of 300 million yuan (US$44 million), in collaboration and with assistance from the French government 's CIRI lab . In 2007 a scientific review paper stated that the Canadian Science Centre for Human and Animal Health , which was designed in the early 1990s, "has become the prototype for modern BSL4 laboratories". Starting with the 2020 COVID-19 pandemic near the facilities of the WIV, work in biocontainment facilities has been politicized, especially in the US Senate for example as the result of Rand Paul 's work. Russia asked questions on 25 October 2022 in the United Nations over the presence in Ukraine of biolabs. In April 2023, Sudan's descent into civil war caused worries at the World Health Organization over its National Public Laboratory as contending factions battled over its area and NPL staff were kicked out in favor of installing a military base at its premises. At the time, the facility contained organisms rated at BSL-2. Biosafety level 1 (BSL-1) is suitable for work with well-characterized agents which do not cause disease in healthy humans. In general, these agents should pose minimal potential hazard to laboratory personnel and the environment. At this level, precautions are limited relative to other levels. Laboratory personnel must wash their hands upon entering and exiting the lab. Research with these agents may be performed on standard open laboratory benches without the use of special containment equipment. However, eating and drinking are generally prohibited in laboratory areas. Potentially infectious material must be decontaminated before disposal, either by adding a chemical such as bleach or isopropanol or by packaging for decontamination elsewhere. Personal protective equipment is only required for circumstances where personnel might be exposed to hazardous material. BSL-1 laboratories must have a door which can be closed to limit access to the lab. However, it is not necessary for BSL-1 labs to be isolated from the general building. This level of biosafety is appropriate for work with several kinds of microorganisms including non-pathogenic strains of Escherichia coli and Staphylococcus , Bacillus subtilis , Saccharomyces cerevisiae and other organisms not suspected to contribute to human disease. Due to the relative ease and safety of maintaining a BSL-1 laboratory, these are the types of laboratories generally used as teaching spaces for high schools and colleges . At this level, all precautions used at Biosafety level 1 are followed, and some additional precautions are taken. BSL-2 differs from BSL-1 in that: Biosafety level 2 is suitable for work involving agents of moderate potential hazard to personnel and the environment. This includes various microbes that cause mild disease to humans, or are difficult to contract via aerosol in a lab setting. Examples of pathogens classified as "Risk Group 2" in the United States include hepatitis A , B , and C viruses, human immunodeficiency virus (HIV), pathogenic strains of Escherichia coli and Staphylococcus , Salmonella , Plasmodium falciparum , and Toxoplasma gondii . Notably, the European Union departs from the United States and classifies HIV and hepatitis B – G as Risk Group 3 agents best handled at BSL-3. Prions , the infectious agents that transmit prion diseases such as vCJD , are typically handled under Biosafety Level 2 or higher. This is due to the lack of any evidence of aerosol transmission and relatively higher infective dose of prion diseases, though some circumstances (such as handling animal-infective prions in a facility which cares for vulnerable animals) would require BSL-3 conditions. Biosafety level 3 is appropriate for work involving microbes which can cause serious and potentially lethal disease via the inhalation route. This type of work can be done in clinical, diagnostic, teaching, research, or production facilities. Here, the precautions undertaken in BSL-1 and BSL-2 labs are followed, as well as additional measures including: In addition, the facility which houses the BSL-3 laboratory must have certain features to ensure appropriate containment. The entrance to the laboratory must be separated from areas of the building with unrestricted traffic flow. Additionally, the laboratory must be behind two sets of self-closing doors (to reduce the risk of aerosols escaping). The construction of the laboratory is such that it can be easily cleaned. Carpets are not permitted, and any seams in the floors, walls, and ceilings are sealed to allow for easy cleaning and decontamination. Additionally, windows must be sealed, and a ventilation system installed which forces air to flow from the "clean" areas of the lab to the areas where infectious agents are handled. Air from the laboratory must be filtered before it can be recirculated. A 2015 study by USA Today journalists identified more than 200 lab sites in the U.S. that were accredited biosafety levels 3 or 4. The Proceedings of a Workshop on "Developing Norms for the Provision of Biological Laboratories in Low-Resource Contexts" provides a list of BSL-3 laboratories in those countries. Biosafety level 3 is commonly used for research and diagnostic work involving various microbes which can be transmitted by aerosols and/or cause severe disease. These include Francisella tularensis , Mycobacterium tuberculosis , Chlamydia psittaci , Venezuelan equine encephalitis virus , Eastern equine encephalitis virus , SARS-CoV-1 , MERS-CoV , Coxiella burnetii , Rift Valley fever virus , Rickettsia rickettsii , several species of Brucella , chikungunya , yellow fever virus , West Nile virus , Yersinia pestis , and SARS-CoV-2 . Biosafety level 4 (BSL-4) is the highest level of biosafety precautions, and is appropriate for work with agents that could easily be aerosol-transmitted within the laboratory and cause severe to fatal disease in humans for which there are no available vaccines or treatments. BSL-4 laboratories are generally set up to be either cabinet laboratories or protective-suit laboratories. In cabinet laboratories, all work must be done within a class III biosafety cabinet . Materials leaving the cabinet must be decontaminated by passing through an autoclave or a tank of disinfectant . The cabinets themselves are required to have seamless edges to allow for easy cleaning. Additionally, the cabinet and all materials within must be free of sharp edges to reduce the risk of damage to the gloves. In a protective-suit laboratory, all work must be done in a class II biosafety cabinet by personnel wearing a positive pressure suit . To exit the BSL-4 laboratory, personnel must pass through a chemical shower for decontamination, then a room for removing the positive-pressure suit, followed by a personal shower. Entry into the BSL-4 laboratory is restricted to trained and authorized individuals, and all persons entering and exiting the laboratory must be recorded. As with BSL-3 laboratories, BSL-4 laboratories must be separated from areas that receive unrestricted traffic. Additionally, airflow is tightly controlled to ensure that air always flows from "clean" areas of the lab to areas where work with infectious agents is being performed. The entrance to the BSL-4 lab must also employ airlocks to minimize the possibility that aerosols from the lab could be removed from the lab. All laboratory waste, including filtered air, water, and trash must also be decontaminated before it can leave the facility. Biosafety level 4 laboratories are used for diagnostic work and research on easily transmitted pathogens which can cause fatal disease. These include a number of viruses known to cause viral hemorrhagic fever such as Marburg virus , Ebola virus , Lassa virus , and Crimean-Congo hemorrhagic fever . Other pathogens handled at BSL-4 include Hendra virus , Nipah virus , and some flaviviruses . Additionally, poorly characterized pathogens which appear closely related to dangerous pathogens are often handled at this level until sufficient data are obtained either to confirm continued work at this level, or to permit working with them at a lower level. This level is also used for work with Variola virus , the causative agent of smallpox , though this work is only performed at the Centers for Disease Control and Prevention in Atlanta, United States, and the State Research Center of Virology and Biotechnology in Koltsovo, Russia. Sample-return missions that bring back to Earth samples obtained from a Category V body must be curated at facilities rated BSL-4. Because the existing BSL-4 facilities in the world do not provide the level of cleanliness necessary to such pristine samples, there is a need to design a facility dedicated to curation of restricted (potentially biohazardous ) extraterrestrial materials . The systems of such facilities must be able to contain unknown biohazards, as the sizes of any putative alien microorganisms are unknown. Ideally, it should filter particles down to 10 nanometers , and release of a particle 50 nanometers or larger is unacceptable under any circumstance. Because NASA and ESA are collaborating on the Mars Sample Return campaign, due to return samples from Mars in the early 2030s, the need for a Sample Receiving Facility (SRF) is becoming more pressing. An SRF is expected to take 7 to 10 years from design to completion, and an additional two years is recommended for the staff to become proficient and accustomed to the facilities. Biosafety level 1 (BSL-1) is suitable for work with well-characterized agents which do not cause disease in healthy humans. In general, these agents should pose minimal potential hazard to laboratory personnel and the environment. At this level, precautions are limited relative to other levels. Laboratory personnel must wash their hands upon entering and exiting the lab. Research with these agents may be performed on standard open laboratory benches without the use of special containment equipment. However, eating and drinking are generally prohibited in laboratory areas. Potentially infectious material must be decontaminated before disposal, either by adding a chemical such as bleach or isopropanol or by packaging for decontamination elsewhere. Personal protective equipment is only required for circumstances where personnel might be exposed to hazardous material. BSL-1 laboratories must have a door which can be closed to limit access to the lab. However, it is not necessary for BSL-1 labs to be isolated from the general building. This level of biosafety is appropriate for work with several kinds of microorganisms including non-pathogenic strains of Escherichia coli and Staphylococcus , Bacillus subtilis , Saccharomyces cerevisiae and other organisms not suspected to contribute to human disease. Due to the relative ease and safety of maintaining a BSL-1 laboratory, these are the types of laboratories generally used as teaching spaces for high schools and colleges . At this level, all precautions used at Biosafety level 1 are followed, and some additional precautions are taken. BSL-2 differs from BSL-1 in that: Biosafety level 2 is suitable for work involving agents of moderate potential hazard to personnel and the environment. This includes various microbes that cause mild disease to humans, or are difficult to contract via aerosol in a lab setting. Examples of pathogens classified as "Risk Group 2" in the United States include hepatitis A , B , and C viruses, human immunodeficiency virus (HIV), pathogenic strains of Escherichia coli and Staphylococcus , Salmonella , Plasmodium falciparum , and Toxoplasma gondii . Notably, the European Union departs from the United States and classifies HIV and hepatitis B – G as Risk Group 3 agents best handled at BSL-3. Prions , the infectious agents that transmit prion diseases such as vCJD , are typically handled under Biosafety Level 2 or higher. This is due to the lack of any evidence of aerosol transmission and relatively higher infective dose of prion diseases, though some circumstances (such as handling animal-infective prions in a facility which cares for vulnerable animals) would require BSL-3 conditions. Biosafety level 3 is appropriate for work involving microbes which can cause serious and potentially lethal disease via the inhalation route. This type of work can be done in clinical, diagnostic, teaching, research, or production facilities. Here, the precautions undertaken in BSL-1 and BSL-2 labs are followed, as well as additional measures including: In addition, the facility which houses the BSL-3 laboratory must have certain features to ensure appropriate containment. The entrance to the laboratory must be separated from areas of the building with unrestricted traffic flow. Additionally, the laboratory must be behind two sets of self-closing doors (to reduce the risk of aerosols escaping). The construction of the laboratory is such that it can be easily cleaned. Carpets are not permitted, and any seams in the floors, walls, and ceilings are sealed to allow for easy cleaning and decontamination. Additionally, windows must be sealed, and a ventilation system installed which forces air to flow from the "clean" areas of the lab to the areas where infectious agents are handled. Air from the laboratory must be filtered before it can be recirculated. A 2015 study by USA Today journalists identified more than 200 lab sites in the U.S. that were accredited biosafety levels 3 or 4. The Proceedings of a Workshop on "Developing Norms for the Provision of Biological Laboratories in Low-Resource Contexts" provides a list of BSL-3 laboratories in those countries. Biosafety level 3 is commonly used for research and diagnostic work involving various microbes which can be transmitted by aerosols and/or cause severe disease. These include Francisella tularensis , Mycobacterium tuberculosis , Chlamydia psittaci , Venezuelan equine encephalitis virus , Eastern equine encephalitis virus , SARS-CoV-1 , MERS-CoV , Coxiella burnetii , Rift Valley fever virus , Rickettsia rickettsii , several species of Brucella , chikungunya , yellow fever virus , West Nile virus , Yersinia pestis , and SARS-CoV-2 . Biosafety level 4 (BSL-4) is the highest level of biosafety precautions, and is appropriate for work with agents that could easily be aerosol-transmitted within the laboratory and cause severe to fatal disease in humans for which there are no available vaccines or treatments. BSL-4 laboratories are generally set up to be either cabinet laboratories or protective-suit laboratories. In cabinet laboratories, all work must be done within a class III biosafety cabinet . Materials leaving the cabinet must be decontaminated by passing through an autoclave or a tank of disinfectant . The cabinets themselves are required to have seamless edges to allow for easy cleaning. Additionally, the cabinet and all materials within must be free of sharp edges to reduce the risk of damage to the gloves. In a protective-suit laboratory, all work must be done in a class II biosafety cabinet by personnel wearing a positive pressure suit . To exit the BSL-4 laboratory, personnel must pass through a chemical shower for decontamination, then a room for removing the positive-pressure suit, followed by a personal shower. Entry into the BSL-4 laboratory is restricted to trained and authorized individuals, and all persons entering and exiting the laboratory must be recorded. As with BSL-3 laboratories, BSL-4 laboratories must be separated from areas that receive unrestricted traffic. Additionally, airflow is tightly controlled to ensure that air always flows from "clean" areas of the lab to areas where work with infectious agents is being performed. The entrance to the BSL-4 lab must also employ airlocks to minimize the possibility that aerosols from the lab could be removed from the lab. All laboratory waste, including filtered air, water, and trash must also be decontaminated before it can leave the facility. Biosafety level 4 laboratories are used for diagnostic work and research on easily transmitted pathogens which can cause fatal disease. These include a number of viruses known to cause viral hemorrhagic fever such as Marburg virus , Ebola virus , Lassa virus , and Crimean-Congo hemorrhagic fever . Other pathogens handled at BSL-4 include Hendra virus , Nipah virus , and some flaviviruses . Additionally, poorly characterized pathogens which appear closely related to dangerous pathogens are often handled at this level until sufficient data are obtained either to confirm continued work at this level, or to permit working with them at a lower level. This level is also used for work with Variola virus , the causative agent of smallpox , though this work is only performed at the Centers for Disease Control and Prevention in Atlanta, United States, and the State Research Center of Virology and Biotechnology in Koltsovo, Russia. Sample-return missions that bring back to Earth samples obtained from a Category V body must be curated at facilities rated BSL-4. Because the existing BSL-4 facilities in the world do not provide the level of cleanliness necessary to such pristine samples, there is a need to design a facility dedicated to curation of restricted (potentially biohazardous ) extraterrestrial materials . The systems of such facilities must be able to contain unknown biohazards, as the sizes of any putative alien microorganisms are unknown. Ideally, it should filter particles down to 10 nanometers , and release of a particle 50 nanometers or larger is unacceptable under any circumstance. Because NASA and ESA are collaborating on the Mars Sample Return campaign, due to return samples from Mars in the early 2030s, the need for a Sample Receiving Facility (SRF) is becoming more pressing. An SRF is expected to take 7 to 10 years from design to completion, and an additional two years is recommended for the staff to become proficient and accustomed to the facilities. Sample-return missions that bring back to Earth samples obtained from a Category V body must be curated at facilities rated BSL-4. Because the existing BSL-4 facilities in the world do not provide the level of cleanliness necessary to such pristine samples, there is a need to design a facility dedicated to curation of restricted (potentially biohazardous ) extraterrestrial materials . The systems of such facilities must be able to contain unknown biohazards, as the sizes of any putative alien microorganisms are unknown. Ideally, it should filter particles down to 10 nanometers , and release of a particle 50 nanometers or larger is unacceptable under any circumstance. Because NASA and ESA are collaborating on the Mars Sample Return campaign, due to return samples from Mars in the early 2030s, the need for a Sample Receiving Facility (SRF) is becoming more pressing. An SRF is expected to take 7 to 10 years from design to completion, and an additional two years is recommended for the staff to become proficient and accustomed to the facilities. According to a U.S. Government Accountability Office (GAO) report published on 4 October 2007, a total of 1,356 CDC/USDA registered BSL-3 facilities were identified throughout the United States. Approximately 36% of these laboratories are located in academia. 15 BSL-4 facilities were identified in the U.S. in 2007, including nine at federal labs. As of May 2021, there are 42 BSL-4 facilities in operation around the world, with a further 17 planned or under construction. The following is a list of existing BSL-4 facilities worldwide.A North Carolina Mosquito & Vector Control Association (NCMVCA) study highlighted safety concerns. In the United States, laboratories can be funded by federal, state, private, non-profit, or academically. The last accounts for 72% of the funding. High-containment labs that are registered with the Centers for Disease Control and Prevention (CDC) and the U.S. Department of Agriculture's (USDA) Select Agent Program must adhere to Department of Defense standards. Since BSL3 and 4 laboratories in the United States are regulated by either the CDC or USDA or another federal agency (depending on the pathogens they handle), no single federal agency is responsible for regulating or tracking the number of these labs. U.S. high-containment laboratories that handle pathogens which are declared as " select agents " must be inspected periodically by the CDC or USDA, adhere to certain standards, and maintain ongoing education on biosecurity and biosafety policies as mandated by law.

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Rift Valley fever

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MRNA vaccine

An mRNA vaccine is a type of vaccine that uses a copy of a molecule called messenger RNA (mRNA) to produce an immune response. The vaccine delivers molecules of antigen -encoding mRNA into immune cells , which use the designed mRNA as a blueprint to build foreign protein that would normally be produced by a pathogen (such as a virus ) or by a cancer cell . These protein molecules stimulate an adaptive immune response that teaches the body to identify and destroy the corresponding pathogen or cancer cells. The mRNA is delivered by a co-formulation of the RNA encapsulated in lipid nanoparticles that protect the RNA strands and help their absorption into the cells. Reactogenicity , the tendency of a vaccine to produce adverse reactions, is similar to that of conventional non-RNA vaccines. People susceptible to an autoimmune response may have an adverse reaction to messenger RNA vaccines. The advantages of mRNA vaccines over traditional vaccines are ease of design, speed and lower cost of production, the induction of both cellular and humoral immunity , and lack of interaction with the genomic DNA . While some messenger RNA vaccines, such as the Pfizer–BioNTech COVID-19 vaccine , have the disadvantage of requiring ultracold storage before distribution, other mRNA vaccines, such as the Moderna vaccine, or the Walvax COVID-19 vaccine used in Indonesia (and the now abandoned CureVac vaccine candidate, as well), do not have such requirements. In RNA therapeutics , messenger RNA vaccines have attracted considerable interest as COVID-19 vaccines . In December 2020, Pfizer–BioNTech and Moderna obtained authorization for their mRNA-based COVID-19 vaccines. On 2 December, the UK Medicines and Healthcare products Regulatory Agency (MHRA) became the first medicines regulator to approve an mRNA vaccine, authorizing the Pfizer–BioNTech vaccine for widespread use. On 11 December, the US Food and Drug Administration (FDA) issued an emergency use authorization for the Pfizer–BioNTech vaccine and a week later similarly authorized the Moderna vaccine. In 2023 the Nobel Prize in Physiology or Medicine was awarded to Katalin Karikó and Drew Weissman for their discoveries concerning modified nucleosides that enabled the development of effective mRNA vaccines against COVID-19. The first successful transfection of designed mRNA packaged within a liposomal nanoparticle into a cell was published in 1989. "Naked" (or unprotected) lab-made mRNA was injected a year later into the muscle of mice. These studies were the first evidence that in vitro transcribed mRNA with a chosen gene was able to deliver the genetic information to produce a desired protein within living cell tissue and led to the concept proposal of messenger RNA vaccines. Liposome-encapsulated mRNA encoding a viral antigen was shown in 1993 to stimulate T cells in mice. The following year self-amplifying mRNA was developed by including both a viral antigen and replicase encoding gene. The method was used in mice to elicit both a humoral and cellular immune response against a viral pathogen. The next year mRNA encoding a tumor antigen was shown to elicit a similar immune response against cancer cells in mice. The first human clinical trial using ex vivo dendritic cells transfected with mRNA encoding tumor antigens ( therapeutic cancer mRNA vaccine ) was started in 2001. Four years later, the successful use of modified nucleosides as a method to transport mRNA inside cells without setting off the body's defense system was reported. Clinical trial results of an mRNA vaccine directly injected into the body against cancer cells were reported in 2008. BioNTech in 2008, and Moderna in 2010, were founded to develop mRNA biotechnologies. The US research agency DARPA launched at this time the biotechnology research program ADEPT to develop emerging technologies for the US military . The agency recognized the potential of nucleic acid technology for defense against pandemics and began to invest in the field. DARPA grants were seen as a vote of confidence that in turn encouraged other government agencies and private investors to invest in mRNA technology. DARPA awarded at the time a $25 million grant to Moderna. The first human clinical trials using an mRNA vaccine against an infectious agent ( rabies ) began in 2013. Over the next few years, clinical trials of mRNA vaccines for a number of other viruses were started. mRNA vaccines for human use were studied for infectious agents such as influenza , Zika virus , cytomegalovirus , and Chikungunya virus . The COVID-19 pandemic , and sequencing of the causative virus SARS-CoV-2 at the beginning of 2020, led to the rapid development of the first approved mRNA vaccines. BioNTech and Moderna in December of the same year obtained approval for their mRNA-based COVID-19 vaccines . On 2 December, seven days after its final eight-week trial, the UK Medicines and Healthcare products Regulatory Agency (MHRA) became the first global medicines regulator in history to approve an mRNA vaccine, granting emergency authorization for Pfizer–BioNTech's BNT162b2 COVID-19 vaccine for widespread use. On 11 December, the FDA gave emergency use authorization for the Pfizer–BioNTech COVID-19 vaccine and a week later similar approval for the Moderna COVID-19 vaccine . Other mRNA vaccines continue to be developed, since the approval of the first mRNA vaccines. Moderna announced the development of mRNA vaccines for 15 diseases: Chikungunya virus , COVID-19, Crimean-Congo haemorrhagic fever , Dengue , Ebola virus disease , HIV , Malaria , Marburg virus disease , Lassa fever , Middle East respiratory syndrome coronavirus (MERS-CoV) , Nipah and henipaviral diseases, Rift Valley fever , Severe fever with Thrombocytopenia syndrome , Tuberculosis and Zika . The first successful transfection of designed mRNA packaged within a liposomal nanoparticle into a cell was published in 1989. "Naked" (or unprotected) lab-made mRNA was injected a year later into the muscle of mice. These studies were the first evidence that in vitro transcribed mRNA with a chosen gene was able to deliver the genetic information to produce a desired protein within living cell tissue and led to the concept proposal of messenger RNA vaccines. Liposome-encapsulated mRNA encoding a viral antigen was shown in 1993 to stimulate T cells in mice. The following year self-amplifying mRNA was developed by including both a viral antigen and replicase encoding gene. The method was used in mice to elicit both a humoral and cellular immune response against a viral pathogen. The next year mRNA encoding a tumor antigen was shown to elicit a similar immune response against cancer cells in mice. The first human clinical trial using ex vivo dendritic cells transfected with mRNA encoding tumor antigens ( therapeutic cancer mRNA vaccine ) was started in 2001. Four years later, the successful use of modified nucleosides as a method to transport mRNA inside cells without setting off the body's defense system was reported. Clinical trial results of an mRNA vaccine directly injected into the body against cancer cells were reported in 2008. BioNTech in 2008, and Moderna in 2010, were founded to develop mRNA biotechnologies. The US research agency DARPA launched at this time the biotechnology research program ADEPT to develop emerging technologies for the US military . The agency recognized the potential of nucleic acid technology for defense against pandemics and began to invest in the field. DARPA grants were seen as a vote of confidence that in turn encouraged other government agencies and private investors to invest in mRNA technology. DARPA awarded at the time a $25 million grant to Moderna. The first human clinical trials using an mRNA vaccine against an infectious agent ( rabies ) began in 2013. Over the next few years, clinical trials of mRNA vaccines for a number of other viruses were started. mRNA vaccines for human use were studied for infectious agents such as influenza , Zika virus , cytomegalovirus , and Chikungunya virus . The COVID-19 pandemic , and sequencing of the causative virus SARS-CoV-2 at the beginning of 2020, led to the rapid development of the first approved mRNA vaccines. BioNTech and Moderna in December of the same year obtained approval for their mRNA-based COVID-19 vaccines . On 2 December, seven days after its final eight-week trial, the UK Medicines and Healthcare products Regulatory Agency (MHRA) became the first global medicines regulator in history to approve an mRNA vaccine, granting emergency authorization for Pfizer–BioNTech's BNT162b2 COVID-19 vaccine for widespread use. On 11 December, the FDA gave emergency use authorization for the Pfizer–BioNTech COVID-19 vaccine and a week later similar approval for the Moderna COVID-19 vaccine . Other mRNA vaccines continue to be developed, since the approval of the first mRNA vaccines. Moderna announced the development of mRNA vaccines for 15 diseases: Chikungunya virus , COVID-19, Crimean-Congo haemorrhagic fever , Dengue , Ebola virus disease , HIV , Malaria , Marburg virus disease , Lassa fever , Middle East respiratory syndrome coronavirus (MERS-CoV) , Nipah and henipaviral diseases, Rift Valley fever , Severe fever with Thrombocytopenia syndrome , Tuberculosis and Zika . The goal of a vaccine is to stimulate the adaptive immune system to create antibodies that precisely target that particular pathogen . The markers on the pathogen that the antibodies target are called antigens . Traditional vaccines stimulate an antibody response by injecting either antigens , an attenuated (weakened) virus, an inactivated (dead) virus, or a recombinant antigen-encoding viral vector (harmless carrier virus with an antigen transgene ) into the body. These antigens and viruses are prepared and grown outside the body. In contrast, mRNA vaccines introduce a short-lived synthetically created fragment of the RNA sequence of a virus into the individual being vaccinated. These mRNA fragments are taken up by dendritic cells through phagocytosis . The dendritic cells use their internal machinery ( ribosomes ) to read the mRNA and produce the viral antigens that the mRNA encodes. The body degrades the mRNA fragments within a few days of introduction. Although non-immune cells can potentially also absorb vaccine mRNA, produce antigens, and display the antigens on their surfaces, dendritic cells absorb the mRNA globules much more readily. The mRNA fragments are translated in the cytoplasm and do not affect the body's genomic DNA, located separately in the cell nucleus . Once the viral antigens are produced by the host cell, the normal adaptive immune system processes are followed. Antigens are broken down by proteasomes . Class I and class II MHC molecules then attach to the antigen and transport it to the cellular membrane, "activating" the dendritic cell. Once activated, dendritic cells migrate to lymph nodes , where they present the antigen to T cells and B cells . This triggers the production of antibodies specifically targeted to the antigen, ultimately resulting in immunity . The central component of a mRNA vaccine is its mRNA construct. The in vitro transcribed mRNA is generated from an engineered plasmid DNA, which has an RNA polymerase promoter and sequence which corresponds to the mRNA construct. By combining T7 phage RNA polymerase and the plasmid DNA, the mRNA can be transcribed in the lab. Efficacy of the vaccine is dependent on the stability and structure of the designed mRNA. The in vitro transcribed mRNA has the same structural components as natural mRNA in eukaryotic cells . It has a 5' cap , a 5'-untranslated region (UTR) and 3'-UTR , an open reading frame (ORF), which encodes the relevant antigen, and a 3'-poly(A) tail . By modifying these different components of the synthetic mRNA, the stability and translational ability of the mRNA can be enhanced, and in turn, the efficacy of the vaccine improved. The mRNA can be improved by using synthetic 5'-cap analogues which enhance the stability and increase protein translation. Similarly, regulatory elements in the 5'-untranslated region and the 3'-untranslated region can be altered, and the length of the poly(A) tail optimized, to stabilize the mRNA and increase protein production. The mRNA nucleotides can be modified to both decrease innate immune activation and increase the mRNA's half-life in the host cell. The nucleic acid sequence and codon usage impacts protein translation. Enriching the sequence with guanine-cytosine content improves mRNA stability and half-life and, in turn, protein production. Replacing rare codons with synonymous codons frequently used by the host cell also enhances protein production. For a vaccine to be successful, sufficient mRNA must enter the host cell cytoplasm to stimulate production of the specific antigens. Entry of mRNA molecules, however, faces a number of difficulties. Not only are mRNA molecules too large to cross the cell membrane by simple diffusion , they are also negatively charged like the cell membrane, which causes a mutual electrostatic repulsion . Additionally, mRNA is easily degraded by RNAases in skin and blood. Various methods have been developed to overcome these delivery hurdles. The method of vaccine delivery can be broadly classified by whether mRNA transfer into cells occurs within ( in vivo ) or outside ( ex vivo ) the organism. Dendritic cells display antigens on their surfaces , leading to interactions with T cells to initiate an immune response. Dendritic cells can be collected from patients and programmed with the desired mRNA, then administered back into patients to create an immune response. The simplest way that ex vivo dendritic cells take up mRNA molecules is through endocytosis , a fairly inefficient pathway in the laboratory setting that can be significantly improved through electroporation . Since the discovery that the direct administration of in vitro transcribed mRNA leads to the expression of antigens in the body, in vivo approaches have been investigated. They offer some advantages over ex vivo methods, particularly by avoiding the cost of harvesting and adapting dendritic cells from patients and by imitating a regular infection. Different routes of injection , such as into the skin , blood , or muscles , result in varying levels of mRNA uptake, making the choice of administration route a critical aspect of in vivo delivery. One study showed, in comparing different routes, that lymph node injection leads to the largest T-cell response. Naked mRNA injection means that the delivery of the vaccine is only done in a buffer solution . This mode of mRNA uptake has been known since the 1990s. The first worldwide clinical studies used intradermal injections of naked mRNA for vaccination. A variety of methods have been used to deliver naked mRNA, such as subcutaneous, intravenous, and intratumoral injections. Although naked mRNA delivery causes an immune response, the effect is relatively weak, and after injection the mRNA is often rapidly degraded. Cationic polymers can be mixed with mRNA to generate protective coatings called polyplexes . These protect the recombinant mRNA from ribonucleases and assist its penetration in cells. Protamine is a natural cationic peptide and has been used to encapsulate mRNA for vaccination. [ non-primary source needed ] The first time the FDA approved the use of lipid nanoparticles as a drug delivery system was in 2018, when the agency approved the first siRNA drug, Onpattro . Encapsulating the mRNA molecule in lipid nanoparticles was a critical breakthrough for producing viable mRNA vaccines, solving a number of key technical barriers in delivering the mRNA molecule into the host cell. Research into using lipids to deliver siRNA to cells became a foundation for similar research into using lipids to deliver mRNA. However, new lipids had to be invented to encapsulate mRNA strands, which are much longer than siRNA strands. Principally, the lipid provides a layer of protection against degradation, allowing more robust translational output. In addition, the customization of the lipid's outer layer allows the targeting of desired cell types through ligand interactions. However, many studies have also highlighted the difficulty of studying this type of delivery, demonstrating that there is an inconsistency between in vivo and in vitro applications of nanoparticles in terms of cellular intake. The nanoparticles can be administered to the body and transported via multiple routes, such as intravenously or through the lymphatic system . One issue with lipid nanoparticles is that several of the breakthroughs leading to the practical use of that technology involve the use of microfluidics . Microfluidic reaction chambers are difficult to scale up, since the entire point of microfluidics is to exploit the microscale behaviors of liquids. The only way around this obstacle is to run an extensive number of microfluidic reaction chambers in parallel, a novel task requiring custom-built equipment. For COVID-19 mRNA vaccines, this was the main manufacturing bottleneck. Pfizer used such a parallel approach to solve the scaling problem. After verifying that impingement jet mixers could not be directly scaled up, Pfizer made about 100 of the little mixers (each about the size of a U.S. half-dollar coin ), connected them together with pumps and filters with a "maze of piping," and set up a computer system to regulate flow and pressure through the mixers. Another issue, with the large-scale use of this delivery method, is the availability of the novel lipids used to create lipid nanoparticles, especially ionizable cationic lipids. Before 2020, such lipids were manufactured in small quantities measured in grams or kilograms, and they were used for medical research and a handful of drugs for rare conditions. As the safety and efficacy of mRNA vaccines became clear in 2020, the few companies able to manufacture the requisite lipids were confronted with the challenge of scaling up production to respond to orders for several tons of lipids. In addition to non-viral delivery methods, RNA viruses have been engineered to achieve similar immunological responses. Typical RNA viruses used as vectors include retroviruses , lentiviruses , alphaviruses and rhabdoviruses , each of which can differ in structure and function. Clinical studies have utilized such viruses on a range of diseases in model animals such as mice , chicken and primates . Dendritic cells display antigens on their surfaces , leading to interactions with T cells to initiate an immune response. Dendritic cells can be collected from patients and programmed with the desired mRNA, then administered back into patients to create an immune response. The simplest way that ex vivo dendritic cells take up mRNA molecules is through endocytosis , a fairly inefficient pathway in the laboratory setting that can be significantly improved through electroporation . Since the discovery that the direct administration of in vitro transcribed mRNA leads to the expression of antigens in the body, in vivo approaches have been investigated. They offer some advantages over ex vivo methods, particularly by avoiding the cost of harvesting and adapting dendritic cells from patients and by imitating a regular infection. Different routes of injection , such as into the skin , blood , or muscles , result in varying levels of mRNA uptake, making the choice of administration route a critical aspect of in vivo delivery. One study showed, in comparing different routes, that lymph node injection leads to the largest T-cell response. Naked mRNA injection means that the delivery of the vaccine is only done in a buffer solution . This mode of mRNA uptake has been known since the 1990s. The first worldwide clinical studies used intradermal injections of naked mRNA for vaccination. A variety of methods have been used to deliver naked mRNA, such as subcutaneous, intravenous, and intratumoral injections. Although naked mRNA delivery causes an immune response, the effect is relatively weak, and after injection the mRNA is often rapidly degraded. Cationic polymers can be mixed with mRNA to generate protective coatings called polyplexes . These protect the recombinant mRNA from ribonucleases and assist its penetration in cells. Protamine is a natural cationic peptide and has been used to encapsulate mRNA for vaccination. [ non-primary source needed ] The first time the FDA approved the use of lipid nanoparticles as a drug delivery system was in 2018, when the agency approved the first siRNA drug, Onpattro . Encapsulating the mRNA molecule in lipid nanoparticles was a critical breakthrough for producing viable mRNA vaccines, solving a number of key technical barriers in delivering the mRNA molecule into the host cell. Research into using lipids to deliver siRNA to cells became a foundation for similar research into using lipids to deliver mRNA. However, new lipids had to be invented to encapsulate mRNA strands, which are much longer than siRNA strands. Principally, the lipid provides a layer of protection against degradation, allowing more robust translational output. In addition, the customization of the lipid's outer layer allows the targeting of desired cell types through ligand interactions. However, many studies have also highlighted the difficulty of studying this type of delivery, demonstrating that there is an inconsistency between in vivo and in vitro applications of nanoparticles in terms of cellular intake. The nanoparticles can be administered to the body and transported via multiple routes, such as intravenously or through the lymphatic system . One issue with lipid nanoparticles is that several of the breakthroughs leading to the practical use of that technology involve the use of microfluidics . Microfluidic reaction chambers are difficult to scale up, since the entire point of microfluidics is to exploit the microscale behaviors of liquids. The only way around this obstacle is to run an extensive number of microfluidic reaction chambers in parallel, a novel task requiring custom-built equipment. For COVID-19 mRNA vaccines, this was the main manufacturing bottleneck. Pfizer used such a parallel approach to solve the scaling problem. After verifying that impingement jet mixers could not be directly scaled up, Pfizer made about 100 of the little mixers (each about the size of a U.S. half-dollar coin ), connected them together with pumps and filters with a "maze of piping," and set up a computer system to regulate flow and pressure through the mixers. Another issue, with the large-scale use of this delivery method, is the availability of the novel lipids used to create lipid nanoparticles, especially ionizable cationic lipids. Before 2020, such lipids were manufactured in small quantities measured in grams or kilograms, and they were used for medical research and a handful of drugs for rare conditions. As the safety and efficacy of mRNA vaccines became clear in 2020, the few companies able to manufacture the requisite lipids were confronted with the challenge of scaling up production to respond to orders for several tons of lipids. In addition to non-viral delivery methods, RNA viruses have been engineered to achieve similar immunological responses. Typical RNA viruses used as vectors include retroviruses , lentiviruses , alphaviruses and rhabdoviruses , each of which can differ in structure and function. Clinical studies have utilized such viruses on a range of diseases in model animals such as mice , chicken and primates . Naked mRNA injection means that the delivery of the vaccine is only done in a buffer solution . This mode of mRNA uptake has been known since the 1990s. The first worldwide clinical studies used intradermal injections of naked mRNA for vaccination. A variety of methods have been used to deliver naked mRNA, such as subcutaneous, intravenous, and intratumoral injections. Although naked mRNA delivery causes an immune response, the effect is relatively weak, and after injection the mRNA is often rapidly degraded. Cationic polymers can be mixed with mRNA to generate protective coatings called polyplexes . These protect the recombinant mRNA from ribonucleases and assist its penetration in cells. Protamine is a natural cationic peptide and has been used to encapsulate mRNA for vaccination. [ non-primary source needed ] The first time the FDA approved the use of lipid nanoparticles as a drug delivery system was in 2018, when the agency approved the first siRNA drug, Onpattro . Encapsulating the mRNA molecule in lipid nanoparticles was a critical breakthrough for producing viable mRNA vaccines, solving a number of key technical barriers in delivering the mRNA molecule into the host cell. Research into using lipids to deliver siRNA to cells became a foundation for similar research into using lipids to deliver mRNA. However, new lipids had to be invented to encapsulate mRNA strands, which are much longer than siRNA strands. Principally, the lipid provides a layer of protection against degradation, allowing more robust translational output. In addition, the customization of the lipid's outer layer allows the targeting of desired cell types through ligand interactions. However, many studies have also highlighted the difficulty of studying this type of delivery, demonstrating that there is an inconsistency between in vivo and in vitro applications of nanoparticles in terms of cellular intake. The nanoparticles can be administered to the body and transported via multiple routes, such as intravenously or through the lymphatic system . One issue with lipid nanoparticles is that several of the breakthroughs leading to the practical use of that technology involve the use of microfluidics . Microfluidic reaction chambers are difficult to scale up, since the entire point of microfluidics is to exploit the microscale behaviors of liquids. The only way around this obstacle is to run an extensive number of microfluidic reaction chambers in parallel, a novel task requiring custom-built equipment. For COVID-19 mRNA vaccines, this was the main manufacturing bottleneck. Pfizer used such a parallel approach to solve the scaling problem. After verifying that impingement jet mixers could not be directly scaled up, Pfizer made about 100 of the little mixers (each about the size of a U.S. half-dollar coin ), connected them together with pumps and filters with a "maze of piping," and set up a computer system to regulate flow and pressure through the mixers. Another issue, with the large-scale use of this delivery method, is the availability of the novel lipids used to create lipid nanoparticles, especially ionizable cationic lipids. Before 2020, such lipids were manufactured in small quantities measured in grams or kilograms, and they were used for medical research and a handful of drugs for rare conditions. As the safety and efficacy of mRNA vaccines became clear in 2020, the few companies able to manufacture the requisite lipids were confronted with the challenge of scaling up production to respond to orders for several tons of lipids. In addition to non-viral delivery methods, RNA viruses have been engineered to achieve similar immunological responses. Typical RNA viruses used as vectors include retroviruses , lentiviruses , alphaviruses and rhabdoviruses , each of which can differ in structure and function. Clinical studies have utilized such viruses on a range of diseases in model animals such as mice , chicken and primates . mRNA vaccines offer specific advantages over traditional vaccines . Because mRNA vaccines are not constructed from an active pathogen (or even an inactivated pathogen), they are non-infectious. In contrast, traditional vaccines require the production of pathogens, which, if done at high volumes, could increase the risks of localized outbreaks of the virus at the production facility. Another biological advantage of mRNA vaccines is that since the antigens are produced inside the cell, they stimulate cellular immunity , as well as humoral immunity . mRNA vaccines have the production advantage that they can be designed swiftly. Moderna designed their mRNA-1273 vaccine for COVID-19 in 2 days. They can also be manufactured faster, more cheaply, and in a more standardized fashion (with fewer error rates in production), which can improve responsiveness to serious outbreaks. The Pfizer–BioNTech vaccine originally required 110 days to mass-produce (before Pfizer began to optimize the manufacturing process to only 60 days), which was substantially faster than traditional flu and polio vaccines. Within that larger timeframe, the actual production time is only about 22 days: two weeks for molecular cloning of DNA plasmids and purification of DNA, four days for DNA-to-RNA transcription and purification of mRNA, and four days to encapsulate mRNA in lipid nanoparticles followed by fill and finish . The majority of the days needed for each production run are allocated to rigorous quality control at each stage. In addition to sharing the advantages of theoretical DNA vaccines over established traditional vaccines , mRNA vaccines also have additional advantages over DNA vaccines. The mRNA is translated in the cytosol , so there is no need for the RNA to enter the cell nucleus , and the risk of being integrated into the host genome is averted. Modified nucleosides (for example, pseudouridines , 2'-O-methylated nucleosides) can be incorporated to mRNA to suppress immune response stimulation to avoid immediate degradation and produce a more persistent effect through enhanced translation capacity. The open reading frame (ORF) and untranslated regions (UTR) of mRNA can be optimized for different purposes (a process called sequence engineering of mRNA), for example through enriching the guanine-cytosine content or choosing specific UTRs known to increase translation. An additional ORF coding for a replication mechanism can be added to amplify antigen translation and therefore immune response, decreasing the amount of starting material needed. mRNA vaccines offer specific advantages over traditional vaccines . Because mRNA vaccines are not constructed from an active pathogen (or even an inactivated pathogen), they are non-infectious. In contrast, traditional vaccines require the production of pathogens, which, if done at high volumes, could increase the risks of localized outbreaks of the virus at the production facility. Another biological advantage of mRNA vaccines is that since the antigens are produced inside the cell, they stimulate cellular immunity , as well as humoral immunity . mRNA vaccines have the production advantage that they can be designed swiftly. Moderna designed their mRNA-1273 vaccine for COVID-19 in 2 days. They can also be manufactured faster, more cheaply, and in a more standardized fashion (with fewer error rates in production), which can improve responsiveness to serious outbreaks. The Pfizer–BioNTech vaccine originally required 110 days to mass-produce (before Pfizer began to optimize the manufacturing process to only 60 days), which was substantially faster than traditional flu and polio vaccines. Within that larger timeframe, the actual production time is only about 22 days: two weeks for molecular cloning of DNA plasmids and purification of DNA, four days for DNA-to-RNA transcription and purification of mRNA, and four days to encapsulate mRNA in lipid nanoparticles followed by fill and finish . The majority of the days needed for each production run are allocated to rigorous quality control at each stage. In addition to sharing the advantages of theoretical DNA vaccines over established traditional vaccines , mRNA vaccines also have additional advantages over DNA vaccines. The mRNA is translated in the cytosol , so there is no need for the RNA to enter the cell nucleus , and the risk of being integrated into the host genome is averted. Modified nucleosides (for example, pseudouridines , 2'-O-methylated nucleosides) can be incorporated to mRNA to suppress immune response stimulation to avoid immediate degradation and produce a more persistent effect through enhanced translation capacity. The open reading frame (ORF) and untranslated regions (UTR) of mRNA can be optimized for different purposes (a process called sequence engineering of mRNA), for example through enriching the guanine-cytosine content or choosing specific UTRs known to increase translation. An additional ORF coding for a replication mechanism can be added to amplify antigen translation and therefore immune response, decreasing the amount of starting material needed. Because mRNA is fragile, some vaccines must be kept at very low temperatures to avoid degrading and thus giving little effective immunity to the recipient. Pfizer–BioNTech's BNT162b2 mRNA vaccine has to be kept between −80 and −60 °C (−112 and −76 °F) . Moderna says their mRNA-1273 vaccine can be stored between −25 and −15 °C (−13 and 5 °F) , which is comparable to a home freezer, and that it remains stable between 2 and 8 °C (36 and 46 °F) for up to 30 days. In November 2020, Nature reported, "While it's possible that differences in LNP formulations or mRNA secondary structures could account for the thermostability differences [between Moderna and BioNtech], many experts suspect both vaccine products will ultimately prove to have similar storage requirements and shelf lives under various temperature conditions." Several platforms are being studied that may allow storage at higher temperatures. Before 2020, no mRNA technology platform (drug or vaccine) had been authorized for use in humans, so there was a risk of unknown effects. The 2020 COVID-19 pandemic required faster production capability of mRNA vaccines, made them attractive to national health organisations, and led to debate about the type of initial authorization mRNA vaccines should get (including emergency use authorization or expanded access authorization ) after the eight-week period of post-final human trials. Reactogenicity is similar to that of conventional, non-RNA vaccines. However, those susceptible to an autoimmune response may have an adverse reaction to mRNA vaccines. The mRNA strands in the vaccine may elicit an unintended immune reaction – this entails the body believing itself to be sick, and the person feeling as if they are as a result. To minimize this, mRNA sequences in mRNA vaccines are designed to mimic those produced by host cells. Strong but transient reactogenic effects were reported in trials of novel COVID-19 mRNA vaccines; most people will not experience severe side effects which include fever and fatigue. Severe side effects are defined as those that prevent daily activity. Because mRNA is fragile, some vaccines must be kept at very low temperatures to avoid degrading and thus giving little effective immunity to the recipient. Pfizer–BioNTech's BNT162b2 mRNA vaccine has to be kept between −80 and −60 °C (−112 and −76 °F) . Moderna says their mRNA-1273 vaccine can be stored between −25 and −15 °C (−13 and 5 °F) , which is comparable to a home freezer, and that it remains stable between 2 and 8 °C (36 and 46 °F) for up to 30 days. In November 2020, Nature reported, "While it's possible that differences in LNP formulations or mRNA secondary structures could account for the thermostability differences [between Moderna and BioNtech], many experts suspect both vaccine products will ultimately prove to have similar storage requirements and shelf lives under various temperature conditions." Several platforms are being studied that may allow storage at higher temperatures. Before 2020, no mRNA technology platform (drug or vaccine) had been authorized for use in humans, so there was a risk of unknown effects. The 2020 COVID-19 pandemic required faster production capability of mRNA vaccines, made them attractive to national health organisations, and led to debate about the type of initial authorization mRNA vaccines should get (including emergency use authorization or expanded access authorization ) after the eight-week period of post-final human trials. Reactogenicity is similar to that of conventional, non-RNA vaccines. However, those susceptible to an autoimmune response may have an adverse reaction to mRNA vaccines. The mRNA strands in the vaccine may elicit an unintended immune reaction – this entails the body believing itself to be sick, and the person feeling as if they are as a result. To minimize this, mRNA sequences in mRNA vaccines are designed to mimic those produced by host cells. Strong but transient reactogenic effects were reported in trials of novel COVID-19 mRNA vaccines; most people will not experience severe side effects which include fever and fatigue. Severe side effects are defined as those that prevent daily activity. The COVID-19 mRNA vaccines from Moderna and Pfizer–BioNTech have efficacy rates of 90 to 95 percent [ citation needed ] . Prior mRNA, drug trials on pathogens other than COVID-19 were not effective and had to be abandoned in the early phases of trials. The reason for the efficacy of the new mRNA vaccines is not clear. Physician-scientist Margaret Liu stated that the efficacy of the new COVID-19 mRNA vaccines could be due to the "sheer volume of resources" that went into development, or that the vaccines might be "triggering a nonspecific inflammatory response to the mRNA that could be heightening its specific immune response, given that the modified nucleoside technique reduced inflammation but hasn't eliminated it completely", and that "this may also explain the intense reactions such as aches and fevers reported in some recipients of the mRNA SARS-CoV-2 vaccines". These reactions though severe were transient and another view is that they were believed to be a reaction to the lipid drug delivery molecules. There is misinformation implying that mRNA vaccines could alter DNA in the nucleus. mRNA in the cytosol is very rapidly degraded before it would have time to gain entry into the cell nucleus. In fact, mRNA vaccines must be stored at very low temperature and free from RNAses to prevent mRNA degradation. Retrovirus can be single-stranded RNA (just as many SARS-CoV-2 vaccines are single-stranded RNA) which enters the cell nucleus and uses reverse transcriptase to make DNA from the RNA in the cell nucleus. A retrovirus has mechanisms to be imported into the nucleus, but other mRNA (such as the vaccine) lack these mechanisms. Once inside the nucleus, creation of DNA from RNA cannot occur without a reverse transcriptase and appropriate primers , which both accompany a retrovirus, but which would not be present for other exogenous mRNA (such as a vaccine) even if it could enter the nucleus. mRNA vaccines use either non-amplifying (conventional) mRNA or self-amplifying mRNA. Pfizer–BioNTech and Moderna vaccines use non-amplifying mRNA. Both mRNA types continue to be investigated as vaccine methods against other potential pathogens and cancer. The initial mRNA vaccines use a non-amplifying mRNA construct. Non-amplifying mRNA has only one open reading frame that codes for the antigen of interest. The total amount of mRNA available to the cell is equal to the amount delivered by the vaccine. Dosage strength is limited by the amount of mRNA that can be delivered by the vaccine. Non-amplifying vaccines replace uridine with N1-Methylpseudouridine in an attempt to reduce toxicity. Self-amplifying mRNA (saRNA) vaccines replicate their mRNA after transfection. Self-amplifying mRNA has two open reading frames . The first frame, like conventional mRNA, codes for the antigen of interest. The second frame codes for an RNA-dependent RNA polymerase (and its helper proteins) which replicates the mRNA construct in the cell. This allows smaller vaccine doses. The mechanisms and consequently the evaluation of self-amplifying mRNA may be different, as self-amplifying mRNA is a much bigger molecule. SaRNA vaccines being researched include a malaria vaccine . Gritstone bio started in 2021 a phase 1 trial of an saRNA COVID-19 vaccine, used as a booster vaccine . The vaccine is designed to target both the spike protein of the SARS‑CoV‑2 virus, and viral proteins that may be less prone to genetic variation, to provide greater protection against SARS‑CoV‑2 variants. saRNA vaccines must use uridine, which is required for reproduction to occur. The initial mRNA vaccines use a non-amplifying mRNA construct. Non-amplifying mRNA has only one open reading frame that codes for the antigen of interest. The total amount of mRNA available to the cell is equal to the amount delivered by the vaccine. Dosage strength is limited by the amount of mRNA that can be delivered by the vaccine. Non-amplifying vaccines replace uridine with N1-Methylpseudouridine in an attempt to reduce toxicity. Self-amplifying mRNA (saRNA) vaccines replicate their mRNA after transfection. Self-amplifying mRNA has two open reading frames . The first frame, like conventional mRNA, codes for the antigen of interest. The second frame codes for an RNA-dependent RNA polymerase (and its helper proteins) which replicates the mRNA construct in the cell. This allows smaller vaccine doses. The mechanisms and consequently the evaluation of self-amplifying mRNA may be different, as self-amplifying mRNA is a much bigger molecule. SaRNA vaccines being researched include a malaria vaccine . Gritstone bio started in 2021 a phase 1 trial of an saRNA COVID-19 vaccine, used as a booster vaccine . The vaccine is designed to target both the spike protein of the SARS‑CoV‑2 virus, and viral proteins that may be less prone to genetic variation, to provide greater protection against SARS‑CoV‑2 variants. saRNA vaccines must use uridine, which is required for reproduction to occur.

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Rift Valley fever

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List of abbreviations for diseases and disorders

This list contains acronyms and initials related to diseases (infectious or non-infectious) and medical disorders.

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Rift Valley fever

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Paramyxoviridae

Paramyxoviridae (from Greek para- "by the side of" and myxa " mucus ") is a family of negative-strand RNA viruses in the order Mononegavirales . Vertebrates serve as natural hosts. Diseases associated with this family include measles , mumps , and respiratory tract infections . The family has four subfamilies, 17 genera, three of which are unassigned to a subfamily, and 78 species. Virions are enveloped and can be spherical or pleomorphic and capable of producing filamentous virions. The diameter is around 150 nm. Genomes are linear, around 15kb in length. Fusion proteins and attachment proteins appear as spikes on the virion surface. Matrix proteins inside the envelope stabilise virus structure. The nucleocapsid core is composed of the genomic RNA, nucleocapsid proteins, phosphoproteins and polymerase proteins.The genome is nonsegmented, negative-sense RNA, 15–19 kilobases in length, and contains six to 10 genes. Extracistronic (noncoding) regions include: Each gene contains transcription start/stop signals at the beginning and end, which are transcribed as part of the gene. Gene sequence within the genome is conserved across the family due to a phenomenon known as transcriptional polarity (see Mononegavirales ) in which genes closest to the 3' end of the genome are transcribed in greater abundance than those towards the 5' end. This is a result of structure of the genome. After each gene is transcribed, the RNA-dependent RNA polymerase pauses to release the new mRNA when it encounters an intergenic sequence. When the RNA polymerase is paused, a chance exists that it will dissociate from the RNA genome. If it dissociates, it must re-enter the genome at the leader sequence, rather than continuing to transcribe the length of the genome. The result is that the further downstream genes are from the leader sequence, the less they will be transcribed by RNA polymerase. Evidence for a single promoter model was verified when viruses were exposed to UV light. UV radiation can cause dimerization of RNA, which prevents transcription by RNA polymerase. If the viral genome follows a multiple promoter model, the level inhibition of transcription should correlate with the length of the RNA gene. However, the genome was best described by a single promoter model. When paramyxovirus genome was exposed to UV light, the level of inhibition of transcription was proportional to the distance from the leader sequence. That is, the further the gene is from the leader sequence, the greater the chance of RNA dimerization inhibiting RNA polymerase. The virus takes advantage of the single promoter model by having its genes arranged in relative order of protein needed for successful infection. For example, nucleocapsid protein, N, is needed in greater amounts than RNA polymerase, L. Viruses in the Paramyxoviridae family are also antigenically stable, meaning that the glycoproteins on the viruses are consistent between different strains of the same type. Two reasons for this phenomenon are posited: The first is that the genome is nonsegmented, thus cannot undergo genetic reassortment . For this process to occur, segments needed as reassortment happen when segments from different strains are mixed together to create a new strain. With no segments, nothing can be mixed with one another, so no antigenic shift occurs. The second reason relates to the idea of antigenic drift . Since RNA-dependent RNA polymerase does not have an error-checking function, many mutations are made when the RNA is processed. These mutations build up and eventually new strains are created. Due to this concept, one would expect that paramyxoviruses should not be antigenically stable; however, the opposite is seen to be true. The main hypothesis behind why the viruses are antigenically stable is that each protein and amino acid has an important function. Thus, any mutation would lead to a decrease or total loss of function, which would in turn cause the new virus to be less efficient. These viruses would not be able to survive as long compared to the more virulent strains, and so would die out. Many paramyxovirus genomes follow the "rule of six" . The total length of the genome is almost always a multiple of six. This is probably due to the advantage of having all RNA bound by N protein (since N binds hexamers of RNA). If RNA is left exposed, the virus does not replicate efficiently. The gene sequence is: Nucleocapsid – phosphoprotein – matrix – fusion – attachment – large (polymerase)Viral replication is cytoplasmic . Entry into the host cell is achieved by viral attachment to host cell. Replication and transcription follow the negative-stranded RNA virus models. Translation takes place by leaky scanning, ribosomal shunting , and RNA termination-reinitiation. The virus exits the host cell by budding. Vertebrates, including humans and birds serve as the natural hosts. Transmission route is airborne particles. The Paramyxoviridae are able to undergo mRNA editing, which produces different proteins from the same mRNA transcript by slipping back one base to read off in a different open reading frame ( ORF ) due to the presence of secondary structures such as pseudoknots. Paramyxoviridae also undergo transcriptional stuttering to produce the poly (A) tail at the end of mRNA transcripts by repeatedly moving back one nucleotide at a time at the end of the RNA template. Family: Paramyxoviridae A number of important human diseases are caused by paramyxoviruses. These include mumps , as well as measles , which caused around 733,000 deaths in 2000. The human parainfluenza viruses (HPIV) are the second most common causes of respiratory tract disease in infants and children. There are four types of HPIVs, known as HPIV-1, HPIV-2, HPIV-3 and HPIV-4. HPIV-1 and HPIV-2 may cause cold-like symptoms, along with croup in children. HPIV-3 is associated with bronchiolitis , bronchitis , and pneumonia . HPIV-4 is less common than the other types, and is known to cause mild to severe respiratory tract illnesses. Paramyxoviruses are also responsible for a range of diseases in other animal species, for example canine distemper virus ( dogs ), phocine distemper virus ( seals ), cetacean morbillivirus ( dolphins and porpoises ), Newcastle disease virus ( birds ), and rinderpest virus ( cattle ). Some paramyxoviruses, such as the henipaviruses , are zoonotic pathogens, occurring naturally in an animal host, but also able to infect humans. Hendra virus and Nipah virus in the genus Henipavirus have emerged in humans and livestock in Australia and Southeast Asia . Both viruses are contagious , highly virulent , and capable of infecting a number of mammalian species and causing potentially fatal disease. Due to the lack of either a licensed human vaccine (a Hendra virus vaccine exists for horses) or antiviral therapies, Hendra virus and Nipah virus are designated as Biosafety level (BSL) 4 agents. The genomic structure of both viruses is that of a typical paramyxovirus. In the past few decades, [ when? ] paramyxoviruses have been discovered from terrestrial, volant , and aquatic animals, demonstrating a vast host range and great viral genetic diversity. As molecular technology advances and viral surveillance programs are implemented, the discovery of new viruses in this group is increasing. The evolution of paramyxoviruses is still debated. Using pneumoviruses (mononegaviral family Pneumoviridae ) as an outgroup, paramyxoviruses can be divided into two clades: one consisting of avulaviruses and rubulaviruses and one consisting of respiroviruses , henipaviruses , and morbilliviruses . Within the second clade the respiroviruses appear to be the basal group. The respirovirus-henipavirus-morbillivirus clade may be basal to the avulavirus-rubulavirus clade.

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SARS-CoV-2

2019-nCoV Severe acute respiratory syndrome coronavirus 2 ( SARS‑CoV‑2 ) is a strain of coronavirus that causes COVID-19 , the respiratory illness responsible for the COVID-19 pandemic . The virus previously had the provisional name 2019 novel coronavirus ( 2019-nCoV ), and has also been called human coronavirus 2019 ( HCoV-19 or hCoV-19 ). First identified in the city of Wuhan , Hubei, China, the World Health Organization designated the outbreak a public health emergency of international concern from January 30, 2020, to May 5, 2023. SARS‑CoV‑2 is a positive-sense single-stranded RNA virus that is contagious in humans. SARS‑CoV‑2 is a strain of the species severe-acute-respiratory-syndrome-related coronavirus (SARSr-CoV), as is SARS-CoV-1 , the virus that caused the 2002–2004 SARS outbreak . There are animal-borne coronavirus strains more closely related to SARS-CoV-2, the most closely known relative being the BANAL-52 bat coronavirus. SARS-CoV-2 is of zoonotic origin; its close genetic similarity to bat coronaviruses suggests it emerged from such a bat-borne virus . Research is ongoing as to whether SARS‑CoV‑2 came directly from bats or indirectly through any intermediate hosts. The virus shows little genetic diversity , indicating that the spillover event introducing SARS‑CoV‑2 to humans is likely to have occurred in late 2019. Epidemiological studies estimate that in the period between December 2019 and September 2020 each infection resulted in an average of 2.4–3.4 new infections when no members of the community were immune and no preventive measures were taken. However, some subsequent variants have become more infectious. The virus is airborne and primarily spreads between people through close contact and via aerosols and respiratory droplets that are exhaled when talking, breathing, or otherwise exhaling, as well as those produced from coughs and sneezes. It enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane protein that regulates the renin–angiotensin system. During the initial outbreak in Wuhan , China, various names were used for the virus; some names used by different sources included "the coronavirus" or "Wuhan coronavirus". In January 2020, the World Health Organization (WHO) recommended "2019 novel coronavirus" (2019-nCoV) as the provisional name for the virus. This was in accordance with WHO's 2015 guidance against using geographical locations, animal species, or groups of people in disease and virus names. On 11 February 2020, the International Committee on Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS‑CoV‑2). To avoid confusion with the disease SARS , the WHO sometimes refers to SARS‑CoV‑2 as "the COVID-19 virus" in public health communications and the name HCoV-19 was included in some research articles. Referring to COVID-19 as the "Wuhan virus" has been described as dangerous by WHO officials, and as xenophobic by many journalists and academics. Human-to-human transmission of SARS‑CoV‑2 was confirmed on 20 January 2020 during the COVID-19 pandemic . Transmission was initially assumed to occur primarily via respiratory droplets from coughs and sneezes within a range of about 1.8 metres (6 ft) . Laser light scattering experiments suggest that speaking is an additional mode of transmission and a far-reaching one, indoors, with little air flow. Other studies have suggested that the virus may be airborne as well, with aerosols potentially being able to transmit the virus. During human-to-human transmission, between 200 and 800 infectious SARS‑CoV‑2 virions are thought to initiate a new infection. If confirmed, aerosol transmission has biosafety implications because a major concern associated with the risk of working with emerging viruses in the laboratory is the generation of aerosols from various laboratory activities which are not immediately recognizable and may affect other scientific personnel. Indirect contact via contaminated surfaces is another possible cause of infection. Preliminary research indicates that the virus may remain viable on plastic ( polypropylene ) and stainless steel ( AISI 304 ) for up to three days, but it does not survive on cardboard for more than one day or on copper for more than four hours. The virus is inactivated by soap, which destabilizes its lipid bilayer . Viral RNA has also been found in stool samples and semen from infected individuals. The degree to which the virus is infectious during the incubation period is uncertain, but research has indicated that the pharynx reaches peak viral load approximately four days after infection or in the first week of symptoms and declines thereafter. The duration of SARS-CoV-2 RNA shedding is generally between 3 and 46 days after symptom onset. A study by a team of researchers from the University of North Carolina found that the nasal cavity is seemingly the dominant initial site of infection, with subsequent aspiration -mediated virus-seeding into the lungs in SARS‑CoV‑2 pathogenesis. They found that there was an infection gradient from high in proximal towards low in distal pulmonary epithelial cultures, with a focal infection in ciliated cells and type 2 pneumocytes in the airway and alveolar regions respectively. Studies have identified a range of animals—such as cats, ferrets, hamsters, non-human primates, minks, tree shrews, raccoon dogs, fruit bats, and rabbits—that are susceptible and permissive to SARS-CoV-2 infection. Some institutions have advised that those infected with SARS‑CoV‑2 restrict their contact with animals. On 1 February 2020, the World Health Organization (WHO) indicated that "transmission from asymptomatic cases is likely not a major driver of transmission". One meta-analysis found that 17% of infections are asymptomatic, and asymptomatic individuals were 42% less likely to transmit the virus. However, an epidemiological model of the beginning of the outbreak in China suggested that "pre-symptomatic shedding may be typical among documented infections" and that subclinical infections may have been the source of a majority of infections. That may explain how out of 217 on board a cruise liner that docked at Montevideo , only 24 of 128 who tested positive for viral RNA showed symptoms. Similarly, a study of ninety-four patients hospitalized in January and February 2020 estimated patients began shedding virus two to three days before symptoms appear and that "a substantial proportion of transmission probably occurred before first symptoms in the index case ". The authors later published a correction that showed that shedding began earlier than first estimated, four to five days before symptoms appear. There is uncertainty about reinfection and long-term immunity. It is not known how common reinfection is, but reports have indicated that it is occurring with variable severity. The first reported case of reinfection was a 33-year-old man from Hong Kong who first tested positive on 26 March 2020, was discharged on 15 April 2020 after two negative tests, and tested positive again on 15 August 2020 (142 days later), which was confirmed by whole-genome sequencing showing that the viral genomes between the episodes belong to different clades . The findings had the implications that herd immunity may not eliminate the virus if reinfection is not an uncommon occurrence and that vaccines may not be able to provide lifelong protection against the virus. Another case study described a 25-year-old man from Nevada who tested positive for SARS‑CoV‑2 on 18 April 2020 and on 5 June 2020 (separated by two negative tests). Since genomic analyses showed significant genetic differences between the SARS‑CoV‑2 variant sampled on those two dates, the case study authors determined this was a reinfection. The man's second infection was symptomatically more severe than the first infection, but the mechanisms that could account for this are not known. On 1 February 2020, the World Health Organization (WHO) indicated that "transmission from asymptomatic cases is likely not a major driver of transmission". One meta-analysis found that 17% of infections are asymptomatic, and asymptomatic individuals were 42% less likely to transmit the virus. However, an epidemiological model of the beginning of the outbreak in China suggested that "pre-symptomatic shedding may be typical among documented infections" and that subclinical infections may have been the source of a majority of infections. That may explain how out of 217 on board a cruise liner that docked at Montevideo , only 24 of 128 who tested positive for viral RNA showed symptoms. Similarly, a study of ninety-four patients hospitalized in January and February 2020 estimated patients began shedding virus two to three days before symptoms appear and that "a substantial proportion of transmission probably occurred before first symptoms in the index case ". The authors later published a correction that showed that shedding began earlier than first estimated, four to five days before symptoms appear. There is uncertainty about reinfection and long-term immunity. It is not known how common reinfection is, but reports have indicated that it is occurring with variable severity. The first reported case of reinfection was a 33-year-old man from Hong Kong who first tested positive on 26 March 2020, was discharged on 15 April 2020 after two negative tests, and tested positive again on 15 August 2020 (142 days later), which was confirmed by whole-genome sequencing showing that the viral genomes between the episodes belong to different clades . The findings had the implications that herd immunity may not eliminate the virus if reinfection is not an uncommon occurrence and that vaccines may not be able to provide lifelong protection against the virus. Another case study described a 25-year-old man from Nevada who tested positive for SARS‑CoV‑2 on 18 April 2020 and on 5 June 2020 (separated by two negative tests). Since genomic analyses showed significant genetic differences between the SARS‑CoV‑2 variant sampled on those two dates, the case study authors determined this was a reinfection. The man's second infection was symptomatically more severe than the first infection, but the mechanisms that could account for this are not known. No natural reservoir for SARS-CoV-2 has been identified. Prior to the emergence of SARS-CoV-2 as a pathogen infecting humans, there had been two previous zoonosis -based coronavirus epidemics, those caused by SARS-CoV-1 and MERS-CoV . The first known infections from SARS‑CoV‑2 were discovered in Wuhan, China. The original source of viral transmission to humans remains unclear, as does whether the virus became pathogenic before or after the spillover event . Because many of the early infectees were workers at the Huanan Seafood Market , it has been suggested that the virus might have originated from the market. However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid expansion of the infections. A March 2021 WHO-convened report stated that human spillover via an intermediate animal host was the most likely explanation, with direct spillover from bats next most likely. Introduction through the food supply chain and the Huanan Seafood Market was considered another possible, but less likely, explanation. An analysis in November 2021, however, said that the earliest-known case had been misidentified and that the preponderance of early cases linked to the Huanan Market argued for it being the source. For a virus recently acquired through a cross-species transmission, rapid evolution is expected. The mutation rate estimated from early cases of SARS-CoV-2 was of 6.54 × 10 −4 per site per year. Coronaviruses in general have high genetic plasticity , but SARS-CoV-2's viral evolution is slowed by the RNA proofreading capability of its replication machinery. For comparison, the viral mutation rate in vivo of SARS-CoV-2 has been found to be lower than that of influenza. Research into the natural reservoir of the virus that caused the 2002–2004 SARS outbreak has resulted in the discovery of many SARS-like bat coronaviruses , most originating in horseshoe bats . The closest match by far, published in Nature (journal) in February 2022, were viruses BANAL-52 (96.8% resemblance to SARS‑CoV‑2), BANAL-103 and BANAL-236, collected in three different species of bats in Feuang , Laos. An earlier source published in February 2020 identified the virus RaTG13 , collected in bats in Mojiang , Yunnan, China to be the closest to SARS‑CoV‑2, with 96.1% resemblance. None of the above are its direct ancestor. Bats are considered the most likely natural reservoir of SARS‑CoV‑2. Differences between the bat coronavirus and SARS‑CoV‑2 suggest that humans may have been infected via an intermediate host; although the source of introduction into humans remains unknown. Although the role of pangolins as an intermediate host was initially posited (a study published in July 2020 suggested that pangolins are an intermediate host of SARS‑CoV‑2-like coronaviruses ), subsequent studies have not substantiated their contribution to the spillover. Evidence against this hypothesis includes the fact that pangolin virus samples are too distant to SARS-CoV-2: isolates obtained from pangolins seized in Guangdong were only 92% identical in sequence to the SARS‑CoV‑2 genome (matches above 90 percent may sound high, but in genomic terms it is a wide evolutionary gap ). In addition, despite similarities in a few critical amino acids, pangolin virus samples exhibit poor binding to the human ACE2 receptor. SARS‑CoV‑2 belongs to the broad family of viruses known as coronaviruses . It is a positive-sense single-stranded RNA (+ssRNA) virus, with a single linear RNA segment. Coronaviruses infect humans, other mammals, including livestock and companion animals, and avian species. Human coronaviruses are capable of causing illnesses ranging from the common cold to more severe diseases such as Middle East respiratory syndrome (MERS, fatality rate ~34%). SARS-CoV-2 is the seventh known coronavirus to infect people, after 229E , NL63 , OC43 , HKU1 , MERS-CoV , and the original SARS-CoV . Like the SARS-related coronavirus implicated in the 2003 SARS outbreak, SARS‑CoV‑2 is a member of the subgenus Sarbecovirus ( beta-CoV lineage B). Coronaviruses undergo frequent recombination. The mechanism of recombination in unsegmented RNA viruses such as SARS-CoV-2 is generally by copy-choice replication, in which gene material switches from one RNA template molecule to another during replication. The SARS-CoV-2 RNA sequence is approximately 30,000 bases in length, relatively long for a coronavirus—which in turn carry the largest genomes among all RNA families. Its genome consists nearly entirely of protein-coding sequences, a trait shared with other coronaviruses. A distinguishing feature of SARS‑CoV‑2 is its incorporation of a polybasic site cleaved by furin , which appears to be an important element enhancing its virulence. It was suggested that the acquisition of the furin-cleavage site in the SARS-CoV-2 S protein was essential for zoonotic transfer to humans. The furin protease recognizes the canonical peptide sequence R X[ R / K ] R ↓X where the cleavage site is indicated by a down arrow and X is any amino acid . In SARS-CoV-2 the recognition site is formed by the incorporated 12 codon nucleotide sequence CCT CGG CGG GCA which corresponds to the amino acid sequence P RR A . This sequence is upstream of an arginine and serine which forms the S1/S2 cleavage site ( P RR A R ↓ S ) of the spike protein. Although such sites are a common naturally-occurring feature of other viruses within the Subfamily Orthocoronavirinae, it appears in few other viruses from the Beta-CoV genus, and it is unique among members of its subgenus for such a site. The furin cleavage site PRRAR↓ is highly similar to that of the feline coronavirus , an alphacoronavirus 1 strain. Viral genetic sequence data can provide critical information about whether viruses separated by time and space are likely to be epidemiologically linked. With a sufficient number of sequenced genomes , it is possible to reconstruct a phylogenetic tree of the mutation history of a family of viruses. By 12 January 2020, five genomes of SARS‑CoV‑2 had been isolated from Wuhan and reported by the Chinese Center for Disease Control and Prevention (CCDC) and other institutions; the number of genomes increased to 42 by 30 January 2020. A phylogenetic analysis of those samples showed they were "highly related with at most seven mutations relative to a common ancestor ", implying that the first human infection occurred in November or December 2019. Examination of the topology of the phylogenetic tree at the start of the pandemic also found high similarities between human isolates. As of 21 August 2021 , [ update ] 3,422 SARS‑CoV‑2 genomes, belonging to 19 strains, sampled on all continents except Antarctica were publicly available. On 11 February 2020, the International Committee on Taxonomy of Viruses announced that according to existing rules that compute hierarchical relationships among coronaviruses based on five conserved sequences of nucleic acids, the differences between what was then called 2019-nCoV and the virus from the 2003 SARS outbreak were insufficient to make them separate viral species . Therefore, they identified 2019-nCoV as a virus of Severe acute respiratory syndrome–related coronavirus . In July 2020, scientists reported that a more infectious SARS‑CoV‑2 variant with spike protein variant G614 has replaced D614 as the dominant form in the pandemic. Coronavirus genomes and subgenomes encode six open reading frames (ORFs). In October 2020, researchers discovered a possible overlapping gene named ORF3d , in the SARS‑CoV‑2 genome . It is unknown if the protein produced by ORF3d has any function, but it provokes a strong immune response. ORF3d has been identified before, in a variant of coronavirus that infects pangolins . A phylogenetic tree based on whole-genome sequences of SARS-CoV-2 and related coronaviruses is: ( Bat ) Rc-o319 , 81% to SARS-CoV-2, Rhinolophus cornutus , Iwate , Japan Bat SL-ZXC21 , 88% to SARS-CoV-2, Rhinolophus pusillus , Zhoushan , Zhejiang Bat SL-ZC45 , 88% to SARS-CoV-2, Rhinolophus pusillus , Zhoushan, Zhejiang Pangolin SARSr-CoV-GX, 85.3% to SARS-CoV-2, Manis javanica , smuggled from Southeast Asia Pangolin SARSr-CoV-GD, 90.1% to SARS-CoV-2, Manis javanica , smuggled from Southeast Asia Bat RshSTT182, 92.6% to SARS-CoV-2, Rhinolophus shameli , Steung Treng , Cambodia Bat RshSTT200, 92.6% to SARS-CoV-2, Rhinolophus shameli , Steung Treng, Cambodia (Bat) RacCS203 , 91.5% to SARS-CoV-2, Rhinolophus acuminatus , Chachoengsao , Thailand (Bat) RmYN02 , 93.3% to SARS-CoV-2, Rhinolophus malayanus , Mengla , Yunnan (Bat) RpYN06 , 94.4% to SARS-CoV-2, Rhinolophus pusillus , Xishuangbanna , Yunnan (Bat) RaTG13 , 96.1% to SARS-CoV-2, Rhinolophus affinis , Mojiang , Yunnan (Bat) BANAL-52 , 96.8% to SARS-CoV-2, Rhinolophus malayanus , Vientiane , Laos SARS-CoV-2 SARS-CoV-1 , 79% to SARS-CoV-2 There are many thousands of variants of SARS-CoV-2, which can be grouped into the much larger clades . Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR). Several notable variants of SARS-CoV-2 emerged in late 2020. The World Health Organization has currently declared five variants of concern , which are as follows: Other notable variants include 6 other WHO-designated variants under investigation and Cluster 5 , which emerged among mink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct. A phylogenetic tree based on whole-genome sequences of SARS-CoV-2 and related coronaviruses is: ( Bat ) Rc-o319 , 81% to SARS-CoV-2, Rhinolophus cornutus , Iwate , Japan Bat SL-ZXC21 , 88% to SARS-CoV-2, Rhinolophus pusillus , Zhoushan , Zhejiang Bat SL-ZC45 , 88% to SARS-CoV-2, Rhinolophus pusillus , Zhoushan, Zhejiang Pangolin SARSr-CoV-GX, 85.3% to SARS-CoV-2, Manis javanica , smuggled from Southeast Asia Pangolin SARSr-CoV-GD, 90.1% to SARS-CoV-2, Manis javanica , smuggled from Southeast Asia Bat RshSTT182, 92.6% to SARS-CoV-2, Rhinolophus shameli , Steung Treng , Cambodia Bat RshSTT200, 92.6% to SARS-CoV-2, Rhinolophus shameli , Steung Treng, Cambodia (Bat) RacCS203 , 91.5% to SARS-CoV-2, Rhinolophus acuminatus , Chachoengsao , Thailand (Bat) RmYN02 , 93.3% to SARS-CoV-2, Rhinolophus malayanus , Mengla , Yunnan (Bat) RpYN06 , 94.4% to SARS-CoV-2, Rhinolophus pusillus , Xishuangbanna , Yunnan (Bat) RaTG13 , 96.1% to SARS-CoV-2, Rhinolophus affinis , Mojiang , Yunnan (Bat) BANAL-52 , 96.8% to SARS-CoV-2, Rhinolophus malayanus , Vientiane , Laos SARS-CoV-2 SARS-CoV-1 , 79% to SARS-CoV-2 There are many thousands of variants of SARS-CoV-2, which can be grouped into the much larger clades . Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR). Several notable variants of SARS-CoV-2 emerged in late 2020. The World Health Organization has currently declared five variants of concern , which are as follows: Other notable variants include 6 other WHO-designated variants under investigation and Cluster 5 , which emerged among mink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct. There are many thousands of variants of SARS-CoV-2, which can be grouped into the much larger clades . Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR). Several notable variants of SARS-CoV-2 emerged in late 2020. The World Health Organization has currently declared five variants of concern , which are as follows: Other notable variants include 6 other WHO-designated variants under investigation and Cluster 5 , which emerged among mink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct. Each SARS-CoV-2 virion is 60–140 nanometres (2.4 × 10 −6 –5.5 × 10 −6 in) in diameter; its mass within the global human populace has been estimated as being between 0.1 and 10 kilograms. Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S ( spike ), E ( envelope ), M ( membrane ), and N ( nucleocapsid ) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create the viral envelope . Coronavirus S proteins are glycoproteins and also type I membrane proteins (membranes containing a single transmembrane domain oriented on the extracellular side). They are divided into two functional parts (S1 and S2). In SARS-CoV-2, the spike protein, which has been imaged at the atomic level using cryogenic electron microscopy , is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell; specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion. As of early 2022, about 7 million SARS-CoV-2 genomes had been sequenced and deposited into public databases and another 800,000 or so were added each month. By September 2023, the GISAID EpiCoV database contained more than 16 million genome sequences. SARS-CoV-2 has a linear, positive-sense , single-stranded RNA genome about 30,000 bases long. Its genome has a bias against cytosine (C) and guanine (G) nucleotides , like other coronaviruses. The genome has the highest composition of U (32.2%), followed by A (29.9%), and a similar composition of G (19.6%) and C (18.3%). The nucleotide bias arises from the mutation of guanines and cytosines to adenosines and uracils , respectively. The mutation of CG dinucleotides is thought to arise to avoid the zinc finger antiviral protein related defense mechanism of cells, and to lower the energy to unbind the genome during replication and translation (adenosine and uracil base pair via two hydrogen bonds , cytosine and guanine via three). The depletion of CG dinucleotides in its genome has led the virus to have a noticeable codon usage bias . For instance, arginine's six different codons have a relative synonymous codon usage of AGA (2.67), CGU (1.46), AGG (.81), CGC (.58), CGA (.29), and CGG (.19). A similar codon usage bias trend is seen in other SARS–related coronaviruses. Virus infections start when viral particles bind to host surface cellular receptors. Protein modeling experiments on the spike protein of the virus soon suggested that SARS‑CoV‑2 has sufficient affinity to the receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism of cell entry . By 22 January 2020, a group in China working with the full virus genome and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS‑CoV‑2. Studies have shown that SARS‑CoV‑2 has a higher affinity to human ACE2 than the original SARS virus. SARS‑CoV‑2 may also use basigin to assist in cell entry. Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS‑CoV‑2. The host protein neuropilin 1 (NRP1) may aid the virus in host cell entry using ACE2. After a SARS‑CoV‑2 virion attaches to a target cell, the cell's TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host receptor ACE2. After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin , a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus , which infect more cells. SARS‑CoV‑2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response . Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020). Each SARS-CoV-2 virion is 60–140 nanometres (2.4 × 10 −6 –5.5 × 10 −6 in) in diameter; its mass within the global human populace has been estimated as being between 0.1 and 10 kilograms. Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S ( spike ), E ( envelope ), M ( membrane ), and N ( nucleocapsid ) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create the viral envelope . Coronavirus S proteins are glycoproteins and also type I membrane proteins (membranes containing a single transmembrane domain oriented on the extracellular side). They are divided into two functional parts (S1 and S2). In SARS-CoV-2, the spike protein, which has been imaged at the atomic level using cryogenic electron microscopy , is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell; specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion. As of early 2022, about 7 million SARS-CoV-2 genomes had been sequenced and deposited into public databases and another 800,000 or so were added each month. By September 2023, the GISAID EpiCoV database contained more than 16 million genome sequences. SARS-CoV-2 has a linear, positive-sense , single-stranded RNA genome about 30,000 bases long. Its genome has a bias against cytosine (C) and guanine (G) nucleotides , like other coronaviruses. The genome has the highest composition of U (32.2%), followed by A (29.9%), and a similar composition of G (19.6%) and C (18.3%). The nucleotide bias arises from the mutation of guanines and cytosines to adenosines and uracils , respectively. The mutation of CG dinucleotides is thought to arise to avoid the zinc finger antiviral protein related defense mechanism of cells, and to lower the energy to unbind the genome during replication and translation (adenosine and uracil base pair via two hydrogen bonds , cytosine and guanine via three). The depletion of CG dinucleotides in its genome has led the virus to have a noticeable codon usage bias . For instance, arginine's six different codons have a relative synonymous codon usage of AGA (2.67), CGU (1.46), AGG (.81), CGC (.58), CGA (.29), and CGG (.19). A similar codon usage bias trend is seen in other SARS–related coronaviruses. Virus infections start when viral particles bind to host surface cellular receptors. Protein modeling experiments on the spike protein of the virus soon suggested that SARS‑CoV‑2 has sufficient affinity to the receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism of cell entry . By 22 January 2020, a group in China working with the full virus genome and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS‑CoV‑2. Studies have shown that SARS‑CoV‑2 has a higher affinity to human ACE2 than the original SARS virus. SARS‑CoV‑2 may also use basigin to assist in cell entry. Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS‑CoV‑2. The host protein neuropilin 1 (NRP1) may aid the virus in host cell entry using ACE2. After a SARS‑CoV‑2 virion attaches to a target cell, the cell's TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host receptor ACE2. After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin , a host cysteine protease, cleaves it. The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus , which infect more cells. SARS‑CoV‑2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response . Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020). Very few drugs are known to effectively inhibit SARS‑CoV‑2. Masitinib is a clinically safe drug and was recently found to inhibit its main protease , 3CLpro and showed >200-fold reduction in viral titers in the lungs and nose in mice. However, it is not approved for the treatment of COVID-19 in humans as of August 2021. [ needs update ] In December 2021, the United States granted emergency use authorization to Nirmatrelvir/ritonavir for the treatment of the virus; the European Union , United Kingdom , and Canada followed suit with full authorization soon after. One study found that Nirmatrelvir/ritonavir reduced the risk of hospitalization and death by 88%. COVID Moonshot is an international collaborative open-science project started in March 2020 with the goal of developing an un- patented oral antiviral drug for treatment of SARS-CoV-2. Retrospective tests collected within the Chinese surveillance system revealed no clear indication of substantial unrecognized circulation of SARS‑CoV‑2 in Wuhan during the latter part of 2019. A meta-analysis from November 2020 estimated the basic reproduction number ( R 0 {\displaystyle R_{0}} ) of the virus to be between 2.39 and 3.44. This means each infection from the virus is expected to result in 2.39 to 3.44 new infections when no members of the community are immune and no preventive measures are taken. The reproduction number may be higher in densely populated conditions such as those found on cruise ships . Human behavior affects the R0 value and hence estimates of R0 differ between different countries, cultures, and social norms. For instance, one study found relatively low R0 (~3.5) in Sweden, Belgium and the Netherlands, while Spain and the US had significantly higher R0 values (5.9 to 6.4, respectively). There have been about 96,000 confirmed cases of infection in mainland China. While the proportion of infections that result in confirmed cases or progress to diagnosable disease remains unclear, one mathematical model estimated that 75,815 people were infected on 25 January 2020 in Wuhan alone, at a time when the number of confirmed cases worldwide was only 2,015. Before 24 February 2020, over 95% of all deaths from COVID-19 worldwide had occurred in Hubei province , where Wuhan is located. As of 10 March 2023 , the percentage had decreased to 0.047% . As of 10 March 2023 , there were 676,609,955 total confirmed cases of SARS‑CoV‑2 infection. The total number of deaths attributed to the virus was 6,881,955 .

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Rift Valley fever

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Eastern equine encephalitis

Eastern equine encephalitis ( EEE ), commonly called Triple E or sleeping sickness (not to be confused with African trypanosomiasis ), is a disease caused by a zoonotic mosquito-vectored Togavirus that is present in North, Central, and South America, and the Caribbean. EEE was first recognized in Massachusetts , United States, in 1831, when 75 horses died mysteriously of viral encephalitis . Epizootics in horses have continued to occur regularly in the United States. It can also be identified in donkeys and zebras. Due to the rarity of the disease, its occurrence can cause economic impact beyond the cost of horses and poultry. EEE is found today in the eastern part of the United States and is often associated with coastal plains. It can most commonly be found in East Coast and Gulf Coast states. In Florida, about one to two human cases are reported a year, although over 60 cases of equine encephalitis are reported. In years in which conditions are favorable for the disease, the number of equine cases is over 200. Diagnosing equine encephalitis is challenging because many of the symptoms are shared with other illnesses and patients can be asymptomatic. Confirmations may require a sample of cerebral spinal fluid or brain tissue, although CT scans and MRI scans are used to detect encephalitis. This could be an indication that the need to test for EEE is necessary. If a biopsy of the cerebral spinal fluid is taken, it is sent to a specialized laboratory for testing. Eastern equine encephalitis virus (EEEV) is closely related to Venezuelan equine encephalitis virus and western equine encephalitis virus .The incubation period for Eastern equine encephalitis virus (EEEV) disease ranges from 4 to 10 days. The illness can progress either systematically or encephalitically, depending on the person's age. Encephalitic disease involves swelling of the brain and can be asymptomatic, while the systemic illness occurs very abruptly. Those with the systemic illness usually recover within 1–2 weeks. While the encephalitis is more common among infants, in adults and children, it usually manifests after experiencing the systemic illness. Symptoms include high fever , muscle pain , altered mental status , headache , meningeal irritation, photophobia , and seizures , which occur 3–10 days after the bite of an infected mosquito . Due to the virus's effect on the brain, patients who survive can be left with mental and physical impairments, such as personality disorders, paralysis, seizures, and intellectual impairment. The causative agent, later identified as a togavirus , was first isolated from infected horse brains in 1933. In 1938, the first confirmed human cases were identified when 30 children died of encephalitis in the Northeastern United States. These cases coincided with outbreaks in horses in the same regions. The fatality rate in humans is 33%, and currently no cure is known for human infections. This virus has four variations in the types in lineage. The most common to the human disease is group 1, which is considered to be endemic in North America and the Caribbean, while the other three lineages, groups IIA, IIB, and III, are typically found in Central and South America, causing equine illness. These two clades may actually be distinct viruses. The North American strains appear to be monotypic with a mutation rate of 2.7 × 10 −4 substitutions/site/year (s/s/y). It appears to have diverged from the other strains 922 to 4,856 years ago. The other strains are divided into two main clades and a third smaller one. The two main clades diverged between 577 and 2,927 years ago. The mutation rate in the genome has been estimated to be 1.2 × 10 −4 s/s/y. [ citation needed ] EEEV is capable of infecting a wide range of animals, including mammals , birds , reptiles , and amphibians . The virus is maintained in nature through a bird — mosquito cycle. Two mosquito species are primarily involved in this portion of the cycle; they are Culiseta melanura and Culiseta morsitans [ Wikidata ] . These mosquitoes feed on the blood of birds. The frequency of the virus found in nature increases throughout the summer as more birds and more mosquitoes become infected. [ citation needed ] Transmission of EEEV to mammals (including humans) occurs via other mosquito species, which feed on the blood of both birds and mammals. These other mosquitoes are referred to as "bridge vectors" because they carry the virus from the avian hosts to other types of hosts, particularly mammals. The bridge vectors include Aedes taeniorhynchus , Aedes vexans , Coquillettidia perturbans , Ochlerotatus canadensis , and Ochlerotatus sollicitans . Ochlerotatus canadensis also frequently bites turtles. [ citation needed ] Humans, horses, and most other infected mammals do not circulate enough viruses in their blood to infect additional mosquitoes. Some cases of EEE have been contracted through laboratory exposures or from exposure of the eyes, lungs, or skin wounds to brain or spinal cord matter from infected animals. [ citation needed ]The causative agent, later identified as a togavirus , was first isolated from infected horse brains in 1933. In 1938, the first confirmed human cases were identified when 30 children died of encephalitis in the Northeastern United States. These cases coincided with outbreaks in horses in the same regions. The fatality rate in humans is 33%, and currently no cure is known for human infections. This virus has four variations in the types in lineage. The most common to the human disease is group 1, which is considered to be endemic in North America and the Caribbean, while the other three lineages, groups IIA, IIB, and III, are typically found in Central and South America, causing equine illness. These two clades may actually be distinct viruses. The North American strains appear to be monotypic with a mutation rate of 2.7 × 10 −4 substitutions/site/year (s/s/y). It appears to have diverged from the other strains 922 to 4,856 years ago. The other strains are divided into two main clades and a third smaller one. The two main clades diverged between 577 and 2,927 years ago. The mutation rate in the genome has been estimated to be 1.2 × 10 −4 s/s/y. [ citation needed ]EEEV is capable of infecting a wide range of animals, including mammals , birds , reptiles , and amphibians . The virus is maintained in nature through a bird — mosquito cycle. Two mosquito species are primarily involved in this portion of the cycle; they are Culiseta melanura and Culiseta morsitans [ Wikidata ] . These mosquitoes feed on the blood of birds. The frequency of the virus found in nature increases throughout the summer as more birds and more mosquitoes become infected. [ citation needed ] Transmission of EEEV to mammals (including humans) occurs via other mosquito species, which feed on the blood of both birds and mammals. These other mosquitoes are referred to as "bridge vectors" because they carry the virus from the avian hosts to other types of hosts, particularly mammals. The bridge vectors include Aedes taeniorhynchus , Aedes vexans , Coquillettidia perturbans , Ochlerotatus canadensis , and Ochlerotatus sollicitans . Ochlerotatus canadensis also frequently bites turtles. [ citation needed ] Humans, horses, and most other infected mammals do not circulate enough viruses in their blood to infect additional mosquitoes. Some cases of EEE have been contracted through laboratory exposures or from exposure of the eyes, lungs, or skin wounds to brain or spinal cord matter from infected animals. [ citation needed ]The disease can be prevented in horses with the use of vaccinations , which are usually given with vaccinations for other diseases, most commonly western equine encephalitis virus , Venezuelan equine encephalitis virus , and tetanus . Most vaccinations for EEE consist of the killed virus. For humans, no vaccine for EEE is available; prevention involves reducing the risk of exposure. Using insect repellent, wearing protective clothing, and reducing the amount of standing water is the best means for prevention. No cure for EEE has been found. Treatment consists of corticosteroids , anticonvulsants , and supportive measures (treating symptoms) such as intravenous fluids, tracheal intubation , and antipyretics . [ citation needed ] About 4% of humans known to be infected develop symptoms, with a total of about six cases per year in the US. A third of these cases die, and many survivors suffer permanent brain damage. Several states in the Northeast U.S. have had increased virus activity since 2004. Between 2004 and 2006, at least ten human cases of EEE were reported in Massachusetts. In 2006, about 500,000 acres (2,000 km 2 ) in southeastern Massachusetts were treated with mosquito adulticides to reduce the risk of humans contracting EEE. Several human cases were reported in New Hampshire, as well. On 19 July 2012, the virus was identified in a mosquito of the species Coquillettidia perturbans in Nickerson State Park on Cape Cod, Massachusetts . On 28 July 2012, the virus was found in mosquitos in Pittsfield, Massachusetts . As of September 2019 [ update ] , a notable uptick in cases erupted in New England and Michigan, prompting some health departments to declare an outbreak. As of 31 October 2019 [ update ] , five people died in Michigan, three people died in Connecticut, one person died in Rhode Island, one person died in Alabama, one person died in Indiana, and three people died in Massachusetts. The virus was also found in goats, in turkeys, in deer, and in horses. As of September 9, 2020, there were 5 confirmed human cases between Massachusetts and Wisconsin. As of October 9, 2020, one person died in Michigan, and one person died in Wisconsin. In October 2007, a citizen of Livingston, West Lothian , Scotland became the first European victim of this disease. The man had visited New Hampshire during the summer of 2007, on a fishing vacation, and was diagnosed as having EEE on 13 September 2007. He fell ill with the disease on 31 August 2007, just one day after flying home, and later fell into a coma. He later awoke from the coma with severe brain injuries. Several states in the Northeast U.S. have had increased virus activity since 2004. Between 2004 and 2006, at least ten human cases of EEE were reported in Massachusetts. In 2006, about 500,000 acres (2,000 km 2 ) in southeastern Massachusetts were treated with mosquito adulticides to reduce the risk of humans contracting EEE. Several human cases were reported in New Hampshire, as well. On 19 July 2012, the virus was identified in a mosquito of the species Coquillettidia perturbans in Nickerson State Park on Cape Cod, Massachusetts . On 28 July 2012, the virus was found in mosquitos in Pittsfield, Massachusetts . As of September 2019 [ update ] , a notable uptick in cases erupted in New England and Michigan, prompting some health departments to declare an outbreak. As of 31 October 2019 [ update ] , five people died in Michigan, three people died in Connecticut, one person died in Rhode Island, one person died in Alabama, one person died in Indiana, and three people died in Massachusetts. The virus was also found in goats, in turkeys, in deer, and in horses. As of September 9, 2020, there were 5 confirmed human cases between Massachusetts and Wisconsin. As of October 9, 2020, one person died in Michigan, and one person died in Wisconsin. In October 2007, a citizen of Livingston, West Lothian , Scotland became the first European victim of this disease. The man had visited New Hampshire during the summer of 2007, on a fishing vacation, and was diagnosed as having EEE on 13 September 2007. He fell ill with the disease on 31 August 2007, just one day after flying home, and later fell into a coma. He later awoke from the coma with severe brain injuries. EEEV was one of more than a dozen agents that the United States researched as potential biological weapons before the nation suspended its biological-weapons program in 1969, a few years before signing (1972) and then ratifying (1975) the Biological Weapons Convention . From its natural reservoir in birds, EEEV is known to infect reptiles and amphibians as well as both humans and other mammals, including horses. After inoculation by the vector, the virus travels via lymphatics to lymph nodes, and replicates in macrophages and neutrophils, resulting in lymphopenia, leukopenia, and fever. Subsequent replication occurs in other organs, leading to viremia. Symptoms in horses occur 1–3 weeks after infection, and begin with a fever that may reach as high as 106 °F (41 °C). The fever usually lasts for 24–48 hours. [ medical citation needed ] Nervous signs appear during the fever that include sensitivity to sound, periods of excitement, and restlessness. Brain lesions appear, causing drowsiness, drooping ears, circling, aimless wandering, head pressing , inability to swallow, and abnormal gait. Paralysis follows, causing the horse to have difficulty raising its head. The horse usually suffers complete paralysis and death 2–4 days after symptoms appear. Mortality rates among horses with the eastern strain range from 70 to 90%. [ medical citation needed ]After inoculation by the vector, the virus travels via lymphatics to lymph nodes, and replicates in macrophages and neutrophils, resulting in lymphopenia, leukopenia, and fever. Subsequent replication occurs in other organs, leading to viremia. Symptoms in horses occur 1–3 weeks after infection, and begin with a fever that may reach as high as 106 °F (41 °C). The fever usually lasts for 24–48 hours. [ medical citation needed ] Nervous signs appear during the fever that include sensitivity to sound, periods of excitement, and restlessness. Brain lesions appear, causing drowsiness, drooping ears, circling, aimless wandering, head pressing , inability to swallow, and abnormal gait. Paralysis follows, causing the horse to have difficulty raising its head. The horse usually suffers complete paralysis and death 2–4 days after symptoms appear. Mortality rates among horses with the eastern strain range from 70 to 90%. [ medical citation needed ]

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Rift Valley fever

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Sarah Gilbert

Dame Sarah Catherine Gilbert DBE FRS (born April 1962) is an English vaccinologist who is a Professor of Vaccinology at the University of Oxford and co-founder of Vaccitech . She specialises in the development of vaccines against influenza and emerging viral pathogens. She led the development and testing of the universal flu vaccine , which underwent clinical trials in 2011. In January 2020, she read a report on ProMED-mail about four people in China suffering from a strange kind of pneumonia of unknown origin in Wuhan . Within two weeks, a vaccine had been designed at Oxford against the new pathogen, which later became known as COVID-19 . On 30 December 2020, the Oxford–AstraZeneca COVID-19 vaccine she co-developed with the Oxford Vaccine Group was approved for use in the UK. As of January 2022, more than 2.5 billion doses of the vaccine have been released to more than 170 countries worldwide. Sarah Catherine Gilbert was born in Kettering , Northamptonshire . Her father was an office manager for a shoemakers and her mother was a primary school teacher. Gilbert attended Kettering High School for Girls , where she realised that she wanted to work in medicine. She earned nine O-Levels with six A grades. She graduated with a Bachelor of Science degree in biological sciences from the University of East Anglia (UEA) in 1983. While at UEA she began playing the saxophone , which she would practise in the woods around the UEA Broad so as not to disturb others in her halls. She moved to the University of Hull for her doctoral degree, where she investigated the genetics and biochemistry of the yeast Rhodosporidium toruloides , graduating with a PhD in 1986. After earning her doctoral degree, Gilbert worked as a postdoctoral researcher in industry at the Brewing Industry Research Foundation before moving to the Leicester Biocentre. In 1990, Gilbert joined Delta Biotechnology, a biopharmaceutical company that manufactured drugs in Nottingham . In 1994, Gilbert returned to academia, joining the laboratory of Adrian V. S. Hill . Her early research considered host–parasite interactions in malaria . She became a University lecturer in 1999 and she was made a Reader in Vaccinology at the University of Oxford in 2004. She was made Professor at the Jenner Institute in 2010. With the support of the Wellcome Trust , Gilbert started work on the design and creation of novel influenza vaccinations . In particular, her research considers the development and preclinical testing of viral vaccinations, which embed a pathogenic protein inside a safe virus. These viral vaccinations induce a T cell response, which can be used against viral diseases, malaria and cancer. Gilbert was involved with the development and testing of the universal flu vaccine . Unlike conventional vaccinations, the universal flu vaccine did not stimulate the production of antibodies, but instead triggers the immune system to create T cells that are specific for influenza. It makes use of one of the core proteins ( nucleoprotein and matrix protein 1) inside the Influenza A virus , not the external proteins that exist on the outside coat. As the immune system weakens with age, conventional vaccinations are not effective for elderly. The universal flu vaccine does not need to be reformatted every year and stops people from needing a seasonal flu vaccine. Her first clinical trials, which were in 2008, made use of the Influenza A virus subtype H3N2 , and included daily monitoring of the patient's symptoms. It was the first study that it was possible to stimulate T cells in response to a flu virus, and that this stimulation would protect people from getting the flu. Her research has demonstrated that the adenoviral vector ChAdOx1 can be used to make vaccinations that are protective against Middle East respiratory syndrome (MERS) in mice and able to induce immune response against MERS in humans. The same vector was also used to create a vaccine against Nipah which was effective in hamsters (but never proven in humans), in addition to a potential vaccine for Rift Valley Fever that was protective in sheep, goats, and cattle (but not proven in humans). Gilbert has been involved with the development of a new vaccination to protect against coronavirus since the beginning of the COVID-19 pandemic . She leads the work on this vaccine candidate alongside Andrew Pollard , Teresa Lambe , Sandy Douglas, Catherine Green and Adrian Hill . As with her earlier work, the COVID-19 vaccine makes use of an adenoviral vector, which stimulates an immune response against the coronavirus spike protein. Plans were announced to start animal studies in March 2020, and recruitment began of 510 human participants for a phase I/II trial on 27 March. In April 2020, Gilbert was interviewed about the developments by Andrew Marr on BBC television. That same month, Gilbert was reported as saying that her candidate vaccine could be available by September 2020, if everything goes to plan with the clinical trial, which has received funding from sources such as the Coalition for Epidemic Preparedness Innovations . Gilbert delivered an update in September 2020 that the vaccine, AZD1222 , was being produced by AstraZeneca while phase III trials were ongoing. Because of her vaccine research, Gilbert featured on The Times ' 'Science Power List' in May 2020. In 2021, Gilbert and Catherine Green published Vaxxers: the inside story of the Oxford AstraZeneca vaccine and the race against the virus . Gilbert was the subject of BBC Radio 4 's The Life Scientific in September 2020. She was also on the list of the BBC's 100 Women announced on 23 November 2020, and became a senior associated research fellow at Christ Church, Oxford . Gilbert was awarded the Rosalind Franklin medal for her services to science by Humanists UK at its annual Rosalind Franklin Lecture on 5 March 2021, at which she delivered a lecture titled 'Racing against the virus'. The lecture detailed the history of the science of vaccination and recounted the progress of the Oxford/AstraZeneca vaccine . In June 2021, Gilbert received a standing ovation at the 2021 Wimbledon Championships . In 2021, as a role model (Barbie Shero), Sarah Gilbert had a Barbie doll made in her honour by the toy manufacturer Mattel . Gilbert gave birth to triplets in 1998. Her partner gave up his career to be their primary parent . As of 2020 [ update ] , all of the triplets are studying biochemistry at university. Gilbert has an h-index of 95 according to Google Scholar . Her publications include:

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Rift Valley fever

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Peter Daszak

Peter Daszak is a British zoologist , consultant and public expert on disease ecology , in particular on zoonosis . He is the president of EcoHealth Alliance , a nonprofit non-governmental organization that supports various programs on global health and pandemic prevention. He is also a member of the Center for Infection and Immunity at the Columbia University Mailman School of Public Health . He lives in Suffern, New York . Daszak was involved in investigations into the initial outbreak which eventually developed into the COVID-19 pandemic and became a member of the World Health Organization team sent to investigate the origins of the COVID-19 pandemic in China.Daszak earned a B.Sc. in zoology in 1987, at Bangor University and a Ph.D. in parasitic infectious diseases in 1994 at University of East London . Daszak worked at the School of Life Sciences, Kingston University , in Surrey, England in the 1990s. In the late 1990s Daszak moved to the United States and was affiliated with the Institute of Ecology at the University of Georgia and the National Center for Infectious Diseases, Centers for Disease Control and Prevention , in Atlanta , Georgia . Around 2001 he became executive director at a collaborative think-tank in New York City , the Consortium for Conservation Medicine. He has adjunct positions at two universities in the U.K. and three universities in the U.S., including the Columbia University Mailman School of Public Health. He was one of the early adopters of conservation medicine . The Society for Conservation Biology symposium in 2000, had focused on the "complex problem of emerging diseases". He said in 2001 that there were "almost no examples of emerging wildlife diseases not driven by human environmental change...[a]nd few human emerging diseases don't include some domestic animal or wildlife component." His research has focused on investigating and predicting the impacts of new diseases on wildlife, livestock, and human populations, and he has been involved in research studies on epidemics such as the Nipah virus infection , the Australian Hendra outbreaks , the 2002–2004 SARS outbreak , Avian influenza , and the West Nile virus . Starting in 2014, Daszak was Principal Investigator of a six-year NIH project which was awarded to the EcoHealth Alliance and which focused on the emergence of novel zoonotic coronaviruses with a bat origin. Among the aims of the project was to characterize the diversity and distribution of Severe acute respiratory syndrome–related coronavirus (SARSr-CoV) in bats, viruses with a significant risk of spillover, in southern China, based on data from spike protein sequences, infectious clone technology, infection experiments (both in vitro and in vivo), as well as analysis of receptor binding. The six 1-year projects received $3.75 million in funding from the National Institute of Allergy and Infectious Diseases (NIAID), part of the U.S. National Institutes of Health agency. Daszak has served on committees of the International Union for Conservation of Nature , World Health Organization (WHO), National Academy of Sciences , and United States Department of the Interior . He is a member of the National Academy of Medicine and Chair of the National Academies of Sciences, Engineering, and Medicine (NASEM)'s Forum on Microbial Threats and sits on the supervisory board of the One Health Commission Council of Advisors. During times of large virus outbreaks Daszak has been invited to speak as an expert on epidemics involving diseases moving across the species barrier from animals to humans. At the time of the Ebola outbreak in West Africa in 2014, Daszak said "Our research shows that new approaches to reducing emerging pandemic threats at the source would be more cost-effective than trying to mobilize a global response after a disease has emerged". In October 2019, when the U.S. federal government "quietly" ended the ten-year old program called PREDICT , operated by United States Agency for International Development (USAID)'s emerging threats division, Daszak said that, compared to the $5 billion the U.S. spent fighting Ebola in West Africa, PREDICT—which cost $250 million—was much less expensive. Daszak further stated, "PREDICT was an approach to heading off pandemics, instead of sitting there waiting for them to emerge, and then mobilizing." As of 2021 [ update ] , Daszak is the president of the New York-headquartered NGO EcoHealth Alliance. His research focuses on global emergent diseases such as Severe Acute Respiratory Syndrome (SARS), Nipah virus , Middle East Respiratory Syndrome (MERS), Rift Valley fever , Ebola virus , and COVID-19 . The organization has administered more than $100 million in U.S. federal grants to fund overseas laboratory experiments. After the outbreak of the COVID-19 pandemic , Daszak noted in The New York Times that he and other disease ecologists had warned the WHO in 2018 that the next pandemic "would be caused by an unknown, novel pathogen that hadn't yet entered the human population", probably in a region with significant human-animal interaction. The group included this hypothetical " Disease X " pathogen on a list of eight diseases which they recommended should be given highest priority in regard to research and development efforts, such as finding better diagnostic methods and developing vaccines . He said, "As the world stands today on the edge of the pandemic precipice, it's worth taking a moment to consider whether Covid-19 is the disease our group was warning about." Prior to the pandemic, Daszak and EcoHealth Alliance were the only U.S.-based organization researching coronavirus evolution and transmission in China, where they partnered with the Wuhan Institute of Virology , among others. On 1 April 2020, following the beginning of the COVID-19 pandemic in the United States , the USAID granted $2.26 million to the EcoHealth program for a six-month emergency extension of the program whose funding has expired in September 2019. The University of California announced that the extension would support "detection of SARS-CoV-2 cases in Africa, Asia and the Middle East to inform the public health response" as well as investigation of "the animal source or sources of SARS-CoV-2 using data and samples collected over the past 10 years in Asia and Southeast Asia." An open letter co-authored by Daszak, signed by 27 scientists and published in The Lancet on 19 February 2020, stated: "We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin ...and overwhelmingly conclude that this coronavirus originated in wildlife." It further warned that blaming Chinese researchers for the virus' origin jeopardised the fight against the disease. In June 2021, The Lancet published an addendum in which Daszak listed his cooperation with researchers in China, and he also recused himself from The Lancet ' s inquiry commission focused on COVID-19 origins. EcoHealth Alliance's project funding was "abruptly terminated" on 24 April 2020, by the National Institutes of Health . The move met with criticism, including by a group of 77 Nobel Prize laureates who wrote to NIH Director Francis Collins that they "are gravely concerned" by the decision and called the funding cut "counterintuitive, given the urgent need to better understand the virus that causes COVID-19 and identify drugs that will save lives." An article on 8 May 2020 in the journal Science stated that the unusual 24 April decision to cut EcoHealth's funding had occurred shortly after "President Donald Trump alleged – without providing evidence – that the pandemic virus had escaped from a Chinese laboratory supported by the NIH grant, and vowed to end the funding." In May 2020, Daszak "said there was 'zero evidence' that the virus" was created in the Wuhan Institute of Virology during an appearance on "60 Minutes." In 2020 Daszak was named by the World Health Organization as the sole U.S.-based representative on a team sent to investigate the origins of the COVID-19 pandemic , a team that also included Marion Koopmans , Hung Nguyen, and Fabian Leendertz. Daszak had previously collaborated for many years with Shi Zhengli , the director of the Wuhan Institute of Virology , on efforts to trace SARSr-CoV viruses to bats after the 2002–2004 SARS outbreak . Some critics, including journalist Nicholas Wade and biologist Richard H. Ebright , alleged that Daszak had a conflict of interest investigating the virus' origins in China. In 2021, a complaint was issued by a few Republican representatives asking for Daszak to be expelled from the National Academy of Medicine (NAM) based on conduct allegations. In 2022 this request was denied by the NAM, citing "no evidence" of the alleged breach in conduct. The conduct probe by NAM to exonerate Daszak drew wider circles as the Republican minority staff of a bipartisan Senate committee led by Senator Richard Burr concluded "that the pandemic most likely began when the virus somehow escaped from WIV". Some NAM members called the probe into Daszak "frivolous and political", and wrote that such accusations against China are detrimental to pandemic preparedness, and hinder international collaboration to confront pandemics effectively. After the outbreak of the COVID-19 pandemic , Daszak noted in The New York Times that he and other disease ecologists had warned the WHO in 2018 that the next pandemic "would be caused by an unknown, novel pathogen that hadn't yet entered the human population", probably in a region with significant human-animal interaction. The group included this hypothetical " Disease X " pathogen on a list of eight diseases which they recommended should be given highest priority in regard to research and development efforts, such as finding better diagnostic methods and developing vaccines . He said, "As the world stands today on the edge of the pandemic precipice, it's worth taking a moment to consider whether Covid-19 is the disease our group was warning about." Prior to the pandemic, Daszak and EcoHealth Alliance were the only U.S.-based organization researching coronavirus evolution and transmission in China, where they partnered with the Wuhan Institute of Virology , among others. On 1 April 2020, following the beginning of the COVID-19 pandemic in the United States , the USAID granted $2.26 million to the EcoHealth program for a six-month emergency extension of the program whose funding has expired in September 2019. The University of California announced that the extension would support "detection of SARS-CoV-2 cases in Africa, Asia and the Middle East to inform the public health response" as well as investigation of "the animal source or sources of SARS-CoV-2 using data and samples collected over the past 10 years in Asia and Southeast Asia." An open letter co-authored by Daszak, signed by 27 scientists and published in The Lancet on 19 February 2020, stated: "We stand together to strongly condemn conspiracy theories suggesting that COVID-19 does not have a natural origin ...and overwhelmingly conclude that this coronavirus originated in wildlife." It further warned that blaming Chinese researchers for the virus' origin jeopardised the fight against the disease. In June 2021, The Lancet published an addendum in which Daszak listed his cooperation with researchers in China, and he also recused himself from The Lancet ' s inquiry commission focused on COVID-19 origins. EcoHealth Alliance's project funding was "abruptly terminated" on 24 April 2020, by the National Institutes of Health . The move met with criticism, including by a group of 77 Nobel Prize laureates who wrote to NIH Director Francis Collins that they "are gravely concerned" by the decision and called the funding cut "counterintuitive, given the urgent need to better understand the virus that causes COVID-19 and identify drugs that will save lives." An article on 8 May 2020 in the journal Science stated that the unusual 24 April decision to cut EcoHealth's funding had occurred shortly after "President Donald Trump alleged – without providing evidence – that the pandemic virus had escaped from a Chinese laboratory supported by the NIH grant, and vowed to end the funding." In May 2020, Daszak "said there was 'zero evidence' that the virus" was created in the Wuhan Institute of Virology during an appearance on "60 Minutes." In 2020 Daszak was named by the World Health Organization as the sole U.S.-based representative on a team sent to investigate the origins of the COVID-19 pandemic , a team that also included Marion Koopmans , Hung Nguyen, and Fabian Leendertz. Daszak had previously collaborated for many years with Shi Zhengli , the director of the Wuhan Institute of Virology , on efforts to trace SARSr-CoV viruses to bats after the 2002–2004 SARS outbreak . Some critics, including journalist Nicholas Wade and biologist Richard H. Ebright , alleged that Daszak had a conflict of interest investigating the virus' origins in China. In 2021, a complaint was issued by a few Republican representatives asking for Daszak to be expelled from the National Academy of Medicine (NAM) based on conduct allegations. In 2022 this request was denied by the NAM, citing "no evidence" of the alleged breach in conduct. The conduct probe by NAM to exonerate Daszak drew wider circles as the Republican minority staff of a bipartisan Senate committee led by Senator Richard Burr concluded "that the pandemic most likely began when the virus somehow escaped from WIV". Some NAM members called the probe into Daszak "frivolous and political", and wrote that such accusations against China are detrimental to pandemic preparedness, and hinder international collaboration to confront pandemics effectively. In 1999, Daszak received a meritorious service award from the Centers for Disease Control and Prevention . In 2018, he was elected to the National Academy of Medicine . He is commemorated in the names of the centipede Cryptops daszaki, as well as the apicomplexan parasite Isospora daszaki.

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Neglected tropical diseases

Neglected tropical diseases ( NTDs ) are a diverse group of tropical infections that are common in low-income populations in developing regions of Africa , Asia , and the Americas . They are caused by a variety of pathogens , such as viruses , bacteria , protozoa , and parasitic worms ( helminths ). These diseases are contrasted with the "big three" infectious diseases ( HIV/AIDS , tuberculosis , and malaria ), which generally receive greater treatment and research funding. In sub-Saharan Africa, the effect of neglected tropical diseases as a group is comparable to that of malaria and tuberculosis. NTD co-infection can also make HIV/AIDS and tuberculosis more deadly. Some treatments for NTDs are relatively inexpensive. For example, treatment for schistosomiasis costs US$0.20 per child per year. Nevertheless, in 2010 it was estimated that control of neglected diseases would require funding of between US$2 billion and $3 billion over the subsequent five to seven years. Some pharmaceutical companies have committed to donating all the drug therapies required, and mass drug administration efforts (for example, mass deworming ) have been successful in several countries. While preventive measures are often more accessible in the developed world , they are not universally available in poorer areas. Within developed countries, neglected tropical diseases affect the very poorest in society. In the United States, there are up to 1.46 million families, including 2.8 million children, living on less than two dollars per day. In developed countries, the burdens of neglected tropical diseases are often overshadowed by other public health issues. However, many of the same issues put populations at risk in developed as well as developing nations. For example, other problems stemming from poverty, such as lack of adequate housing , can expose individuals to the vectors of these diseases. Twenty neglected tropical diseases are prioritized by the World Health Organization (WHO), though other organizations define NTDs differently. Chromoblastomycosis and other deep mycoses , scabies and other ectoparasites , and snakebite envenomation were added to the WHO list in 2017. These diseases are common in 149 countries, affecting more than 1.4 billion people (including more than 500 million children) and costing developing economies billions of dollars every year. They resulted in 142,000 deaths in 2013, down from 204,000 deaths in 1990. The importance of neglected tropical diseases has been underestimated since many are asymptomatic and have long incubation periods . The connection between death and a neglected tropical disease that has been latent for a long period is often not realized. Areas of high endemicity are often geographically isolated, making treatment and prevention much more difficult. There are three other major reasons that these diseases have been overlooked: they mainly affect the poorest countries of the developing world ; in recent years public health efforts have focused heavily on decreasing the prevalence of HIV/AIDS, tuberculosis, and malaria (far more resources are given to those three diseases because of their higher mortality rates and higher public awareness of them); and neglected tropical diseases do not currently have a prominent cultural figure to champion their elimination. Neglected tropical diseases are often associated with social stigma , making their treatment more complex. Public health research has only recently begun to focus on stigma as a component of the issue. From the 1960s onward, approximately one citation a year related to social stigma. In 2006, there were 458. Stigma greatly affects disease control by decreasing help-seeking and treatment adherence. Disease control programs since the 1980s, have begun to integrate stigma mitigation into their offerings. In India , a leprosy program prioritized the message that "leprosy is curable, not hereditary" in order to inspire optimism in highly affected communities. The goal was to make leprosy a disease "like any other", so as to reduce stigma. At the same time, medical resources were optimized to fulfill the promise that the disease could be cured. Treatment and prevention of neglected tropical diseases are not seen as profitable, so patents and profit play no role in stimulating innovation. Like all non-commercial areas, these communities affected by these diseases are reliant on governments and philanthropy (including industry philanthropy). Currently, the pharmaceutical industry views research and development as highly risky. For this reason, resources are not often put into the field of NTDs, and new chemical products are often expensive. A review of public and private initiatives found that of the 1,393 new chemical products that were marketed between 1975 and 1999, only 16 were related to tropical diseases and tuberculosis. The same review found that there was a 13-fold greater chance of a newly marketed drug being for central nervous system disorders or cancer than for an NTD. Because of a lack of economic incentives for the pharmaceutical industry, successful NTD treatment programs have often relied on donations. The Mectizan Donation Program has donated over 1.8 billion tablets of ivermectin . While developed countries often rely on government-run and private partnerships to fund such projects, developing nations frequently have significantly lower per-person spending on these diseases. A 2006 report found that the Gates Foundation funded most extra activities to counter these diseases. Since 2008, the concept of "neglected diseases of poverty" has been developed and explored. This group of diseases, which overlaps with neglected tropical diseases, also pose a threat to human health in developed nations. In the United States alone, there are at least 12 million people with neglected parasitic infections. They make up a hidden disease burden among the poorest people in wealthy societies . In developed nations, lack of knowledge in the healthcare industry and lack of conclusive diagnostic tests perpetuate the neglect of this group of diseases. In the United States, high rates of parasitic infection can be distributed along geographic, racial, and socio-economic lines. Among African Americans , there may be up to 2.8 million cases of toxocariasis . Toxocariasis, trichomoniasis , and some other neglected infections occur in the United States at the same rate as in Nigeria . Within the Hispanic community, neglected infections are concentrated near the US–Mexico border . Vector-borne illnesses are especially high, with some rates approaching those of Latin America . Chagas disease was found in the US as early as the 1970s. However, in the developed world, diseases that are associated with poverty are often not addressed comprehensively. This may be due to a lack of economic incentives and public policy failings. A lack of awareness prevents effective policy generation and leaves healthcare services unequipped to address the issue. Additionally, little effort is put into creating and maintaining large data sets on neglected diseases in the United States and other developed nations. The first summit on the issue was held by the Adler Institute on Social Exclusion in the United States in 2009. In Europe , a similar trend is seen. Neglected tropical diseases are concentrated in eastern and southern Europe , where poverty levels are highest. The most prevalent diseases in this region are ascariasis , trichuriasis , zoonotic helminth infections , and visceral leishmaniasis . Migration paths to Europe, most notably to Spain , have brought diseases to Europe as well. As many as 6,000 cases of Chagas disease have been introduced in this way. In response to a growing awareness of the burden on these populations, the European Centre for Disease Prevention and Control has laid out ten public health guidelines. They cover a variety of topics, from health education and promotion to community partnerships and the development of a minority healthcare workforce. Neglected tropical diseases are often associated with social stigma , making their treatment more complex. Public health research has only recently begun to focus on stigma as a component of the issue. From the 1960s onward, approximately one citation a year related to social stigma. In 2006, there were 458. Stigma greatly affects disease control by decreasing help-seeking and treatment adherence. Disease control programs since the 1980s, have begun to integrate stigma mitigation into their offerings. In India , a leprosy program prioritized the message that "leprosy is curable, not hereditary" in order to inspire optimism in highly affected communities. The goal was to make leprosy a disease "like any other", so as to reduce stigma. At the same time, medical resources were optimized to fulfill the promise that the disease could be cured. Treatment and prevention of neglected tropical diseases are not seen as profitable, so patents and profit play no role in stimulating innovation. Like all non-commercial areas, these communities affected by these diseases are reliant on governments and philanthropy (including industry philanthropy). Currently, the pharmaceutical industry views research and development as highly risky. For this reason, resources are not often put into the field of NTDs, and new chemical products are often expensive. A review of public and private initiatives found that of the 1,393 new chemical products that were marketed between 1975 and 1999, only 16 were related to tropical diseases and tuberculosis. The same review found that there was a 13-fold greater chance of a newly marketed drug being for central nervous system disorders or cancer than for an NTD. Because of a lack of economic incentives for the pharmaceutical industry, successful NTD treatment programs have often relied on donations. The Mectizan Donation Program has donated over 1.8 billion tablets of ivermectin . While developed countries often rely on government-run and private partnerships to fund such projects, developing nations frequently have significantly lower per-person spending on these diseases. A 2006 report found that the Gates Foundation funded most extra activities to counter these diseases. Since 2008, the concept of "neglected diseases of poverty" has been developed and explored. This group of diseases, which overlaps with neglected tropical diseases, also pose a threat to human health in developed nations. In the United States alone, there are at least 12 million people with neglected parasitic infections. They make up a hidden disease burden among the poorest people in wealthy societies . In developed nations, lack of knowledge in the healthcare industry and lack of conclusive diagnostic tests perpetuate the neglect of this group of diseases. In the United States, high rates of parasitic infection can be distributed along geographic, racial, and socio-economic lines. Among African Americans , there may be up to 2.8 million cases of toxocariasis . Toxocariasis, trichomoniasis , and some other neglected infections occur in the United States at the same rate as in Nigeria . Within the Hispanic community, neglected infections are concentrated near the US–Mexico border . Vector-borne illnesses are especially high, with some rates approaching those of Latin America . Chagas disease was found in the US as early as the 1970s. However, in the developed world, diseases that are associated with poverty are often not addressed comprehensively. This may be due to a lack of economic incentives and public policy failings. A lack of awareness prevents effective policy generation and leaves healthcare services unequipped to address the issue. Additionally, little effort is put into creating and maintaining large data sets on neglected diseases in the United States and other developed nations. The first summit on the issue was held by the Adler Institute on Social Exclusion in the United States in 2009. In Europe , a similar trend is seen. Neglected tropical diseases are concentrated in eastern and southern Europe , where poverty levels are highest. The most prevalent diseases in this region are ascariasis , trichuriasis , zoonotic helminth infections , and visceral leishmaniasis . Migration paths to Europe, most notably to Spain , have brought diseases to Europe as well. As many as 6,000 cases of Chagas disease have been introduced in this way. In response to a growing awareness of the burden on these populations, the European Centre for Disease Prevention and Control has laid out ten public health guidelines. They cover a variety of topics, from health education and promotion to community partnerships and the development of a minority healthcare workforce. There is some debate among the WHO, CDC , and infectious disease experts over which diseases are classified as neglected tropical diseases. Feasey, a researcher in neglected tropical diseases, notes 13 neglected tropical diseases: ascariasis , Buruli ulcer , Chagas disease , dracunculiasis , hookworm infection, human African trypanosomiasis , leishmaniasis , leprosy , lymphatic filariasis , onchocerciasis , schistosomiasis , trachoma , and trichuriasis . Fenwick recognizes 12 "core" neglected tropical diseases: the same as above, excluding hookworm. These diseases result from four classes of causative pathogens : (i) protozoa (Chagas disease, human African trypanosomiasis, and leishmaniasis); (ii) bacteria (Buruli ulcer, leprosy, trachoma, and yaws ), (iii) helminths or metazoan worms ( cysticercosis / taeniasis , dracunculiasis, echinococcosis , foodborne trematodiases , lymphatic filariasis, onchocerciasis, schistosomiasis, and soil-transmitted helminthiasis ); and (iv) viruses ( dengue , chikungunya , and rabies ). [ citation needed ] The WHO recognizes the twenty diseases below as neglected tropical diseases. Helminth infections: Viral infections: Bacterial infections: Fungal infections: Ectoparasites: Non-infectious diseases caused by toxin exposure: The World Health Organization's 2010 report on neglected tropical diseases offers an expanded list including dengue, rabies, yaws, cysticercosis, echinococcosis, and foodborne trematode infections . Buruli ulcer is caused by the bacterium Mycobacterium ulcerans . It is related to the bacteria that cause tuberculosis and leprosy. Mycobacterium ulcerans produces a toxin, mycolactone , that destroys tissue. The prevalence of Buruli ulcer is unknown. The risk of mortality is low, although secondary infections can be lethal. Morbidity takes the form of deformity, disability, and skin lesions, which can be prevented through early treatment with antibiotics and surgery. It is found in Africa, Asia, Australia, and Latin America. Chagas disease is also known as American trypanosomiasis. There are approximately 15 million people infected with Chagas disease. Morbidity rates are higher for immunocompromised individuals, children, and the elderly, but can be very low if the disease is treated early. Chagas disease does not kill victims rapidly, instead causing years of debilitating chronic symptoms. It is caused by the vector-borne protozoa Trypanosoma cruzi . It is spread by contact with Trypanosoma cruzi -infected feces of the triatomine ( assassin bug ). The protozoan can enter the body via the bug's bite, skin breaks, or mucous membranes . Infection can result from eating infected food or coming into contact with contaminated bodily fluids. There are two phases of Chagas disease. The acute phase is usually asymptomatic. The first symptoms are usually skin chancres , unilateral purplish orbital oedema , local lymphadenopathy , and fever , accompanied by a variety of other symptoms depending on the infection site. The chronic phase occurs in 30 percent of all infections and can take three forms: asymptomatic (most prevalent), cardiac, and digestive lesions. Chagas disease can be prevented by avoiding insect bites through insecticide spraying, home improvement, bed nets, hygienic food, medical care, laboratory practices, and testing. It can be diagnosed through a serological test, although the test is not very accurate. Treatment is with medication, which may have severe side effects. There are 50–100 million dengue virus infections annually. Dengue fever is usually not fatal, but infection with one of four serotypes can increase later susceptibility to other serotypes, resulting in a potentially fatal disease called severe dengue. Dengue fever is caused by a flavivirus which is spread mostly by the bite of the Aedes aegypti mosquito. No treatment for either dengue or severe dengue exists beyond palliative care . The symptoms are high fever and flu-like symptoms. It is found in Asia, Latin America, and Northern Australia. Chikungunya is an arboviral disease transmitted by A. albopictus and A. aegypti mosquitoes. The virus was first isolated from an outbreak in Tanzania in 1952. Chikungunya virus is a member of the genus Alphavirus and family Togaviridae . The word "chikungunya" is from the Makonde language and means "that which bends up", referring to the effect of debilitating joint pain on the patient. Symptoms, generally appearing 5–7 days after exposure, can be confused with dengue and include fever, rash, headache, joint pain, and swelling. The disease mainly occurs in Africa and Asia. Dracunculiasis is also known as Guinea-worm disease. In 2019, 53 cases were reported across four countries, a substantial decrease from 3,500,000 cases in 1986. It is not fatal, but can cause months of inactivity. It is caused by drinking water contaminated by water fleas infected with guinea-worm larvae. Approximately one year after infection, a painful blister forms and one or more worms emerge. Worms can be up to 1 metre long. It is usually treated by World Health Organization volunteers who clean and bandage wounds caused by worms and return daily to pull the worm out a few more inches. Dracunculiasis is preventable by water filtration, immediate case identification to prevent spread, health education, and treating ponds with larvicide. An eradication program has been able to reduce prevalence. As of 2014 [ update ] , the four endemic countries are Chad , Ethiopia , Mali , and South Sudan . The rate of echinococcosis is higher in rural areas, and there are more than one million people infected currently. It is caused by ingesting parasites in animal feces. There are two versions of the disease: cystic and alveolar . Both versions involve an asymptomatic incubation period of several years. In the cystic version, liver cysts cause abdominal pain , nausea , and vomiting , while cysts in the lungs cause chronic cough , chest pain , and shortness of breath . In alveolar echinococcosis, a primary cyst develops, usually in the liver, in addition to weight loss, abdominal pain, malaise , and signs of liver failure . Untreated alveolar echinococcosis is fatal. Surgery and drugs can be used to treat echinococcosis. It can be prevented by deworming dogs, sanitation, proper disposal of animal feces, health education, and livestock vaccination. Cystic echinococcosis is found in the eastern portion of the Mediterranean region, northern Africa, southern and eastern Europe, the southern portion of South America, and Central Asia. Alveolar echinococcosis is found in western and northern China, Russia, Europe, and northern North America. It can be diagnosed through imaging techniques and serological tests . There are limited data available on the prevalence of yaws , although it primarily affects children. The mortality risk is very low, but the disease causes disfigurement and disability if untreated. The most common symptom is skin lesions. It is a chronic bacterial infection, transmitted by skin contact, and caused by the spirochete bacterium Treponema pallidum pertenue . It is treated with antibiotics and can be prevented through hygiene and sanitation. Yaws is most prevalent in warm, moist tropical regions of the Americas, Africa, Asia, and the Pacific. Foodborne trematode infections include clonorchiasis , opisthorchiasis , fascioliasis , and paragonimiasis . These infections are all zoonotic , primarily affecting domestic or wild animals, but can also be transmitted to humans. They are acquired by eating food, such as raw fish, contaminated with the larval stages of the parasites. At least 40 million people are thought to be infected. African trypanosomiasis (African sleeping sickness) is a somewhat rare protozoal disease, with fewer than 10,000 cases currently. Human African trypanosomiasis is vector-borne and spreads through the bite of the tsetse fly . The most common symptoms are fever, headache, lymphadenopathy , sleeping disturbances, personality changes, cognitive decline, and coma . The disease is always fatal if untreated. The current forms of treatment are highly toxic and ineffective, as resistance is spreading. It is diagnosed through an inexpensive serological test. [ medical citation needed ] The three forms of leishmaniasis , a protozoal disease, are visceral ( Kala-azar ), cutaneous , and mucocutaneous. There are an estimated 12 million people infected. It is fatal if untreated, and 20,000 deaths from visceral leishmaniasis occur annually. It is a vector-borne disease caused by the bite of sandflies . At least 90 percent of visceral leishmaniasis occurs in Bangladesh , Brazil , Ethiopia , India , South Sudan , and Sudan . Cutaneous leishmaniasis occurs in Afghanistan , Algeria , Brazil, Colombia , Iran , Pakistan , Peru , Saudi Arabia , and Syria . Around 90 percent of mucocutaneous leishmaniasis occurs in Bolivia , Brazil, and Peru. A vaccine is under development to prevent leishmaniasis. The only other method of prevention is avoidance of sandfly bites. Diagnosis can be made by clinical signs, serological tests, or parasitological tests. Leishmaniasis can be treated with expensive medications. According to recent figures from the WHO, 208,619 new cases of leprosy were reported in 2018 from 127 countries. It is most prevalent in India (69% of cases), Brazil, Indonesia , Nigeria , the Democratic Republic of the Congo , Madagascar , and East Africa from Mozambique to Ethiopia, with the highest relative incidence in India, Brazil, and Nepal . There are one to two million individuals currently disabled or disfigured due to past or present leprosy. It is caused by bacteria and transmitted through droplets from the mouth and nose of infected individuals. Leprosy causes disfigurement and physical disabilities if untreated. It is curable if treated early. Treatment requires multidrug therapy. The BCG vaccine has some preventative effect against leprosy. Leprosy has a 5–20 year incubation period, and the symptoms are damage to the skin, nerves, eyes, and limbs. Lymphatic filariasis is also known as elephantiasis . There are approximately 120 million individuals infected and 40 million with deformities. Approximately two-thirds of cases are in Southwest Asia, and one-third are in Africa. Lymphatic filariasis is rarely fatal but has lifelong implications, such as lymphoedema of the limbs, genital disease, and painful recurrent attacks. Most people are asymptomatic but have lymphatic damage. Up to 40 percent of infected individuals have kidney damage. It is a vector-borne disease, caused by nematode worms that are transmitted by mosquitoes. It can be treated with cost-effective antihelminthic treatments, and washing skin can slow or even reverse damage. It is diagnosed with a finger-prick blood test. Noma, an opportunistic bacterial infection causing gangrenous necrosis of the mouth, was added to the World Health Organization's list of neglected tropical diseases in December 2023. Onchocerciasis is also known as river blindness. There are 20.9 million people infected, and prevalence is higher in rural areas. Over 99 percent of cases are in sub-Saharan Africa . It causes blindness, skin rashes, lesions, intense itching, and skin depigmentation. It is a vector-borne disease, caused by blackflies infected with filarial worms. It can be treated with ivermectin and prevented by insecticide spraying or preventative dosing with ivermectin. There are two forms of rabies : furious and paralytic. It is mostly found in Asia and Africa. There is a higher prevalence in rural areas, and it disproportionately affects children. Rabies is fatal after symptoms develop. It is caused by a lyssavirus transmitted through wounds or bites from infected animals. The first symptoms are fever and pain near the infection site, which occur after a one- to three-month incubation period. Furious rabies (the more common type) causes hyperactivity, hydrophobia, and aerophobia; death by cardio-respiratory arrest occurs within days. Paralytic rabies causes a slow progression from paralysis to coma to death. There are 60,000 deaths from rabies annually. It can be prevented in dogs by vaccination and by cleaning and disinfecting bite wounds and post-exposure prophylaxis . Rabies is undiagnosable before symptoms develop. It can be detected through tissue testing after symptoms develop. There are over 200 million cases of schistosomiasis . Approximately 85 percent of cases are in sub-Saharan Africa. The disease can be fatal by causing bladder cancer and hematemesis . Schistosoma species have a complex life cycle that alternates between humans and freshwater snails. Infection occurs when the skin comes into contact with contaminated fresh water in which snails that carry the parasite are living. Symptoms for schistosomiasis are not caused by the worms but by the body's reaction to the eggs. The eggs that do not pass out of the body can become lodged in the intestine or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties. The symptoms are usually haematuria , bladder obstruction, renal failure , bladder cancer , periportal fibrosis, bladder fibrosis, liver fibrosis, portal hypertension , cervical lesions, ascites , and esophageal varices . Inexpensive praziquantel can be used to treat individuals with schistosomiasis, but it cannot prevent reinfection. The cost of prevention is US$0.32 per child per year. Mass deworming treatment with praziquantel, better access to safe water, sanitation, and health education can all be used to prevent schistosomiasis. Vaccines are under development. It can be diagnosed through a serological test, but the test often produces false negatives. Soil-transmitted helminthiasis is the most prevalent neglected tropical disease. The four major worm species responsible for soil-transmitted helminthiasis are Ascaris ( roundworms ), Trichuris ( whipworm ), the hookworms Necator americanus and Ancylostoma duodenale , and Strongyloides stercoralis . There are 1.5 billion people currently infected. Soil-transmitted helminthiasis occurs in sub-Saharan Africa, the Americas, China, and East Asia. The mortality risk is very low. The most common symptoms are anemia, stunted growth , intestinal problems, lack of energy, and compromised physical and cognitive development. Infected children often fall behind in schooling. The severity of symptoms depends on the number of worms in the body. Parasitic worms are generally transmitted via exposure to infected human feces and soil that are spread in the environment, for example, due to open defecation . The most common treatment is medicine. It can be prevented through hygienically prepared food and clean water, improved sanitation , periodic deworming, and health education. The World Health Organization recommends mass deworming without prior diagnosis. Cysticercosis is a tapeworm larvae infection, while taeniasis is infection with adult tapeworms . Both are found in Asia, Africa, and Latin America, particularly on farms in which pigs are exposed to human excrement. Cysticercosis is the most common preventable cause of epilepsy in the developing world. Cysticercosis occurs after ingestion of contaminated food, water, or soil. Cysts and lesions can cause headaches , blindness , seizures , hydrocephalus , meningitis , and dementia . Neurocysticercosis , or the parasitic infection of the nervous system, can be fatal. Taeniasis is not fatal. It is usually contracted after eating undercooked contaminated pork. Taeniasis has mild symptoms, including abdominal pain, nausea, diarrhea, or constipation. [ citation needed ] Drugs are used to treat both diseases. Infection can be prevented through stricter meat-inspection standards, livestock confinement, improved hygiene and sanitation, health education, safe meat preparation, and identifying and treating human and pig carriers. There are 21.4 million people infected with trachoma , of whom 2.2 million are partially blind and 1.2 million are blind. It is found in Africa, Asia, Central and South America, the Middle East, and Australia. The disease disproportionately affects women and children. The mortality risk is very low, although multiple re-infections eventually lead to blindness. The symptoms are internally scarred eyelids, followed by eyelids turning inward. Trachoma is caused by a micro-organism that spreads through eye discharges (on hands, cloth, etc.) and by "eye-seeking flies". It is treated with antibiotics. The only known prevention method is interpersonal hygiene. [ citation needed ] Chromoblastomycosis is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis ). It can be caused by many different types of fungi which become implanted under the skin , often by thorns or splinters. Chromoblastomycosis spreads very slowly. [ citation needed ] Other important endemic mycoses with common systemic involvement are histoplasmosis, paracoccidioidomycosis, coccidioidomycosis, blastomycosis and talaromycosis. These infections are also seldomly seen in returning travelers in western countries Snakebite was added to the list in 2017, after years of criticism of the WHO by activists for not making it a priority. The greatest burden of snakebite morbidity is in India and Southeast Asia. Globally, there are an estimated 421,000 envenomings each year (about 1 in 4 snakebites) and 20,000 deaths, but snakebites often go unreported. A policy analysis however found that the placement of snakebite in the global health agenda of WHO is fragile due to reluctance acceptance of the disease in the neglected tropical disease community and the perceived colonial nature of the network driving the agenda. Buruli ulcer is caused by the bacterium Mycobacterium ulcerans . It is related to the bacteria that cause tuberculosis and leprosy. Mycobacterium ulcerans produces a toxin, mycolactone , that destroys tissue. The prevalence of Buruli ulcer is unknown. The risk of mortality is low, although secondary infections can be lethal. Morbidity takes the form of deformity, disability, and skin lesions, which can be prevented through early treatment with antibiotics and surgery. It is found in Africa, Asia, Australia, and Latin America. Chagas disease is also known as American trypanosomiasis. There are approximately 15 million people infected with Chagas disease. Morbidity rates are higher for immunocompromised individuals, children, and the elderly, but can be very low if the disease is treated early. Chagas disease does not kill victims rapidly, instead causing years of debilitating chronic symptoms. It is caused by the vector-borne protozoa Trypanosoma cruzi . It is spread by contact with Trypanosoma cruzi -infected feces of the triatomine ( assassin bug ). The protozoan can enter the body via the bug's bite, skin breaks, or mucous membranes . Infection can result from eating infected food or coming into contact with contaminated bodily fluids. There are two phases of Chagas disease. The acute phase is usually asymptomatic. The first symptoms are usually skin chancres , unilateral purplish orbital oedema , local lymphadenopathy , and fever , accompanied by a variety of other symptoms depending on the infection site. The chronic phase occurs in 30 percent of all infections and can take three forms: asymptomatic (most prevalent), cardiac, and digestive lesions. Chagas disease can be prevented by avoiding insect bites through insecticide spraying, home improvement, bed nets, hygienic food, medical care, laboratory practices, and testing. It can be diagnosed through a serological test, although the test is not very accurate. Treatment is with medication, which may have severe side effects. There are 50–100 million dengue virus infections annually. Dengue fever is usually not fatal, but infection with one of four serotypes can increase later susceptibility to other serotypes, resulting in a potentially fatal disease called severe dengue. Dengue fever is caused by a flavivirus which is spread mostly by the bite of the Aedes aegypti mosquito. No treatment for either dengue or severe dengue exists beyond palliative care . The symptoms are high fever and flu-like symptoms. It is found in Asia, Latin America, and Northern Australia. Chikungunya is an arboviral disease transmitted by A. albopictus and A. aegypti mosquitoes. The virus was first isolated from an outbreak in Tanzania in 1952. Chikungunya virus is a member of the genus Alphavirus and family Togaviridae . The word "chikungunya" is from the Makonde language and means "that which bends up", referring to the effect of debilitating joint pain on the patient. Symptoms, generally appearing 5–7 days after exposure, can be confused with dengue and include fever, rash, headache, joint pain, and swelling. The disease mainly occurs in Africa and Asia. Dracunculiasis is also known as Guinea-worm disease. In 2019, 53 cases were reported across four countries, a substantial decrease from 3,500,000 cases in 1986. It is not fatal, but can cause months of inactivity. It is caused by drinking water contaminated by water fleas infected with guinea-worm larvae. Approximately one year after infection, a painful blister forms and one or more worms emerge. Worms can be up to 1 metre long. It is usually treated by World Health Organization volunteers who clean and bandage wounds caused by worms and return daily to pull the worm out a few more inches. Dracunculiasis is preventable by water filtration, immediate case identification to prevent spread, health education, and treating ponds with larvicide. An eradication program has been able to reduce prevalence. As of 2014 [ update ] , the four endemic countries are Chad , Ethiopia , Mali , and South Sudan . The rate of echinococcosis is higher in rural areas, and there are more than one million people infected currently. It is caused by ingesting parasites in animal feces. There are two versions of the disease: cystic and alveolar . Both versions involve an asymptomatic incubation period of several years. In the cystic version, liver cysts cause abdominal pain , nausea , and vomiting , while cysts in the lungs cause chronic cough , chest pain , and shortness of breath . In alveolar echinococcosis, a primary cyst develops, usually in the liver, in addition to weight loss, abdominal pain, malaise , and signs of liver failure . Untreated alveolar echinococcosis is fatal. Surgery and drugs can be used to treat echinococcosis. It can be prevented by deworming dogs, sanitation, proper disposal of animal feces, health education, and livestock vaccination. Cystic echinococcosis is found in the eastern portion of the Mediterranean region, northern Africa, southern and eastern Europe, the southern portion of South America, and Central Asia. Alveolar echinococcosis is found in western and northern China, Russia, Europe, and northern North America. It can be diagnosed through imaging techniques and serological tests . There are limited data available on the prevalence of yaws , although it primarily affects children. The mortality risk is very low, but the disease causes disfigurement and disability if untreated. The most common symptom is skin lesions. It is a chronic bacterial infection, transmitted by skin contact, and caused by the spirochete bacterium Treponema pallidum pertenue . It is treated with antibiotics and can be prevented through hygiene and sanitation. Yaws is most prevalent in warm, moist tropical regions of the Americas, Africa, Asia, and the Pacific. Foodborne trematode infections include clonorchiasis , opisthorchiasis , fascioliasis , and paragonimiasis . These infections are all zoonotic , primarily affecting domestic or wild animals, but can also be transmitted to humans. They are acquired by eating food, such as raw fish, contaminated with the larval stages of the parasites. At least 40 million people are thought to be infected. African trypanosomiasis (African sleeping sickness) is a somewhat rare protozoal disease, with fewer than 10,000 cases currently. Human African trypanosomiasis is vector-borne and spreads through the bite of the tsetse fly . The most common symptoms are fever, headache, lymphadenopathy , sleeping disturbances, personality changes, cognitive decline, and coma . The disease is always fatal if untreated. The current forms of treatment are highly toxic and ineffective, as resistance is spreading. It is diagnosed through an inexpensive serological test. [ medical citation needed ]The three forms of leishmaniasis , a protozoal disease, are visceral ( Kala-azar ), cutaneous , and mucocutaneous. There are an estimated 12 million people infected. It is fatal if untreated, and 20,000 deaths from visceral leishmaniasis occur annually. It is a vector-borne disease caused by the bite of sandflies . At least 90 percent of visceral leishmaniasis occurs in Bangladesh , Brazil , Ethiopia , India , South Sudan , and Sudan . Cutaneous leishmaniasis occurs in Afghanistan , Algeria , Brazil, Colombia , Iran , Pakistan , Peru , Saudi Arabia , and Syria . Around 90 percent of mucocutaneous leishmaniasis occurs in Bolivia , Brazil, and Peru. A vaccine is under development to prevent leishmaniasis. The only other method of prevention is avoidance of sandfly bites. Diagnosis can be made by clinical signs, serological tests, or parasitological tests. Leishmaniasis can be treated with expensive medications. According to recent figures from the WHO, 208,619 new cases of leprosy were reported in 2018 from 127 countries. It is most prevalent in India (69% of cases), Brazil, Indonesia , Nigeria , the Democratic Republic of the Congo , Madagascar , and East Africa from Mozambique to Ethiopia, with the highest relative incidence in India, Brazil, and Nepal . There are one to two million individuals currently disabled or disfigured due to past or present leprosy. It is caused by bacteria and transmitted through droplets from the mouth and nose of infected individuals. Leprosy causes disfigurement and physical disabilities if untreated. It is curable if treated early. Treatment requires multidrug therapy. The BCG vaccine has some preventative effect against leprosy. Leprosy has a 5–20 year incubation period, and the symptoms are damage to the skin, nerves, eyes, and limbs. Lymphatic filariasis is also known as elephantiasis . There are approximately 120 million individuals infected and 40 million with deformities. Approximately two-thirds of cases are in Southwest Asia, and one-third are in Africa. Lymphatic filariasis is rarely fatal but has lifelong implications, such as lymphoedema of the limbs, genital disease, and painful recurrent attacks. Most people are asymptomatic but have lymphatic damage. Up to 40 percent of infected individuals have kidney damage. It is a vector-borne disease, caused by nematode worms that are transmitted by mosquitoes. It can be treated with cost-effective antihelminthic treatments, and washing skin can slow or even reverse damage. It is diagnosed with a finger-prick blood test. Noma, an opportunistic bacterial infection causing gangrenous necrosis of the mouth, was added to the World Health Organization's list of neglected tropical diseases in December 2023. Onchocerciasis is also known as river blindness. There are 20.9 million people infected, and prevalence is higher in rural areas. Over 99 percent of cases are in sub-Saharan Africa . It causes blindness, skin rashes, lesions, intense itching, and skin depigmentation. It is a vector-borne disease, caused by blackflies infected with filarial worms. It can be treated with ivermectin and prevented by insecticide spraying or preventative dosing with ivermectin. There are two forms of rabies : furious and paralytic. It is mostly found in Asia and Africa. There is a higher prevalence in rural areas, and it disproportionately affects children. Rabies is fatal after symptoms develop. It is caused by a lyssavirus transmitted through wounds or bites from infected animals. The first symptoms are fever and pain near the infection site, which occur after a one- to three-month incubation period. Furious rabies (the more common type) causes hyperactivity, hydrophobia, and aerophobia; death by cardio-respiratory arrest occurs within days. Paralytic rabies causes a slow progression from paralysis to coma to death. There are 60,000 deaths from rabies annually. It can be prevented in dogs by vaccination and by cleaning and disinfecting bite wounds and post-exposure prophylaxis . Rabies is undiagnosable before symptoms develop. It can be detected through tissue testing after symptoms develop. There are over 200 million cases of schistosomiasis . Approximately 85 percent of cases are in sub-Saharan Africa. The disease can be fatal by causing bladder cancer and hematemesis . Schistosoma species have a complex life cycle that alternates between humans and freshwater snails. Infection occurs when the skin comes into contact with contaminated fresh water in which snails that carry the parasite are living. Symptoms for schistosomiasis are not caused by the worms but by the body's reaction to the eggs. The eggs that do not pass out of the body can become lodged in the intestine or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and learning difficulties. The symptoms are usually haematuria , bladder obstruction, renal failure , bladder cancer , periportal fibrosis, bladder fibrosis, liver fibrosis, portal hypertension , cervical lesions, ascites , and esophageal varices . Inexpensive praziquantel can be used to treat individuals with schistosomiasis, but it cannot prevent reinfection. The cost of prevention is US$0.32 per child per year. Mass deworming treatment with praziquantel, better access to safe water, sanitation, and health education can all be used to prevent schistosomiasis. Vaccines are under development. It can be diagnosed through a serological test, but the test often produces false negatives. Soil-transmitted helminthiasis is the most prevalent neglected tropical disease. The four major worm species responsible for soil-transmitted helminthiasis are Ascaris ( roundworms ), Trichuris ( whipworm ), the hookworms Necator americanus and Ancylostoma duodenale , and Strongyloides stercoralis . There are 1.5 billion people currently infected. Soil-transmitted helminthiasis occurs in sub-Saharan Africa, the Americas, China, and East Asia. The mortality risk is very low. The most common symptoms are anemia, stunted growth , intestinal problems, lack of energy, and compromised physical and cognitive development. Infected children often fall behind in schooling. The severity of symptoms depends on the number of worms in the body. Parasitic worms are generally transmitted via exposure to infected human feces and soil that are spread in the environment, for example, due to open defecation . The most common treatment is medicine. It can be prevented through hygienically prepared food and clean water, improved sanitation , periodic deworming, and health education. The World Health Organization recommends mass deworming without prior diagnosis. Cysticercosis is a tapeworm larvae infection, while taeniasis is infection with adult tapeworms . Both are found in Asia, Africa, and Latin America, particularly on farms in which pigs are exposed to human excrement. Cysticercosis is the most common preventable cause of epilepsy in the developing world. Cysticercosis occurs after ingestion of contaminated food, water, or soil. Cysts and lesions can cause headaches , blindness , seizures , hydrocephalus , meningitis , and dementia . Neurocysticercosis , or the parasitic infection of the nervous system, can be fatal. Taeniasis is not fatal. It is usually contracted after eating undercooked contaminated pork. Taeniasis has mild symptoms, including abdominal pain, nausea, diarrhea, or constipation. [ citation needed ] Drugs are used to treat both diseases. Infection can be prevented through stricter meat-inspection standards, livestock confinement, improved hygiene and sanitation, health education, safe meat preparation, and identifying and treating human and pig carriers. There are 21.4 million people infected with trachoma , of whom 2.2 million are partially blind and 1.2 million are blind. It is found in Africa, Asia, Central and South America, the Middle East, and Australia. The disease disproportionately affects women and children. The mortality risk is very low, although multiple re-infections eventually lead to blindness. The symptoms are internally scarred eyelids, followed by eyelids turning inward. Trachoma is caused by a micro-organism that spreads through eye discharges (on hands, cloth, etc.) and by "eye-seeking flies". It is treated with antibiotics. The only known prevention method is interpersonal hygiene. [ citation needed ]Chromoblastomycosis is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis ). It can be caused by many different types of fungi which become implanted under the skin , often by thorns or splinters. Chromoblastomycosis spreads very slowly. [ citation needed ] Other important endemic mycoses with common systemic involvement are histoplasmosis, paracoccidioidomycosis, coccidioidomycosis, blastomycosis and talaromycosis. These infections are also seldomly seen in returning travelers in western countries Snakebite was added to the list in 2017, after years of criticism of the WHO by activists for not making it a priority. The greatest burden of snakebite morbidity is in India and Southeast Asia. Globally, there are an estimated 421,000 envenomings each year (about 1 in 4 snakebites) and 20,000 deaths, but snakebites often go unreported. A policy analysis however found that the placement of snakebite in the global health agenda of WHO is fragile due to reluctance acceptance of the disease in the neglected tropical disease community and the perceived colonial nature of the network driving the agenda. Several NTDs, such as leprosy , cause severe deformities that result in social stigma. Stigma is considered to be the "hidden burden" of NTDs and is not accounted for in measures such as disability-adjusted life years (DALYs). Other NTDs that carry heavy social stigma include onchocerciasis , lymphatic filariasis , plague , Buruli ulcer , leishmaniasis , and Chagas disease . Lymphatic filariasis, for example, causes severe deformities that can result in denial of marriage and inability to work. Studies in Ghana and Sri Lanka have demonstrated that support groups for patients with lymphatic filariasis can increase participants' self-esteem, quality of life, and social relations through social support and providing practical advice on how to manage their illness. The social effects of neglected tropical diseases have been shown to affect men and women in different ways. Men are socially stigmatized in a way that detrimentally affects their economic prospects. Women are more likely to be affected in the areas of marriage and family. A 2012 review found that infection with a neglected tropical disease predisposes individuals to poor mental health. This is partially due to the social stigma that surrounds NTDs, but is also likely caused by the subsequent lack of access to health and social services. Overall, being a member of the infected community was found to cut individuals off from multiple aspects of society via civic rights, educational opportunities, and employment. A high prevalence of post-traumatic stress disorder (PTSD) and depression was found among people who had survived snakebites. More research needs to be directed to understanding psychological aspects of NTDs to understand their effects more fully and to direct strategies to manage them better in healthcare systems where mental health professionals are scarce. NTDs disproportionately affect women and children. There is also added risk of hookworm infection during pregnancy and potential to transfer diseases such as Chagas during pregnancy. A study in Uganda found that women were able to obtain treatment more easily than men because they had fewer occupational responsibilities and were more trusting of treatments, but ignorance of the effects of medicines during pregnancy prevented adequate care. The paper concludes that gender should be considered when designing treatment programs in Uganda. Additionally, women often bear a heavier social stigma in relation to the pressure to marry. [ dubious – discuss ] [ failed verification ] The cost of treatment of some of these diseases, such as Buruli ulcer, can be almost the average household income for families in the highest quarter of incomes, while for those in the lowest quarter it can be over twice the yearly income. These enormous financial costs often cause deferral of treatment and financial ruin. These diseases also cost the government in terms of healthcare provision and lost worker productivity through morbidity and shortened life spans. In Kenya, for example, deworming is estimated to increase average adult income by 40 percent, which is a benefit-to-cost ratio of 100. Each untreated case of trachoma is estimated to cost US$118 in lost productivity. Each case of schistosomiasis causes a loss of 45.4 days of work per year. Most of the diseases cost the economies of developing countries millions of dollars. Large-scale prevention campaigns are predicted to increase agricultural output and education levels. The low cost of treatment for NTDs can be attributed to the large scale of the programs, free provision of drugs by pharmaceutical companies, delivery modes of drugs, and unpaid volunteers who distribute the drugs. The economic burden of NTDs is undervalued and therefore the corresponding economic effect and cost-effectiveness of decreasing prevalence of NTDs is underestimated. The investment return on measures to control NTDs is estimated to be between 14 and 30 percent, depending on the disease and region. Coinfection is a major concern with NTDs, making them more damaging than their mortality rates might suggest. Because factors such as poverty, inadequate healthcare and inadequate sanitation practices contribute to all NTDs, they are often found in overlapping distributions. Helminth infections , as the most common infection of humans, are often found to be in multi-infection systems. For example, in Brazil, low socioeconomic status contributes to overcrowded housing. In these same areas, coinfection by Necator americanus and Schistosoma mansoni is common. The effect of each worm weakens the immune system , making infection from the other more likely and more severe. For this reason, coinfection carries a higher risk of mortality. NTDs may also play a role in infection with other diseases, such as malaria , HIV/AIDS , and tuberculosis . The ability of helminths to manipulate the immune system may create a physiological environment that could exacerbate the progression of HIV/AIDS. Some evidence from Senegal , Malawi , and Thailand has shown that helminth infections raise the risk of malarial infection. Several NTDs, such as leprosy , cause severe deformities that result in social stigma. Stigma is considered to be the "hidden burden" of NTDs and is not accounted for in measures such as disability-adjusted life years (DALYs). Other NTDs that carry heavy social stigma include onchocerciasis , lymphatic filariasis , plague , Buruli ulcer , leishmaniasis , and Chagas disease . Lymphatic filariasis, for example, causes severe deformities that can result in denial of marriage and inability to work. Studies in Ghana and Sri Lanka have demonstrated that support groups for patients with lymphatic filariasis can increase participants' self-esteem, quality of life, and social relations through social support and providing practical advice on how to manage their illness. The social effects of neglected tropical diseases have been shown to affect men and women in different ways. Men are socially stigmatized in a way that detrimentally affects their economic prospects. Women are more likely to be affected in the areas of marriage and family. A 2012 review found that infection with a neglected tropical disease predisposes individuals to poor mental health. This is partially due to the social stigma that surrounds NTDs, but is also likely caused by the subsequent lack of access to health and social services. Overall, being a member of the infected community was found to cut individuals off from multiple aspects of society via civic rights, educational opportunities, and employment. A high prevalence of post-traumatic stress disorder (PTSD) and depression was found among people who had survived snakebites. More research needs to be directed to understanding psychological aspects of NTDs to understand their effects more fully and to direct strategies to manage them better in healthcare systems where mental health professionals are scarce. NTDs disproportionately affect women and children. There is also added risk of hookworm infection during pregnancy and potential to transfer diseases such as Chagas during pregnancy. A study in Uganda found that women were able to obtain treatment more easily than men because they had fewer occupational responsibilities and were more trusting of treatments, but ignorance of the effects of medicines during pregnancy prevented adequate care. The paper concludes that gender should be considered when designing treatment programs in Uganda. Additionally, women often bear a heavier social stigma in relation to the pressure to marry. [ dubious – discuss ] [ failed verification ]Several NTDs, such as leprosy , cause severe deformities that result in social stigma. Stigma is considered to be the "hidden burden" of NTDs and is not accounted for in measures such as disability-adjusted life years (DALYs). Other NTDs that carry heavy social stigma include onchocerciasis , lymphatic filariasis , plague , Buruli ulcer , leishmaniasis , and Chagas disease . Lymphatic filariasis, for example, causes severe deformities that can result in denial of marriage and inability to work. Studies in Ghana and Sri Lanka have demonstrated that support groups for patients with lymphatic filariasis can increase participants' self-esteem, quality of life, and social relations through social support and providing practical advice on how to manage their illness. The social effects of neglected tropical diseases have been shown to affect men and women in different ways. Men are socially stigmatized in a way that detrimentally affects their economic prospects. Women are more likely to be affected in the areas of marriage and family. A 2012 review found that infection with a neglected tropical disease predisposes individuals to poor mental health. This is partially due to the social stigma that surrounds NTDs, but is also likely caused by the subsequent lack of access to health and social services. Overall, being a member of the infected community was found to cut individuals off from multiple aspects of society via civic rights, educational opportunities, and employment. A high prevalence of post-traumatic stress disorder (PTSD) and depression was found among people who had survived snakebites. More research needs to be directed to understanding psychological aspects of NTDs to understand their effects more fully and to direct strategies to manage them better in healthcare systems where mental health professionals are scarce. NTDs disproportionately affect women and children. There is also added risk of hookworm infection during pregnancy and potential to transfer diseases such as Chagas during pregnancy. A study in Uganda found that women were able to obtain treatment more easily than men because they had fewer occupational responsibilities and were more trusting of treatments, but ignorance of the effects of medicines during pregnancy prevented adequate care. The paper concludes that gender should be considered when designing treatment programs in Uganda. Additionally, women often bear a heavier social stigma in relation to the pressure to marry. [ dubious – discuss ] [ failed verification ]The cost of treatment of some of these diseases, such as Buruli ulcer, can be almost the average household income for families in the highest quarter of incomes, while for those in the lowest quarter it can be over twice the yearly income. These enormous financial costs often cause deferral of treatment and financial ruin. These diseases also cost the government in terms of healthcare provision and lost worker productivity through morbidity and shortened life spans. In Kenya, for example, deworming is estimated to increase average adult income by 40 percent, which is a benefit-to-cost ratio of 100. Each untreated case of trachoma is estimated to cost US$118 in lost productivity. Each case of schistosomiasis causes a loss of 45.4 days of work per year. Most of the diseases cost the economies of developing countries millions of dollars. Large-scale prevention campaigns are predicted to increase agricultural output and education levels. The low cost of treatment for NTDs can be attributed to the large scale of the programs, free provision of drugs by pharmaceutical companies, delivery modes of drugs, and unpaid volunteers who distribute the drugs. The economic burden of NTDs is undervalued and therefore the corresponding economic effect and cost-effectiveness of decreasing prevalence of NTDs is underestimated. The investment return on measures to control NTDs is estimated to be between 14 and 30 percent, depending on the disease and region. Coinfection is a major concern with NTDs, making them more damaging than their mortality rates might suggest. Because factors such as poverty, inadequate healthcare and inadequate sanitation practices contribute to all NTDs, they are often found in overlapping distributions. Helminth infections , as the most common infection of humans, are often found to be in multi-infection systems. For example, in Brazil, low socioeconomic status contributes to overcrowded housing. In these same areas, coinfection by Necator americanus and Schistosoma mansoni is common. The effect of each worm weakens the immune system , making infection from the other more likely and more severe. For this reason, coinfection carries a higher risk of mortality. NTDs may also play a role in infection with other diseases, such as malaria , HIV/AIDS , and tuberculosis . The ability of helminths to manipulate the immune system may create a physiological environment that could exacerbate the progression of HIV/AIDS. Some evidence from Senegal , Malawi , and Thailand has shown that helminth infections raise the risk of malarial infection. Coinfection is a major concern with NTDs, making them more damaging than their mortality rates might suggest. Because factors such as poverty, inadequate healthcare and inadequate sanitation practices contribute to all NTDs, they are often found in overlapping distributions. Helminth infections , as the most common infection of humans, are often found to be in multi-infection systems. For example, in Brazil, low socioeconomic status contributes to overcrowded housing. In these same areas, coinfection by Necator americanus and Schistosoma mansoni is common. The effect of each worm weakens the immune system , making infection from the other more likely and more severe. For this reason, coinfection carries a higher risk of mortality. NTDs may also play a role in infection with other diseases, such as malaria , HIV/AIDS , and tuberculosis . The ability of helminths to manipulate the immune system may create a physiological environment that could exacerbate the progression of HIV/AIDS. Some evidence from Senegal , Malawi , and Thailand has shown that helminth infections raise the risk of malarial infection. Prevention and eradication are important because "of the appalling stigma, disfigurement, blindness and disabilities caused by NTDs." The principal aim of the London Declaration on Neglected Tropical Diseases was the elimination or eradication of dracunculiasis , leprosy , lymphatic filariasis , onchocerciasis , trachoma , sleeping sickness , visceral leishmaniasis , and canine rabies within ten years of its launch in January 2012. The declaration is a collaborative effort involving the WHO, the World Bank , the Bill & Melinda Gates Foundation, the world's 13 leading pharmaceutical companies, and government representatives from the US, UK, United Arab Emirates, Bangladesh, Brazil, Mozambique, and Tanzania. While there has been a noticeable uptick in biological research into NTDs, prevention may be supplemented by social and development outreach. Spiegel and coauthors advocated for "social offset", which reallocates some funding for biotechnological research to social programs. This attempts to alleviate some of the factors (such as poverty, poor sanitation, overcrowding and poor healthcare) that greatly exacerbate conditions brought on by NTDs. Projects such as these also strengthen the goal of sustained eliminations rather than quickly addressing symptoms. There are many prevention and eradication campaigns funded by organizations such as the World Health Organization, US Agency for International Development , Bill & Melinda Gates Foundation , and UK Department for International Development . Sustainable Development Goal 3 has the target: "By 2030, [to] end the epidemics of AIDS, tuberculosis, malaria and neglected tropical diseases and combat hepatitis, water-borne diseases and other communicable diseases ." In 2012, WHO published an NTD "roadmap", which contained milestones for 2015 and 2020, and specified targets for eradication, elimination and intensified control of the different NTDs. For example: In 2021, WHO updated their NTD roadmap "Together towards 2030", outlining their approach for 2021–2030. : v–vi The U.S. Food and Drug Administration priority review voucher is an incentive for companies to invest in new drugs and vaccines for tropical diseases. A provision of the Food and Drug Administration Amendments Act of 2007 awards a transferable "priority review voucher" to any company that obtains approval for a treatment for one of the listed diseases. The voucher can later be used to accelerate the review of an unrelated drug. This program is for all tropical diseases and includes medicines for malaria and tuberculosis. The first voucher given was for Coartem , a malaria treatment. The prize was proposed by Duke University faculty Henry Grabowski, Jeffrey Moe, and David Ridley in their 2006 Health Affairs paper "Developing Drugs for Developing Countries". In 2007, United States Senators Sam Brownback (R-KS) and Sherrod Brown (D-OH) sponsored an amendment to the Food and Drug Administration Amendments Act of 2007. President George W. Bush signed the bill in September 2007. [ citation needed ] Deworming treatments in infected children may have some nutritional benefit, as worms are often partially responsible for malnutrition. However, in areas where these infections are common, there is strong evidence that mass deworming campaigns do not have a positive effect on children's average nutritional status, levels of blood haemoglobin , cognitive abilities, performance at school, or survival. To achieve health gains in the longer term, improvements in sanitation and hygiene behaviours are also required, together with deworming treatments. [ citation needed ] The effect of mass deworming on school attendance is disputed. It has been argued that mass deworming has a positive effect on school attendance. The long-term benefits of deworming include a decrease in school absenteeism by 25 percent and an increase in adult earnings by 20 percent. A systematic review, however, found that there is little or no difference in attendance in children who receive mass deworming compared to children who did not. One study found that boys were enrolled in primary school for more years than boys who were in schools that did not offer such programs. Girls in the same study were about a quarter more likely to attend secondary school if they received treatment. Both groups went on to participate in more skilled sectors of the labor market. The economic growth generated from school programs such as this may balance out the actual expenses of the program. However, the results of this study are disputed (due to a high risk of bias in the study), and the positive long-term outcomes of mass deworming remain unclear. Inclusion of NTDs into initiatives for malaria , HIV/AIDS , and tuberculosis , as well as integration of NTD treatment programs, may have advantages given the strong link between these diseases and NTDs. Some neglected tropical diseases share common vectors (sandflies, black flies, and mosquitos). Both medicinal and vector control efforts may be combined. A four-drug rapid-impact package has been proposed that targets multiple diseases together. This package is estimated to cost US$0.40 per patient, with estimated saving of 26–47% compared to treating the diseases separately. While more research must be done in order to understand how NTDs and other diseases interact in both the vector and the human stages, safety assessments have so far produced positive results. Many neglected tropical diseases and other prevalent diseases share common vectors, creating another opportunity for treatment and control integration. One such example of this is malaria and lymphatic filariasis, which are both transmitted by the same or related mosquito vectors. Vector control, through the distribution of insecticide-treated nets, reduces human contact with a wide variety of disease vectors. Integrated vector control may also alleviate pressure on mass drug administration, especially with respect to rapidly evolving drug resistance. Combining vector control and mass drug administration deemphasizes both, making each less susceptible to resistance evolution. Water, sanitation, and hygiene ( WASH ) interventions are essential in preventing many NTDs, such as soil-transmitted helminthiasis . Mass drug administration alone will not protect people from re-infection. A more holistic and integrated approach to NTDs and WASH efforts will benefit both sectors along with the communities they are aiming to serve. This is especially true in areas where more than one NTD is endemic. In August 2015, the World Health Organization unveiled a global strategy and action plan to integrate WASH with other public health interventions to accelerate the elimination of NTDs. The plan aimed to intensify control or eliminate certain NTDs in specific regions by 2020, and referred to the NTD "roadmap" milestones from 2012 that included eradication of dracunculiasis by 2015 and of yaws by 2020, elimination of trachoma and lymphatic filariasis as public health problems by 2020, and intensified control of dengue, schistosomiasis, and soil-transmitted helminthiases. Closer collaboration between WASH and NTD programmes can lead to synergies . They can be achieved through collaborative planning, delivery and evaluation of programmes, strengthening and sharing of evidence, and using monitoring tools to improve the equity of health services. Reasons why WASH plays an important role in NTD prevention and patient care include: Biotechnology companies in the developing world have targeted neglected tropical diseases due to a need to improve global health. Mass drug administration is considered a possible method for eradication, especially for lymphatic filariasis, onchocerciasis, and trachoma, although drug resistance is a potential problem. According to Fenwick, Pfizer donated 70 million doses of drugs in 2011 to eliminate trachoma through the International Trachoma Initiative. Merck has helped The African Programme for the Control of Onchocerciasis (APOC) and Oncho Elimination Programme for the Americas to greatly diminish the effect of onchocerciasis by donating ivermectin . Merck KGaA pledged to give 200 million tablets of praziquantel , the only cure for schistosomiasis , over 10 years. GlaxoSmithKline has donated two billion tablets of medicine for lymphatic filariasis and pledged 400 million deworming tablets per year for five years in 2010. Johnson & Johnson has pledged 200 million deworming tablets per year. Novartis has pledged leprosy treatment, and EISAI pledged two billion tablets to help treat lymphatic filariasis. Non-governmental organizations that focus exclusively on NTDs include the Schistosomiasis Control Initiative , Deworm the World , and the END Fund. Despite under-funding, treatment and prevention of many neglected diseases is cost-effective. The cost of treating a child for infection of soil-transmitted helminths and schistosomes (some of the main causes of neglected diseases) is less than US$0.50 per year when administered as part of school-based mass deworming by Deworm the World. This programme is recommended by Giving What We Can and the Copenhagen Consensus Centre as one of the most efficient and cost-effective solutions. The efforts of the Schistosomiasis Control Initiative to combat neglected diseases include the use of rapid-impact packages: supplying schools with packages including four or five drugs, and training teachers in how to administer them. [ citation needed ] Health Action International based in Amsterdam worked with the WHO to get snakebite envenoming on the list of neglected tropical diseases. An alternative to the profit-driven drug development model emerged in 2000 to address the needs of these neglected patients. Product development partnerships (PDPs) aim at implementing and accelerating the research and development (R&D) of safe and effective health tools (diagnostics, vaccines, drugs) to combat neglected diseases. Drugs for Neglected Disease initiative (DNDi) is one of these PDPs that has already developed new treatments for NTDs. The Sabin Vaccine Institute , founded in 1993, works to address the issues of vaccine-preventable diseases as well as NTDs. They run three main programs: Sabin Vaccine Development, Global Network for Neglected Tropical Diseases , and Vaccine Advocacy and Education. Their product development partnership affiliates them with the Texas Children's Hospital as well as the Baylor College of Medicine . Their major campaign, End7, aims to end seven of the most common NTDs ( elephantiasis , river blindness , snail fever , trachoma , roundworm , whipworm , and hookworm ) by 2020. Through End7, college campuses undertake fundraising and educational initiatives for the broader goals of the campaign. WIPO Re:Search was established in 2011 by the World Intellectual Property Organization in collaboration with BIO Ventures for Global Health (BVGH) and with the active participation of leading pharmaceutical companies and other private and public sector research organizations. It allows organizations to share their intellectual property, compounds, expertise, facilities, and know-how royalty-free with qualified researchers worldwide working on new solutions for NTDs, malaria, and tuberculosis. In 2013, the Government of Japan, five Japanese pharmaceutical companies, the Bill and Melinda Gates Foundation, and the UNDP established a new public–private partnership, the Global Health Innovative Technology Fund . They pledged over US$100 million to the fund over five years, to be awarded as grants to R&D partnerships across sectors in Japan and elsewhere, working to develop new drugs and vaccines for 17 neglected diseases, in addition to HIV, malaria, and tuberculosis. Affordability of the resulting drugs and vaccines is one of the key criteria for grant awards. The London Declaration on Neglected Tropical Diseases, initiated by the Bill and Melinda Gates Foundation launched on 30 January 2012 in London. Inspired by the WHO roadmap to eradicate or prevent transmission for neglected tropical diseases, it aimed to eradicate or reduce NTDs by the year 2020. It was endorsed by governments and organisations around the world, as well as major pharmaceutical companies including Abbott , AstraZeneca , Bayer HealthCare Pharmaceuticals , Becton Dickinson , Bristol-Myers Squibb , Eisai , Gilead Sciences , GlaxoSmithKline , Johnson & Johnson , Merck KGaA , Merck Sharp & Dohme, MSD , Novartis , Pfizer , and Sanofi . It was not a complete success, but millions of lives were saved, the burden of the infections was reduced, and 42 countries eliminated at least one disease. To commemorate the programme, WHO adopted 30 January as the World NTD Day . The Kigali Declaration on Neglected Tropical Diseases was launched at the Kigali Summit on Malaria and Neglected Tropical Diseases (NTDs) hosted by the Government of Rwanda at its capital city Kigali on 23 June 2022. It was signed as a support for the World Health Organization 's 2021–30 road map for NTDs and the target of Sustainable Development Goal 3 to end NTD epidemics; and as a follow-up project of the London Declaration . Supported by WHO, governments of the Commonwealth of Nations pledged the endorsement, along with commitments from GSK plc , Novartis , and Pfizer . An open-access journal dedicated to neglected tropical diseases called PLoS Neglected Tropical Diseases first began publication in 2007. One of the first large-scale initiatives to address NTDs came from a collaboration between Kenneth Warren and the Rockefeller Foundation . Ken Warren is regarded as a pioneer in neglected tropical disease research. The Great Neglected Tropical Diseases Network was a consortium of scientists from all over the world, hand-picked by Warren, working to expand the research base in neglected diseases. Many of the scientists that he recruited had not been involved in NTD research before. The network ran from 1978 to 1988. Warren's vision was to establish units within biological labs across the world, dedicated to R&D . By forming a critical mass of scientists in NTD research, he hoped to attract new students into the field. The interdisciplinary group met annually to update the community on research progress. Much of the work done by this group focused on understanding the mechanisms behind infection. At these informally structured meetings, research partnerships were formed. Warren himself encouraged these partnerships, especially if they bridged the divide between developed and developing nations. Through the Great Neglected Tropical Disease Network, a great number of scientists were brought into the field of parasitology . There are many prevention and eradication campaigns funded by organizations such as the World Health Organization, US Agency for International Development , Bill & Melinda Gates Foundation , and UK Department for International Development . Sustainable Development Goal 3 has the target: "By 2030, [to] end the epidemics of AIDS, tuberculosis, malaria and neglected tropical diseases and combat hepatitis, water-borne diseases and other communicable diseases ." In 2012, WHO published an NTD "roadmap", which contained milestones for 2015 and 2020, and specified targets for eradication, elimination and intensified control of the different NTDs. For example: In 2021, WHO updated their NTD roadmap "Together towards 2030", outlining their approach for 2021–2030. : v–vi The U.S. Food and Drug Administration priority review voucher is an incentive for companies to invest in new drugs and vaccines for tropical diseases. A provision of the Food and Drug Administration Amendments Act of 2007 awards a transferable "priority review voucher" to any company that obtains approval for a treatment for one of the listed diseases. The voucher can later be used to accelerate the review of an unrelated drug. This program is for all tropical diseases and includes medicines for malaria and tuberculosis. The first voucher given was for Coartem , a malaria treatment. The prize was proposed by Duke University faculty Henry Grabowski, Jeffrey Moe, and David Ridley in their 2006 Health Affairs paper "Developing Drugs for Developing Countries". In 2007, United States Senators Sam Brownback (R-KS) and Sherrod Brown (D-OH) sponsored an amendment to the Food and Drug Administration Amendments Act of 2007. President George W. Bush signed the bill in September 2007. [ citation needed ]In 2012, WHO published an NTD "roadmap", which contained milestones for 2015 and 2020, and specified targets for eradication, elimination and intensified control of the different NTDs. For example: In 2021, WHO updated their NTD roadmap "Together towards 2030", outlining their approach for 2021–2030. : v–viThe U.S. Food and Drug Administration priority review voucher is an incentive for companies to invest in new drugs and vaccines for tropical diseases. A provision of the Food and Drug Administration Amendments Act of 2007 awards a transferable "priority review voucher" to any company that obtains approval for a treatment for one of the listed diseases. The voucher can later be used to accelerate the review of an unrelated drug. This program is for all tropical diseases and includes medicines for malaria and tuberculosis. The first voucher given was for Coartem , a malaria treatment. The prize was proposed by Duke University faculty Henry Grabowski, Jeffrey Moe, and David Ridley in their 2006 Health Affairs paper "Developing Drugs for Developing Countries". In 2007, United States Senators Sam Brownback (R-KS) and Sherrod Brown (D-OH) sponsored an amendment to the Food and Drug Administration Amendments Act of 2007. President George W. Bush signed the bill in September 2007. [ citation needed ]Deworming treatments in infected children may have some nutritional benefit, as worms are often partially responsible for malnutrition. However, in areas where these infections are common, there is strong evidence that mass deworming campaigns do not have a positive effect on children's average nutritional status, levels of blood haemoglobin , cognitive abilities, performance at school, or survival. To achieve health gains in the longer term, improvements in sanitation and hygiene behaviours are also required, together with deworming treatments. [ citation needed ] The effect of mass deworming on school attendance is disputed. It has been argued that mass deworming has a positive effect on school attendance. The long-term benefits of deworming include a decrease in school absenteeism by 25 percent and an increase in adult earnings by 20 percent. A systematic review, however, found that there is little or no difference in attendance in children who receive mass deworming compared to children who did not. One study found that boys were enrolled in primary school for more years than boys who were in schools that did not offer such programs. Girls in the same study were about a quarter more likely to attend secondary school if they received treatment. Both groups went on to participate in more skilled sectors of the labor market. The economic growth generated from school programs such as this may balance out the actual expenses of the program. However, the results of this study are disputed (due to a high risk of bias in the study), and the positive long-term outcomes of mass deworming remain unclear. Inclusion of NTDs into initiatives for malaria , HIV/AIDS , and tuberculosis , as well as integration of NTD treatment programs, may have advantages given the strong link between these diseases and NTDs. Some neglected tropical diseases share common vectors (sandflies, black flies, and mosquitos). Both medicinal and vector control efforts may be combined. A four-drug rapid-impact package has been proposed that targets multiple diseases together. This package is estimated to cost US$0.40 per patient, with estimated saving of 26–47% compared to treating the diseases separately. While more research must be done in order to understand how NTDs and other diseases interact in both the vector and the human stages, safety assessments have so far produced positive results. Many neglected tropical diseases and other prevalent diseases share common vectors, creating another opportunity for treatment and control integration. One such example of this is malaria and lymphatic filariasis, which are both transmitted by the same or related mosquito vectors. Vector control, through the distribution of insecticide-treated nets, reduces human contact with a wide variety of disease vectors. Integrated vector control may also alleviate pressure on mass drug administration, especially with respect to rapidly evolving drug resistance. Combining vector control and mass drug administration deemphasizes both, making each less susceptible to resistance evolution. Water, sanitation, and hygiene ( WASH ) interventions are essential in preventing many NTDs, such as soil-transmitted helminthiasis . Mass drug administration alone will not protect people from re-infection. A more holistic and integrated approach to NTDs and WASH efforts will benefit both sectors along with the communities they are aiming to serve. This is especially true in areas where more than one NTD is endemic. In August 2015, the World Health Organization unveiled a global strategy and action plan to integrate WASH with other public health interventions to accelerate the elimination of NTDs. The plan aimed to intensify control or eliminate certain NTDs in specific regions by 2020, and referred to the NTD "roadmap" milestones from 2012 that included eradication of dracunculiasis by 2015 and of yaws by 2020, elimination of trachoma and lymphatic filariasis as public health problems by 2020, and intensified control of dengue, schistosomiasis, and soil-transmitted helminthiases. Closer collaboration between WASH and NTD programmes can lead to synergies . They can be achieved through collaborative planning, delivery and evaluation of programmes, strengthening and sharing of evidence, and using monitoring tools to improve the equity of health services. Reasons why WASH plays an important role in NTD prevention and patient care include: Biotechnology companies in the developing world have targeted neglected tropical diseases due to a need to improve global health. Mass drug administration is considered a possible method for eradication, especially for lymphatic filariasis, onchocerciasis, and trachoma, although drug resistance is a potential problem. According to Fenwick, Pfizer donated 70 million doses of drugs in 2011 to eliminate trachoma through the International Trachoma Initiative. Merck has helped The African Programme for the Control of Onchocerciasis (APOC) and Oncho Elimination Programme for the Americas to greatly diminish the effect of onchocerciasis by donating ivermectin . Merck KGaA pledged to give 200 million tablets of praziquantel , the only cure for schistosomiasis , over 10 years. GlaxoSmithKline has donated two billion tablets of medicine for lymphatic filariasis and pledged 400 million deworming tablets per year for five years in 2010. Johnson & Johnson has pledged 200 million deworming tablets per year. Novartis has pledged leprosy treatment, and EISAI pledged two billion tablets to help treat lymphatic filariasis. Non-governmental organizations that focus exclusively on NTDs include the Schistosomiasis Control Initiative , Deworm the World , and the END Fund. Despite under-funding, treatment and prevention of many neglected diseases is cost-effective. The cost of treating a child for infection of soil-transmitted helminths and schistosomes (some of the main causes of neglected diseases) is less than US$0.50 per year when administered as part of school-based mass deworming by Deworm the World. This programme is recommended by Giving What We Can and the Copenhagen Consensus Centre as one of the most efficient and cost-effective solutions. The efforts of the Schistosomiasis Control Initiative to combat neglected diseases include the use of rapid-impact packages: supplying schools with packages including four or five drugs, and training teachers in how to administer them. [ citation needed ] Health Action International based in Amsterdam worked with the WHO to get snakebite envenoming on the list of neglected tropical diseases. An alternative to the profit-driven drug development model emerged in 2000 to address the needs of these neglected patients. Product development partnerships (PDPs) aim at implementing and accelerating the research and development (R&D) of safe and effective health tools (diagnostics, vaccines, drugs) to combat neglected diseases. Drugs for Neglected Disease initiative (DNDi) is one of these PDPs that has already developed new treatments for NTDs. The Sabin Vaccine Institute , founded in 1993, works to address the issues of vaccine-preventable diseases as well as NTDs. They run three main programs: Sabin Vaccine Development, Global Network for Neglected Tropical Diseases , and Vaccine Advocacy and Education. Their product development partnership affiliates them with the Texas Children's Hospital as well as the Baylor College of Medicine . Their major campaign, End7, aims to end seven of the most common NTDs ( elephantiasis , river blindness , snail fever , trachoma , roundworm , whipworm , and hookworm ) by 2020. Through End7, college campuses undertake fundraising and educational initiatives for the broader goals of the campaign. WIPO Re:Search was established in 2011 by the World Intellectual Property Organization in collaboration with BIO Ventures for Global Health (BVGH) and with the active participation of leading pharmaceutical companies and other private and public sector research organizations. It allows organizations to share their intellectual property, compounds, expertise, facilities, and know-how royalty-free with qualified researchers worldwide working on new solutions for NTDs, malaria, and tuberculosis. In 2013, the Government of Japan, five Japanese pharmaceutical companies, the Bill and Melinda Gates Foundation, and the UNDP established a new public–private partnership, the Global Health Innovative Technology Fund . They pledged over US$100 million to the fund over five years, to be awarded as grants to R&D partnerships across sectors in Japan and elsewhere, working to develop new drugs and vaccines for 17 neglected diseases, in addition to HIV, malaria, and tuberculosis. Affordability of the resulting drugs and vaccines is one of the key criteria for grant awards. The London Declaration on Neglected Tropical Diseases, initiated by the Bill and Melinda Gates Foundation launched on 30 January 2012 in London. Inspired by the WHO roadmap to eradicate or prevent transmission for neglected tropical diseases, it aimed to eradicate or reduce NTDs by the year 2020. It was endorsed by governments and organisations around the world, as well as major pharmaceutical companies including Abbott , AstraZeneca , Bayer HealthCare Pharmaceuticals , Becton Dickinson , Bristol-Myers Squibb , Eisai , Gilead Sciences , GlaxoSmithKline , Johnson & Johnson , Merck KGaA , Merck Sharp & Dohme, MSD , Novartis , Pfizer , and Sanofi . It was not a complete success, but millions of lives were saved, the burden of the infections was reduced, and 42 countries eliminated at least one disease. To commemorate the programme, WHO adopted 30 January as the World NTD Day . The Kigali Declaration on Neglected Tropical Diseases was launched at the Kigali Summit on Malaria and Neglected Tropical Diseases (NTDs) hosted by the Government of Rwanda at its capital city Kigali on 23 June 2022. It was signed as a support for the World Health Organization 's 2021–30 road map for NTDs and the target of Sustainable Development Goal 3 to end NTD epidemics; and as a follow-up project of the London Declaration . Supported by WHO, governments of the Commonwealth of Nations pledged the endorsement, along with commitments from GSK plc , Novartis , and Pfizer . The London Declaration on Neglected Tropical Diseases, initiated by the Bill and Melinda Gates Foundation launched on 30 January 2012 in London. Inspired by the WHO roadmap to eradicate or prevent transmission for neglected tropical diseases, it aimed to eradicate or reduce NTDs by the year 2020. It was endorsed by governments and organisations around the world, as well as major pharmaceutical companies including Abbott , AstraZeneca , Bayer HealthCare Pharmaceuticals , Becton Dickinson , Bristol-Myers Squibb , Eisai , Gilead Sciences , GlaxoSmithKline , Johnson & Johnson , Merck KGaA , Merck Sharp & Dohme, MSD , Novartis , Pfizer , and Sanofi . It was not a complete success, but millions of lives were saved, the burden of the infections was reduced, and 42 countries eliminated at least one disease. To commemorate the programme, WHO adopted 30 January as the World NTD Day . The Kigali Declaration on Neglected Tropical Diseases was launched at the Kigali Summit on Malaria and Neglected Tropical Diseases (NTDs) hosted by the Government of Rwanda at its capital city Kigali on 23 June 2022. It was signed as a support for the World Health Organization 's 2021–30 road map for NTDs and the target of Sustainable Development Goal 3 to end NTD epidemics; and as a follow-up project of the London Declaration . Supported by WHO, governments of the Commonwealth of Nations pledged the endorsement, along with commitments from GSK plc , Novartis , and Pfizer . An open-access journal dedicated to neglected tropical diseases called PLoS Neglected Tropical Diseases first began publication in 2007. One of the first large-scale initiatives to address NTDs came from a collaboration between Kenneth Warren and the Rockefeller Foundation . Ken Warren is regarded as a pioneer in neglected tropical disease research. The Great Neglected Tropical Diseases Network was a consortium of scientists from all over the world, hand-picked by Warren, working to expand the research base in neglected diseases. Many of the scientists that he recruited had not been involved in NTD research before. The network ran from 1978 to 1988. Warren's vision was to establish units within biological labs across the world, dedicated to R&D . By forming a critical mass of scientists in NTD research, he hoped to attract new students into the field. The interdisciplinary group met annually to update the community on research progress. Much of the work done by this group focused on understanding the mechanisms behind infection. At these informally structured meetings, research partnerships were formed. Warren himself encouraged these partnerships, especially if they bridged the divide between developed and developing nations. Through the Great Neglected Tropical Disease Network, a great number of scientists were brought into the field of parasitology . The distribution of neglected tropical disease disproportionally affects about one billion of the world's poorest populations, causing mortality, disability, and morbidity. Lack of funding, resources, and attention can result in treatable and preventable diseases causing death. Factors like political dynamics, poverty, and geographical conditions can make the delivery of NTD control programs difficult. Intersectional collaboration of poverty reduction policies and neglected tropical diseases creates cross-sector approaches to simultaneously address these issues. The six most common NTDs include soil-transmitted helminths (STHs)—specifically roundworms ( Ascaris lumbricoides ), whipworm ( Trichuris trichiura ), and hookworms ( Necator americanus and Ancylostoma duodenale )—schistosomiasis, trachoma, and lymphatic filariasis (LF). These diseases affect one-sixth of the world's population, with 90 percent of the disease burden occurring in sub-Saharan Africa. Information on the frequency of neglected tropical diseases is of low quality. It is currently difficult to summarize all of the information on this family of diseases. One effort to do so is the Global Burden of Disease framework. It aims to create a standardized method of measurement. The principle components of the approach involve 1) the measuring of premature mortality as well as disability, 2) the standardized usage of DALYs ( disability-adjusted life years ), and 3) widespread inclusion of diseases and injury causes with the estimation of missing data. However, the DALY has been criticized as a "systematic undervaluation" of disease burden. King asserts that DALY emphasizes the individual too much while ignoring the effects of the ecology of the disease. In order for the measure to become more valid, it may have to take the context of poverty more into account. King also emphasizes that DALYs may not capture the non-linear effects of poverty on the cost-utility analysis of disease control. The Socio-Demographic Index (SDI) and Healthy Life Expectancy (HALE) are other summary measures that can be used to take into account other factors. HALE is a metric that weights years lived and health loss before death to provide a summary of population health. SDI is a measurement that includes lag-distributed income per capita, average education, and fertility rate. Socioeconomic factors greatly influence the distribution of neglected tropical diseases, and not addressing these factors in models and measurements can lead to ineffective public health policy. NTD interventions include programs to address environmental and social determinants of health (e.g., vector control, water quality, sanitation) as well as programs offering mass drug administration for disease prevention and treatment. Drug treatments exist to confront many of the NTDs and represent some of the world's essential medicines . Despite significant health and economic improvements using available medicines, the low number of new compounds being researched and developed for NTDs is an ongoing and significant challenge. The dearth of candidates in pharmaceutical company drug pipelines is primarily attributed to the high costs of drug development and the fact that NTDs are concentrated among the world's poor. Other disincentives to investment include weak existing infrastructure for distribution and sales as well as concerns regarding intellectual property protection. However, the major stakeholders in NTD drug development—governments, foundations, pharmaceutical companies, academia, and NGOs —are involved in activities to help address the research and development shortfall and meet the many challenges presented by neglected tropical diseases. Initiatives include public-private partnerships, global R&D capacity building, priority vouchers to speed drug approval processes, open source scientific collaborations, and harmonization of global governance structures concerning NTDs. [ citation needed ] The diseases considered neglected tropical diseases vary. Some researchers no longer consider malaria , HIV , and tuberculosis to be neglected due to the amount of public attention and increased funding they have received. Outside "The Big Three", the seven most prevalent neglected tropical diseases in order of their global prevalence are ascariasis , trichuriasis , hookworm infection , schistosomiasis , lymphatic filariasis , and trachoma . These seven are among a larger list of thirteen major NTDs: onchocerciasis , leishmaniasis , Chagas disease , leprosy , human African trypanosomiasis (sleeping sickness), dracunculiasis , and Buruli ulcer . In their 2002 review of the U.S. Food and Drug Administration (FDA) databases and the European Agency for the Evaluation of Medicinal Products , Troullier et al. found that 16 out of 1393 new chemical entities were approved for NTDs between 1975 and 1999 (~1%). Cohen et al. revisited the data and using the same methodology found 32 new chemical entities during the time period. In a second analysis using an expanded list of NTDs based on the G-FINDER survey, the number was slightly higher, with 46 new drugs and vaccines approved (~3% of the total including HIV drugs). Between 2000 and 2009, there has been some increase with an additional 26 newly approved drugs and vaccines for NTDs. A number of factors are recognized as contributing to the low number. The barrier most reported is the high cost of drug development. Estimates are that pharmaceutical companies' development costs to approval fall between $500 million and $2 billion. DiMasi, Hansen, and Grabowski calculated an average of $802 million in year 2000 dollars. Furthermore, the time that drugs are approved for use averages seven years out of the twenty years on patent, meaning a tendency for the market to focus on diseases of developed nations where high prices can be used to recoup research and development costs, and subsidize failed R&D efforts. In short, NTD research and development is considered a high investment risk, given that NTDs predominantly affect the poor in low- and middle-income countries. Additional barriers include drug safety regulatory requirements, intellectual property protection problems, and poor infrastructure for distribution and sales. Although drug companies have not invested heavily in NTDs, in several cases, rather than focus on profits, some have decided to donate key drugs to address NTDs. For example, Merck has had a program since the mid-1980s to donate ivermectin (Mectizan) indefinitely to support the global fight against onchocerciasis. GlaxoSmithKline and several other large pharmaceutical companies have donation programs as well. Drug donation, however, does not ameliorate the deficiency of new chemical entities being researched and developed. This is especially of concern with reports of emerging resistance among existing drugs. Governments, foundations, the non-profit sector, and the private sector have found new connections to help address market deficiencies by providing funding support and spreading both the costs and risks of NTD research and development. The proliferation of public–private partnerships (PPPs) has been recognized as a key innovation in the past decade, helping to unlock existing and new resources. [ citation needed ] Major PPPs for NTDs include: the Sabin Vaccine Institute , Norvartis Vaccines Institute for Global Health, MSD Wellcome Trust Hilleman Laboratories , Infectious Diseases Research Institute, Institut Pasteur and INSERM , WIPO Re:Search, and the International Vaccine Institute . Likewise, a number of new academic drug development centers have been created in recent years drawing in industry partners. Support for these centers is frequently traced to the Bill & Melinda Gates Foundation , the Sandler Foundation , and the Wellcome Trust . Growing NTD research and development capacity in middle-income countries is an area of policy interest. A 2009 study of biotechnology companies in India, China, Brazil, and South Africa revealed 62 NTD products in development and on the market out of approximately 500 products offered (~14%). When products to fight HIV, malaria, and TB were included in the analysis, the number increased to 123 products, approximately 25% of the total products offered. [ citation needed ] Researchers have argued that, unlike most multinationals, small and mid-sized "Global South" companies see significant business opportunities in the development of NTD-related diagnostics, biologics, pharmaceuticals, and services. Potential actions to improve and expand this R&D capacity have been recommended, including expansion of human capital, increased private investment, knowledge and patent sharing, infrastructure building for business incubation, and innovation support. [ citation needed ] Competitive innovation prizes have been used to spur development in a range of fields such as aerospace engineering, clean technology, and genomics. The X-Prize Foundation is launching a competition for high-speed, point-of-care diagnostics for tuberculosis. [ citation needed ] A more widely defined annual "Global Health EnterPrize" for neglected tropical diseases has been proposed to reward health innovators, particularly those based in countries where NTDs represent a serious health burden. [ citation needed ] The Bill & Melinda Gates Foundation offers the Grand Challenges Explorations Opportunities on a rolling basis. This grant program allows individuals from any organization or background to apply to address priority global health issues. Each project award is $100,000 and is drawn from a Foundation funding pool of $100 million. Awardees have tended to offer research projects on topics that are highly speculative but offer potentially game-changing breakthroughs in global health. [ citation needed ] In 2006, Ridley et al. recommended the development of a priority review voucher (PRV) in the journal Health Affairs . It gained interest from Senator Sam Brownback of Kansas, who championed its introduction in the FDA Amendments Act of 2007 . Under the enacted law, FDA approval of a non-NTD drug can be accelerated through the drug review process if paired with a drug that addresses an NTD. The potential economic benefit to a pharmaceutical company is estimated to be potentially as high as $300 million per drug. Three drugs have earned NTD PRVs to date (December 2014): Coartem (by Novartis, for malaria); bedaquiline (by Janssen, for TB); and miltefosine (by Knight, for leishmaniasis). However, the success of the PRV system is now under much scrutiny, given that Knight benefitted by $125 million from the sale of a PRV earned from a drug (miltefosine) that was largely researched and developed by the WHO. Médecins Sans Frontières are now pressuring Knight to guarantee to supply miltefosine at cost price, thus far without success. [ citation needed ] The PRV isn't limited to the pairing of drugs within a single company as it can be transferred between companies. Companies with NTD drug candidates in their pipelines but without a blockbuster drug are able to sell their vouchers, producing financial returns. In the EU, similar priority review incentives are now under consideration to increase the speed of regulatory pricing and reimbursement decisions. [ citation needed ] However, PRVs have been criticized as being open to manipulation and possibly encouraging errors through too rapid regulatory decision-making. Several companies and scientific organizations are participating in open-source initiatives to share drug data and patent information over the web, and facilitate virtual collaboration on NTD research. One rich area to explore is the wealth of genomic data resulting from the sequencing of parasite genomes. These data offer opportunities for the exploration of new therapeutic products using computational and open-source collaboration methods for drug discovery. The Tropical Disease Initiative, for example, has used large amounts of computing power to generate the protein structures for ten parasite genomes. An open-source drug bank was matched algorithmically to determine compounds with protein interaction activity, and two candidates were identified. In general, such methods may hold important opportunities for off-label use of existing approved drugs.In their 2002 review of the U.S. Food and Drug Administration (FDA) databases and the European Agency for the Evaluation of Medicinal Products , Troullier et al. found that 16 out of 1393 new chemical entities were approved for NTDs between 1975 and 1999 (~1%). Cohen et al. revisited the data and using the same methodology found 32 new chemical entities during the time period. In a second analysis using an expanded list of NTDs based on the G-FINDER survey, the number was slightly higher, with 46 new drugs and vaccines approved (~3% of the total including HIV drugs). Between 2000 and 2009, there has been some increase with an additional 26 newly approved drugs and vaccines for NTDs. A number of factors are recognized as contributing to the low number. The barrier most reported is the high cost of drug development. Estimates are that pharmaceutical companies' development costs to approval fall between $500 million and $2 billion. DiMasi, Hansen, and Grabowski calculated an average of $802 million in year 2000 dollars. Furthermore, the time that drugs are approved for use averages seven years out of the twenty years on patent, meaning a tendency for the market to focus on diseases of developed nations where high prices can be used to recoup research and development costs, and subsidize failed R&D efforts. In short, NTD research and development is considered a high investment risk, given that NTDs predominantly affect the poor in low- and middle-income countries. Additional barriers include drug safety regulatory requirements, intellectual property protection problems, and poor infrastructure for distribution and sales. Although drug companies have not invested heavily in NTDs, in several cases, rather than focus on profits, some have decided to donate key drugs to address NTDs. For example, Merck has had a program since the mid-1980s to donate ivermectin (Mectizan) indefinitely to support the global fight against onchocerciasis. GlaxoSmithKline and several other large pharmaceutical companies have donation programs as well. Drug donation, however, does not ameliorate the deficiency of new chemical entities being researched and developed. This is especially of concern with reports of emerging resistance among existing drugs. Governments, foundations, the non-profit sector, and the private sector have found new connections to help address market deficiencies by providing funding support and spreading both the costs and risks of NTD research and development. The proliferation of public–private partnerships (PPPs) has been recognized as a key innovation in the past decade, helping to unlock existing and new resources. [ citation needed ] Major PPPs for NTDs include: the Sabin Vaccine Institute , Norvartis Vaccines Institute for Global Health, MSD Wellcome Trust Hilleman Laboratories , Infectious Diseases Research Institute, Institut Pasteur and INSERM , WIPO Re:Search, and the International Vaccine Institute . Likewise, a number of new academic drug development centers have been created in recent years drawing in industry partners. Support for these centers is frequently traced to the Bill & Melinda Gates Foundation , the Sandler Foundation , and the Wellcome Trust . Growing NTD research and development capacity in middle-income countries is an area of policy interest. A 2009 study of biotechnology companies in India, China, Brazil, and South Africa revealed 62 NTD products in development and on the market out of approximately 500 products offered (~14%). When products to fight HIV, malaria, and TB were included in the analysis, the number increased to 123 products, approximately 25% of the total products offered. [ citation needed ] Researchers have argued that, unlike most multinationals, small and mid-sized "Global South" companies see significant business opportunities in the development of NTD-related diagnostics, biologics, pharmaceuticals, and services. Potential actions to improve and expand this R&D capacity have been recommended, including expansion of human capital, increased private investment, knowledge and patent sharing, infrastructure building for business incubation, and innovation support. [ citation needed ] Competitive innovation prizes have been used to spur development in a range of fields such as aerospace engineering, clean technology, and genomics. The X-Prize Foundation is launching a competition for high-speed, point-of-care diagnostics for tuberculosis. [ citation needed ] A more widely defined annual "Global Health EnterPrize" for neglected tropical diseases has been proposed to reward health innovators, particularly those based in countries where NTDs represent a serious health burden. [ citation needed ] The Bill & Melinda Gates Foundation offers the Grand Challenges Explorations Opportunities on a rolling basis. This grant program allows individuals from any organization or background to apply to address priority global health issues. Each project award is $100,000 and is drawn from a Foundation funding pool of $100 million. Awardees have tended to offer research projects on topics that are highly speculative but offer potentially game-changing breakthroughs in global health. [ citation needed ] In 2006, Ridley et al. recommended the development of a priority review voucher (PRV) in the journal Health Affairs . It gained interest from Senator Sam Brownback of Kansas, who championed its introduction in the FDA Amendments Act of 2007 . Under the enacted law, FDA approval of a non-NTD drug can be accelerated through the drug review process if paired with a drug that addresses an NTD. The potential economic benefit to a pharmaceutical company is estimated to be potentially as high as $300 million per drug. Three drugs have earned NTD PRVs to date (December 2014): Coartem (by Novartis, for malaria); bedaquiline (by Janssen, for TB); and miltefosine (by Knight, for leishmaniasis). However, the success of the PRV system is now under much scrutiny, given that Knight benefitted by $125 million from the sale of a PRV earned from a drug (miltefosine) that was largely researched and developed by the WHO. Médecins Sans Frontières are now pressuring Knight to guarantee to supply miltefosine at cost price, thus far without success. [ citation needed ] The PRV isn't limited to the pairing of drugs within a single company as it can be transferred between companies. Companies with NTD drug candidates in their pipelines but without a blockbuster drug are able to sell their vouchers, producing financial returns. In the EU, similar priority review incentives are now under consideration to increase the speed of regulatory pricing and reimbursement decisions. [ citation needed ] However, PRVs have been criticized as being open to manipulation and possibly encouraging errors through too rapid regulatory decision-making. Several companies and scientific organizations are participating in open-source initiatives to share drug data and patent information over the web, and facilitate virtual collaboration on NTD research. One rich area to explore is the wealth of genomic data resulting from the sequencing of parasite genomes. These data offer opportunities for the exploration of new therapeutic products using computational and open-source collaboration methods for drug discovery. The Tropical Disease Initiative, for example, has used large amounts of computing power to generate the protein structures for ten parasite genomes. An open-source drug bank was matched algorithmically to determine compounds with protein interaction activity, and two candidates were identified. In general, such methods may hold important opportunities for off-label use of existing approved drugs.Governments, foundations, the non-profit sector, and the private sector have found new connections to help address market deficiencies by providing funding support and spreading both the costs and risks of NTD research and development. The proliferation of public–private partnerships (PPPs) has been recognized as a key innovation in the past decade, helping to unlock existing and new resources. [ citation needed ] Major PPPs for NTDs include: the Sabin Vaccine Institute , Norvartis Vaccines Institute for Global Health, MSD Wellcome Trust Hilleman Laboratories , Infectious Diseases Research Institute, Institut Pasteur and INSERM , WIPO Re:Search, and the International Vaccine Institute . Likewise, a number of new academic drug development centers have been created in recent years drawing in industry partners. Support for these centers is frequently traced to the Bill & Melinda Gates Foundation , the Sandler Foundation , and the Wellcome Trust . Growing NTD research and development capacity in middle-income countries is an area of policy interest. A 2009 study of biotechnology companies in India, China, Brazil, and South Africa revealed 62 NTD products in development and on the market out of approximately 500 products offered (~14%). When products to fight HIV, malaria, and TB were included in the analysis, the number increased to 123 products, approximately 25% of the total products offered. [ citation needed ] Researchers have argued that, unlike most multinationals, small and mid-sized "Global South" companies see significant business opportunities in the development of NTD-related diagnostics, biologics, pharmaceuticals, and services. Potential actions to improve and expand this R&D capacity have been recommended, including expansion of human capital, increased private investment, knowledge and patent sharing, infrastructure building for business incubation, and innovation support. [ citation needed ]Competitive innovation prizes have been used to spur development in a range of fields such as aerospace engineering, clean technology, and genomics. The X-Prize Foundation is launching a competition for high-speed, point-of-care diagnostics for tuberculosis. [ citation needed ] A more widely defined annual "Global Health EnterPrize" for neglected tropical diseases has been proposed to reward health innovators, particularly those based in countries where NTDs represent a serious health burden. [ citation needed ] The Bill & Melinda Gates Foundation offers the Grand Challenges Explorations Opportunities on a rolling basis. This grant program allows individuals from any organization or background to apply to address priority global health issues. Each project award is $100,000 and is drawn from a Foundation funding pool of $100 million. Awardees have tended to offer research projects on topics that are highly speculative but offer potentially game-changing breakthroughs in global health. [ citation needed ]In 2006, Ridley et al. recommended the development of a priority review voucher (PRV) in the journal Health Affairs . It gained interest from Senator Sam Brownback of Kansas, who championed its introduction in the FDA Amendments Act of 2007 . Under the enacted law, FDA approval of a non-NTD drug can be accelerated through the drug review process if paired with a drug that addresses an NTD. The potential economic benefit to a pharmaceutical company is estimated to be potentially as high as $300 million per drug. Three drugs have earned NTD PRVs to date (December 2014): Coartem (by Novartis, for malaria); bedaquiline (by Janssen, for TB); and miltefosine (by Knight, for leishmaniasis). However, the success of the PRV system is now under much scrutiny, given that Knight benefitted by $125 million from the sale of a PRV earned from a drug (miltefosine) that was largely researched and developed by the WHO. Médecins Sans Frontières are now pressuring Knight to guarantee to supply miltefosine at cost price, thus far without success. [ citation needed ] The PRV isn't limited to the pairing of drugs within a single company as it can be transferred between companies. Companies with NTD drug candidates in their pipelines but without a blockbuster drug are able to sell their vouchers, producing financial returns. In the EU, similar priority review incentives are now under consideration to increase the speed of regulatory pricing and reimbursement decisions. [ citation needed ] However, PRVs have been criticized as being open to manipulation and possibly encouraging errors through too rapid regulatory decision-making. Several companies and scientific organizations are participating in open-source initiatives to share drug data and patent information over the web, and facilitate virtual collaboration on NTD research. One rich area to explore is the wealth of genomic data resulting from the sequencing of parasite genomes. These data offer opportunities for the exploration of new therapeutic products using computational and open-source collaboration methods for drug discovery. The Tropical Disease Initiative, for example, has used large amounts of computing power to generate the protein structures for ten parasite genomes. An open-source drug bank was matched algorithmically to determine compounds with protein interaction activity, and two candidates were identified. In general, such methods may hold important opportunities for off-label use of existing approved drugs.In 1977, Kenneth S. Warren , an American researcher, invented the concept of what is now "neglected tropical diseases". In 2005 Lorenzo Savioli , a senior United Nations civil servant, was appointed director of the "Department of Control of Neglected Tropical Diseases". The World Health Organization definition of neglected tropical disease has been criticised to be restrictive and described as a form of epistemic injustice, where conditions like snakebite are forced to be framed as a medical problem.

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Rift Valley fever

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Lujo mammarenavirus

Lujo virus LuJo virus Lusaka/Johannesburg virus Lujo is a bisegmented RNA virus —a member of the family Arenaviridae —and a known cause of viral hemorrhagic fever (VHF) in humans. Its name was suggested by the Special Pathogens Unit of the National Institute for Communicable Diseases of the National Health Laboratory Service (NICD-NHLS) by using the first two letters of the names of the cities involved in the 2008 outbreak of the disease, Lusaka (Zambia) and Johannesburg (Republic of South Africa). It is the second pathogenic Arenavirus to be described from the African continent—the first being Lassa virus —and since 2012 has been classed as a " Select Agent " under U.S. law .Only 5 cases of this virus have ever been reported; all 5 were identified in September and October 2008, and 4 were fatal. Those infections that proved fatal caused death within 10–13 days of showing symptoms. All four patients in which infection proved fatal first showed signs of improvement and then went into respiratory distress, displayed neurological problems, and had circulatory issues that resulted in collapse. The discovery of this novel virus was described following a highly fatal nosocomial (hospital) outbreak of VHF in Johannesburg. The identification of this virus was the first new arenavirus discovered in over 40 years. The first case was a female travel agent who lived in the outskirts of Lusaka. She developed a fever which grew worse with time. She was evacuated to Johannesburg for medical treatment. Almost two weeks later, the paramedic that nursed the patient on the flight to South Africa also fell ill and was also brought to Johannesburg for medical treatment. At this time the connection between these two patients was recognized by the attending physician in the Johannesburg hospital. Together with the NICD-NHLS the clinical syndrome of VHF was recognized and specimens from the second patient were submitted for laboratory confirmation. In addition, a cleaner and a nurse that had contact with the first patient also fell ill. A second nurse was infected through contact with the paramedic. The outbreak had a high case fatality rate with 4 of 5 identified cases resulting in death. The Special Pathogens Unit of the NICD-NHLS together with colleagues from the Special Pathogens Unit of the U.S. Centers for Disease Control and Prevention (CDC) identified the etiological agent of the outbreak as an Old World arenavirus using molecular and serological tests. Sequencing and phylogenetic investigation of partial genome sequencing indicated that this virus was not Lassavirus and likely a previously unreported arenavirus. This was corroborated by full genome sequencing that was conducted by the NICD-NHLS, CDC and collaborators from Columbia University in New York . The distribution of this newly described arenavirus is uncertain. To date this virus has only been reported from a patient from Zambia and a subsequent nosocomial outbreak in South Africa . [ citation needed ]Viruses from the Arenaviridae family, to which Lujo virus belongs, almost always have a rodent reservoir , with one virus in the family having a bat reservoir. Contact with an infected rodent host, its urine or fecal matter, inhalation of dust with virus particles, or eating food containing remnants of the virus can result in human infection. Transmission can also occur via human-to-human contact, as evidenced by the 5 cases from 2008, but it is still not completely clear how the first case was contracted. Both bats and rodents should be considered possible contact points, just to be safe. Though it is not known for sure, it is speculated that the human-to-human transmission occurs from contact with bodily fluids. The incubation period is expected to be 7–13 days. VHF symptoms appear similar to other viruses of the same family, such as Lassa fever. The known symptoms include swelling in the neck and face, sore throat, diarrhea, and a rash resembling measles on the face and body. Blood tests of those infected revealed elevated liver values, white blood cell counts that were first low and then elevated over time, and low platelet counts. In-depth research into Lujo virus and its treatment have been difficult because of the lack of economic and cultural stability of the regions where the only known cases have occurred. Under Treatment with oral ribavirin treatment, the patient 5 continued to deteriorate but the treatment shifted to i.v on day 8 it seemed to have cured the only surviving patient with Lujo Virus, but because the 5 affected in 2008 have been the only cases identified, there has not been much opportunity for further research. Sequencing of the viral genome has shown that this virus belongs to the Old World arenavirus group. Comparisons with other viral genome sequences showed that this virus is equidistant from other Old World and New World arenaviruses. It is distantly similar to the other pathogenic African arenavirus, Lassa fever virus. This virus has been associated with an outbreak of five cases of VHF in September and October 2008. In four cases (80% of total known infections) the infection was fatal. The fifth case was treated with ribavirin early after onset of clinical disease (was detected through active contact tracing), an antiviral drug which is effective in treating Lassa fever , and survived; however, complete ribavirin's effectiveness against Lujo virus remains unknown but may be useful as adjunctive therapy.

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Rift Valley fever

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People Who Fell from the Sky

People Who Fell from the Sky is the third and final studio album by American rock band Mind Funk ."Rift Valley Fever – 4:22" "Superchief – 4:55" "Seasick – 4:55" "Deep End – 4:28" "People Who Fell from the Sky – 3:17" "Weird Water – 3:01" "Aluna – 6:18" "1000 Times – 3:47" "Kill the Messenger – 5:40" "Acrobats Falling – 5:41"

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Rift Valley fever

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B virus

B-virus ( Macacine alphaherpesvirus 1 ; McHV-1; formerly Macacine herpesvirus 1 , Cercopithecine herpesvirus 1 , CHV-1 ), Herpesvirus simiae , or Herpes virus B is the Simplexvirus infecting macaque monkeys. B virus is very similar to HSV-1, and as such, this neurotropic virus is not found in the blood. In the natural host, the virus exhibits pathogenesis similar to that of cold sores in humans. There have been a number of accidental infections and fatalities of researchers working with rhesus monkeys ( Rhesus macaque ). When humans are zoonotically infected with B virus, they can present with a severe encephalitis , resulting in permanent neurological dysfunction or death. Severity of the disease increases for untreated patients, with a case fatality rate of approximately 80%. Early diagnosis and subsequent treatment are crucial to human survival of the infection. Personal protective equipment is necessary when working with macaques, especially with animals that have tested positive for the virus. Bites, scratches, and exposures to mucous membranes , including the eye, have led to infection when not cleaned immediately.Macacine alphaherpesvirus 1 was first identified in 1932 following the death of William Brebner, a young physician who was bitten by a rhesus monkey while doing research on polio . He had healed from the bite but later developed a febrile illness, resulting in localized erythema , lymphangitis , lymphadenitis and, ultimately, transverse myelitis . Neurologic tissues obtained during autopsy revealed the presence of an ultrafilterable agent that appeared similar to HSV-1 . This isolate was originally termed "W virus." Within a year of Brebner's death, Albert Sabin identified a novel virus from the same samples, which he later named B virus. Sabin further described the lethality of Macacine alphaherpesvirus 1 by showing that infectivity was independent of the route of inoculation. Additionally, it was observed that Macacine alphaherpesvirus 1 induced immunologic responses similar to HSV-1 and shared similarities to HVP -2 and Langur herpesvirus, two other nonhuman primate alphaherpesviruses. By 1959, Macacine alphaherpesvirus 1 was identified as the causative agent in 17 human cases, 12 of which resulted in death. Approximately 50 cases had been identified by 2002, although only 26 were well documented. Improvements in handling human cases have been made in the past several decades. Between 1987 and 2004, the mortality rate decreased, largely due to the addition of new forms of treatment and improved diagnosis. There have been a total of five fatalities related to Macacine alphaherpesvirus 1 in this period. In 1997 researcher Elizabeth Griffin was splashed in the eye by an infected rhesus monkey while working at the Yerkes National Primate Research Center and she subsequently died. In 2019, a researcher working with monkeys at a Japanese pharmaceutical company became infected and critically ill. In 2021, a veterinarian in China became infected while performing two dissections on rhesus monkeys and subsequently died. Macacine alphaherpesvirus 1 is approximately 200 nm in diameter and has a structure almost identical to that of HSV1 and HSV2 . It has an icosahedral capsid (T=16) consisting of 150 hexons and 12 pentons formed from 6 proteins. The envelope is loose around the viral capsid and contains at least 10 glycoproteins critical for adsorption and penetration into host cells. The tegument , containing at least 14 proteins, lies between the capsid and the envelope. The tegument proteins are involved in nucleic acid metabolism , DNA synthesis , and protein processing . The proteins in the tegument are thymidine kinase , thymidylate synthetase , dUTPase , ribonucleotide reductase , DNA polymerase , DNA helicase , DNA primase , and protein kinases . The B virus genome was fully sequenced in 2003 from an isolate found in a rhesus macaque . Like all herpes viruses, the B virus genome contains double-stranded DNA and is approximately 157 kbp in length. Two unique regions (UL and US) are flanked by a pair of inverted repeats, two of which are found at the termini, with the other two internally located. This arrangement, which is identical in nature to HSV, results in four sequence-oriented isomers. Cytosine and guanine nucleotides represent 75% of the sequence. Sequence analyses suggest that B virus and HSV types 1 and 2 most likely diverged from a common ancestor during the evolution of these pathogens. Each gene-encoded glycoprotein , including gB, gC, gD, gE and gG, has approximately 50% homology with HSV, with a slightly higher predilection towards HSV-2 over HSV-1. Additionally, glycoprotein sequences have demonstrated that all cysteine residues are conserved, as are most glycosylation sites. One key difference between the B virus and the HSVs is that B virus does not have a homolog of the HSV γ 1 34.5 gene, which codes for a neurovirulence factor. This indicates that B virus has different mechanisms from HSV for replicating inside nerve cells , which could explain the drastically different effects of these viruses on humans.Macacine alphaherpesvirus 1 is approximately 200 nm in diameter and has a structure almost identical to that of HSV1 and HSV2 . It has an icosahedral capsid (T=16) consisting of 150 hexons and 12 pentons formed from 6 proteins. The envelope is loose around the viral capsid and contains at least 10 glycoproteins critical for adsorption and penetration into host cells. The tegument , containing at least 14 proteins, lies between the capsid and the envelope. The tegument proteins are involved in nucleic acid metabolism , DNA synthesis , and protein processing . The proteins in the tegument are thymidine kinase , thymidylate synthetase , dUTPase , ribonucleotide reductase , DNA polymerase , DNA helicase , DNA primase , and protein kinases . The B virus genome was fully sequenced in 2003 from an isolate found in a rhesus macaque . Like all herpes viruses, the B virus genome contains double-stranded DNA and is approximately 157 kbp in length. Two unique regions (UL and US) are flanked by a pair of inverted repeats, two of which are found at the termini, with the other two internally located. This arrangement, which is identical in nature to HSV, results in four sequence-oriented isomers. Cytosine and guanine nucleotides represent 75% of the sequence. Sequence analyses suggest that B virus and HSV types 1 and 2 most likely diverged from a common ancestor during the evolution of these pathogens. Each gene-encoded glycoprotein , including gB, gC, gD, gE and gG, has approximately 50% homology with HSV, with a slightly higher predilection towards HSV-2 over HSV-1. Additionally, glycoprotein sequences have demonstrated that all cysteine residues are conserved, as are most glycosylation sites. One key difference between the B virus and the HSVs is that B virus does not have a homolog of the HSV γ 1 34.5 gene, which codes for a neurovirulence factor. This indicates that B virus has different mechanisms from HSV for replicating inside nerve cells , which could explain the drastically different effects of these viruses on humans.In the natural host, the virus exhibits pathogenesis similar to that of cold sores in humans. B virus infection of humans is extremely rare. People typically get infected with B virus if they are bitten or scratched by an infected macaque monkey, or have contact with the monkey's eyes, nose, or mouth. Only one case has been documented of an infected person spreading B virus to another person. Traveling to an area where macaques are known carriers of the virus and interacting in close contact in areas such as temples poses a risk of exposure. However, even in endemic areas, human cases are rare. There have been no known cases of Macacine alphaherpesvirus 1 in travelers. When humans are zoonotically infected with B virus, they can develop encephalitis , resulting in permanent neurological dysfunction or death. The severity of the disease increases for untreated patients. As of 2014, there was a case fatality rate of approximately 80%. As of 2020, there have been 50 documented cases of human B virus infection since the identification of the virus in 1932, 21 of which led to death. At least 20 of the patients developed some degree of encephalitis . B virus is the only identified old-world-monkey herpesvirus that displays severe pathogenicity in humans. [ citation needed ]B virus infection of humans is extremely rare. People typically get infected with B virus if they are bitten or scratched by an infected macaque monkey, or have contact with the monkey's eyes, nose, or mouth. Only one case has been documented of an infected person spreading B virus to another person. Traveling to an area where macaques are known carriers of the virus and interacting in close contact in areas such as temples poses a risk of exposure. However, even in endemic areas, human cases are rare. There have been no known cases of Macacine alphaherpesvirus 1 in travelers. When humans are zoonotically infected with B virus, they can develop encephalitis , resulting in permanent neurological dysfunction or death. The severity of the disease increases for untreated patients. As of 2014, there was a case fatality rate of approximately 80%. As of 2020, there have been 50 documented cases of human B virus infection since the identification of the virus in 1932, 21 of which led to death. At least 20 of the patients developed some degree of encephalitis . B virus is the only identified old-world-monkey herpesvirus that displays severe pathogenicity in humans. [ citation needed ]Personal protective equipment is necessary when working with macaques, especially with animals that have tested positive for the virus. Bites, scratches, and exposures to mucous membranes , including the eye, have led to infection when not cleaned immediately. Early diagnosis and subsequent treatment are crucial to human survival of the infection. Upon potential infection, samples from both the human and, when possible, the macaque should be sent for B virus diagnostic testing. Acyclovir has prevented progression of the disease in some patients and may be lifesaving, though it is thought to be only one-tenth as effective against B virus as against HSV1. Prompt treatment is essential to prevent permanent neurological impairment.

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Rift Valley fever

https://api.wikimedia.org/core/v1/wikipedia/en/page/MERS/html

MERS

Middle East respiratory syndrome ( MERS ) is a viral respiratory infection caused by Middle East respiratory syndrome–related coronavirus (MERS-CoV). Symptoms may range from none, to mild, to severe depending on age and risk level. Typical symptoms include fever , cough , diarrhea , and shortness of breath . The disease is typically more severe in those with other health problems. The first case was identified in June 2012 by Egyptian physician Ali Mohamed Zaki at the Dr. Soliman Fakeeh Hospital in Jeddah , Saudi Arabia, and most cases have occurred in the Arabian Peninsula . Over 2,600 cases have been reported as of January 2021, including 45 cases in the year 2020. About 35% of those who are diagnosed with the disease die from it. Larger outbreaks have occurred in South Korea in 2015 and in Saudi Arabia in 2018 . MERS-CoV is a virus in the coronavirus family believed to be originally from bats. However, humans are typically infected from camels , either during direct contact or indirectly through respiratory droplets. Spread between humans typically requires close contact with an infected person. Its spread is uncommon outside of hospitals. Thus, its risk to the global population is currently deemed to be significantly low. Diagnosis is by rRT-PCR testing of blood and respiratory samples. As of 2021 [ update ] , there is no specific vaccine or treatment for the disease, but a number are being developed. The World Health Organization (WHO) recommends that those who come in contact with camels wash their hands and not touch sick camels. They also recommend that camel-based food products be appropriately cooked. Treatments that help with the symptoms and support body functioning may be used. Previous infection with MERS can confer cross-reactive immunity to SARS-CoV-2 and provide partial protection against COVID-19 . However, co-infection with SARS-CoV-2 and MERS is possible and could lead to a recombination event. Early reports compared the viruses to severe acute respiratory syndrome ( SARS ), and it has been referred to as Saudi Arabia's SARS-like virus. The first person, in June 2012 , had a fever , cough , expectoration , and shortness of breath. One review of 47 laboratory confirmed cases in Saudi Arabia gave the most common presenting symptoms as fever in 98%, cough in 83%, shortness of breath in 72% and myalgia in 32% of people. There were also frequent gastrointestinal symptoms with diarrhea in 26%, vomiting in 21%, abdominal pain in 17% of people. 72% of people required mechanical ventilation . There were also 3.3 males for every female. One study of a hospital-based outbreak of MERS had an estimated incubation period of 5.5 days (95% confidence interval 1.9 to 14.7 days). MERS can range from asymptomatic disease to severe pneumonia leading to acute respiratory distress syndrome (ARDS). Kidney failure , disseminated intravascular coagulation (DIC), and pericarditis have also been reported. Middle East respiratory syndrome is caused by the MERS coronavirus (MERS-CoV), a species with single-stranded RNA belonging to the genus betacoronavirus which is distinct from SARS coronavirus and the common-cold coronavirus. Its genomes are phylogenetically classified into two clades , Clades A and B. Early cases of MERS were of Clade A clusters (EMC/2012 and Jordan-N3/2012), while new cases are genetically different in general (Clade B). The virus grows readily on Vero cells and LLC-MK2 cells. In November 2012, Egyptian virologist Dr. Ali Zaki sent a virus sample from the first confirmed case in Saudi Arabia to virologist Ron Fouchier , a leading coronavirus researcher at the Erasmus Medical Center (EMC) in Rotterdam , the Netherlands. The second laboratory-proven case was in London, confirmed by the UK Health Protection Agency (HPA). The HPA named the virus the London1_novel CoV 2012. A study performed between 2010 and 2013, in which the incidence of MERS was evaluated in 310 dromedary camels , revealed high titers of neutralizing antibodies to MERS-CoV in the blood serum of these animals. A further study sequenced MERS-CoV from nasal swabs of dromedary camels in Saudi Arabia and found they had sequences identical to previously sequenced human isolates. Some individual camels were also found to have more than one genomic variant in their nasopharynx . There is also a 2014 report of a Saudi Arabian man who became ill seven days after applying topical medicine to the noses of several sick camels and later he and one of the camels were found to have identical strains of MERS-CoV. It is still unclear how the virus is transmitted from camels to humans. In 2014, the Saudi Ministry of Agriculture advised people to avoid contact with camels or wear breathing masks when around them. In response "some people have refused to listen to the government's advice" and kiss their camels in defiance of their government's advice. In 2020, the World Health Organization advised avoiding contact with camels and to eat only fully cooked camel meat, pasteurized camel milk, and to avoid drinking camel urine . There has been evidence of limited, but not sustained spread of MERS-CoV from person to person, both in households as well as in health care settings like hospitals. Most transmission has occurred "in the circumstances of close contact with severely ill persons in healthcare or household settings" and there is no evidence of transmission from asymptomatic cases. Cluster sizes have ranged from 1 to 26 people, with an average of 2.7. Middle East respiratory syndrome is caused by the MERS coronavirus (MERS-CoV), a species with single-stranded RNA belonging to the genus betacoronavirus which is distinct from SARS coronavirus and the common-cold coronavirus. Its genomes are phylogenetically classified into two clades , Clades A and B. Early cases of MERS were of Clade A clusters (EMC/2012 and Jordan-N3/2012), while new cases are genetically different in general (Clade B). The virus grows readily on Vero cells and LLC-MK2 cells. In November 2012, Egyptian virologist Dr. Ali Zaki sent a virus sample from the first confirmed case in Saudi Arabia to virologist Ron Fouchier , a leading coronavirus researcher at the Erasmus Medical Center (EMC) in Rotterdam , the Netherlands. The second laboratory-proven case was in London, confirmed by the UK Health Protection Agency (HPA). The HPA named the virus the London1_novel CoV 2012. A study performed between 2010 and 2013, in which the incidence of MERS was evaluated in 310 dromedary camels , revealed high titers of neutralizing antibodies to MERS-CoV in the blood serum of these animals. A further study sequenced MERS-CoV from nasal swabs of dromedary camels in Saudi Arabia and found they had sequences identical to previously sequenced human isolates. Some individual camels were also found to have more than one genomic variant in their nasopharynx . There is also a 2014 report of a Saudi Arabian man who became ill seven days after applying topical medicine to the noses of several sick camels and later he and one of the camels were found to have identical strains of MERS-CoV. It is still unclear how the virus is transmitted from camels to humans. In 2014, the Saudi Ministry of Agriculture advised people to avoid contact with camels or wear breathing masks when around them. In response "some people have refused to listen to the government's advice" and kiss their camels in defiance of their government's advice. In 2020, the World Health Organization advised avoiding contact with camels and to eat only fully cooked camel meat, pasteurized camel milk, and to avoid drinking camel urine . There has been evidence of limited, but not sustained spread of MERS-CoV from person to person, both in households as well as in health care settings like hospitals. Most transmission has occurred "in the circumstances of close contact with severely ill persons in healthcare or household settings" and there is no evidence of transmission from asymptomatic cases. Cluster sizes have ranged from 1 to 26 people, with an average of 2.7. A study performed between 2010 and 2013, in which the incidence of MERS was evaluated in 310 dromedary camels , revealed high titers of neutralizing antibodies to MERS-CoV in the blood serum of these animals. A further study sequenced MERS-CoV from nasal swabs of dromedary camels in Saudi Arabia and found they had sequences identical to previously sequenced human isolates. Some individual camels were also found to have more than one genomic variant in their nasopharynx . There is also a 2014 report of a Saudi Arabian man who became ill seven days after applying topical medicine to the noses of several sick camels and later he and one of the camels were found to have identical strains of MERS-CoV. It is still unclear how the virus is transmitted from camels to humans. In 2014, the Saudi Ministry of Agriculture advised people to avoid contact with camels or wear breathing masks when around them. In response "some people have refused to listen to the government's advice" and kiss their camels in defiance of their government's advice. In 2020, the World Health Organization advised avoiding contact with camels and to eat only fully cooked camel meat, pasteurized camel milk, and to avoid drinking camel urine . There has been evidence of limited, but not sustained spread of MERS-CoV from person to person, both in households as well as in health care settings like hospitals. Most transmission has occurred "in the circumstances of close contact with severely ill persons in healthcare or household settings" and there is no evidence of transmission from asymptomatic cases. Cluster sizes have ranged from 1 to 26 people, with an average of 2.7. According to World Health Organization , the interim case definition is that a confirmed case is identified in a person with a positive lab test by "molecular diagnostics including either a positive PCR on at least two specific genomic targets or a single positive target with sequencing on a second". According to the WHO, a probable case is: In the United States, the Centers for Disease Control and Prevention (CDC) recommend investigating any person with: Fever and pneumonia or acute respiratory distress syndrome (based on clinical or radiological evidence) and either: a history of travel from countries in or near the Arabian Peninsula within 14 days before symptom onset, or close contact with a symptomatic traveler who developed fever and acute respiratory illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian Peninsula or a member of a cluster of people with severe acute respiratory illness (e.g. fever and pneumonia requiring hospitalization) of unknown cause in which MERS-CoV is being evaluated, in consultation with state and local health departments. Fever and symptoms of respiratory illness (not necessarily pneumonia; e.g., cough, shortness of breath) and being in a healthcare facility (as a patient, worker, or visitor) within 14 days before symptom onset in a country or territory in or near the Arabian Peninsula in which recent healthcare-associated cases of MERS have been identified. Fever or symptoms of respiratory illness (not necessarily pneumonia; e.g., cough, shortness of breath) and close contact with a confirmed MERS case while the case was ill. a history of travel from countries in or near the Arabian Peninsula within 14 days before symptom onset, or close contact with a symptomatic traveler who developed fever and acute respiratory illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian Peninsula or a member of a cluster of people with severe acute respiratory illness (e.g. fever and pneumonia requiring hospitalization) of unknown cause in which MERS-CoV is being evaluated, in consultation with state and local health departments. Chest X-ray findings tend to show bilateral patchy infiltrates consistent with viral pneumonitis and acute respiratory distress syndrome (ARDS). Lower lobes tend to be more involved. CT scans show interstitial infiltrates. MERS cases have been reported to have low white blood cell count , and in particular low lymphocytes . For PCR [ clarification needed ] testing, the World Health Organization (WHO) recommends obtaining samples from the lower respiratory tract via bronchoalveolar lavage (BAL), sputum sample or tracheal aspirate as these have the highest viral loads. There have also been studies utilizing upper respiratory sampling via nasopharyngeal swab . Several highly sensitive, confirmatory real-time RT-PCR assays exist for rapid identification of MERS-CoV from patient-derived samples. These assays attempt to amplify upE (targets elements upstream of the E gene), open reading frame 1B (targets the ORF1b gene) and open reading frame 1A (targets the ORF1a gene). The WHO recommends the upE target for screening assays as it is highly sensitive. In addition, hemi-nested sequencing amplicons targeting RdRp (present in all coronaviruses ) and nucleocapsid (N) gene (specific to MERS-CoV) fragments can be generated for confirmation via sequencing. Reports of potential polymorphisms in the N gene between isolates highlight the necessity for sequence-based characterization. [ citation needed ] The WHO recommended testing algorithm is to start with an upE RT-PCR and if positive confirm with ORF 1A assay or RdRp or N gene sequence assay for confirmation. If both an upE and secondary assay are positive it is considered a confirmed case. Protocols for biologically safe immunofluorescence assays (IFA) have also been developed; however, antibodies against betacoronaviruses are known to cross-react within the genus. This effectively limits their use to confirmatory applications. A more specific protein-microarray based assay has also been developed that did not show any cross-reactivity against population samples and serum known to be positive for other betacoronaviruses. Due to the limited validation done so far with serological assays, WHO guidance is that "cases where the testing laboratory has reported positive serological test results in the absence of PCR testing or sequencing, are considered probable cases of MERS-CoV infection, if they meet the other conditions of that case definition." According to the WHO, a probable case is: In the United States, the Centers for Disease Control and Prevention (CDC) recommend investigating any person with: Fever and pneumonia or acute respiratory distress syndrome (based on clinical or radiological evidence) and either: a history of travel from countries in or near the Arabian Peninsula within 14 days before symptom onset, or close contact with a symptomatic traveler who developed fever and acute respiratory illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian Peninsula or a member of a cluster of people with severe acute respiratory illness (e.g. fever and pneumonia requiring hospitalization) of unknown cause in which MERS-CoV is being evaluated, in consultation with state and local health departments. Fever and symptoms of respiratory illness (not necessarily pneumonia; e.g., cough, shortness of breath) and being in a healthcare facility (as a patient, worker, or visitor) within 14 days before symptom onset in a country or territory in or near the Arabian Peninsula in which recent healthcare-associated cases of MERS have been identified. Fever or symptoms of respiratory illness (not necessarily pneumonia; e.g., cough, shortness of breath) and close contact with a confirmed MERS case while the case was ill. a history of travel from countries in or near the Arabian Peninsula within 14 days before symptom onset, or close contact with a symptomatic traveler who developed fever and acute respiratory illness (not necessarily pneumonia) within 14 days after traveling from countries in or near the Arabian Peninsula or a member of a cluster of people with severe acute respiratory illness (e.g. fever and pneumonia requiring hospitalization) of unknown cause in which MERS-CoV is being evaluated, in consultation with state and local health departments.Chest X-ray findings tend to show bilateral patchy infiltrates consistent with viral pneumonitis and acute respiratory distress syndrome (ARDS). Lower lobes tend to be more involved. CT scans show interstitial infiltrates. MERS cases have been reported to have low white blood cell count , and in particular low lymphocytes . For PCR [ clarification needed ] testing, the World Health Organization (WHO) recommends obtaining samples from the lower respiratory tract via bronchoalveolar lavage (BAL), sputum sample or tracheal aspirate as these have the highest viral loads. There have also been studies utilizing upper respiratory sampling via nasopharyngeal swab . Several highly sensitive, confirmatory real-time RT-PCR assays exist for rapid identification of MERS-CoV from patient-derived samples. These assays attempt to amplify upE (targets elements upstream of the E gene), open reading frame 1B (targets the ORF1b gene) and open reading frame 1A (targets the ORF1a gene). The WHO recommends the upE target for screening assays as it is highly sensitive. In addition, hemi-nested sequencing amplicons targeting RdRp (present in all coronaviruses ) and nucleocapsid (N) gene (specific to MERS-CoV) fragments can be generated for confirmation via sequencing. Reports of potential polymorphisms in the N gene between isolates highlight the necessity for sequence-based characterization. [ citation needed ] The WHO recommended testing algorithm is to start with an upE RT-PCR and if positive confirm with ORF 1A assay or RdRp or N gene sequence assay for confirmation. If both an upE and secondary assay are positive it is considered a confirmed case. Protocols for biologically safe immunofluorescence assays (IFA) have also been developed; however, antibodies against betacoronaviruses are known to cross-react within the genus. This effectively limits their use to confirmatory applications. A more specific protein-microarray based assay has also been developed that did not show any cross-reactivity against population samples and serum known to be positive for other betacoronaviruses. Due to the limited validation done so far with serological assays, WHO guidance is that "cases where the testing laboratory has reported positive serological test results in the absence of PCR testing or sequencing, are considered probable cases of MERS-CoV infection, if they meet the other conditions of that case definition." While the mechanism of spread of MERS-CoV is currently not known, based on experience with prior coronaviruses, such as SARS, the WHO currently recommends that all individuals coming into contact with MERS suspects should (in addition to standard precautions): [ citation needed ] Wear a medical mask Wear eye protection (i.e. goggles or a face shield) Wear a clean, non sterile, long sleeved gown; and gloves (some procedures may require sterile gloves) Perform hand hygiene before and after contact with the person and his or her surroundings and immediately after removal of personal protective equipment (PPE) For procedures which carry a risk of aerosolization, such as intubation, the WHO recommends that care providers also: [ citation needed ] Wear a particulate respirator and, when putting on a disposable particulate respirator, always check the seal Wear eye protection (i.e. goggles or a face shield) Wear a clean, non-sterile, long-sleeved gown and gloves (some of these procedures require sterile gloves) Wear an impermeable apron for some procedures with expected high fluid volumes that might penetrate the gown Perform procedures in an adequately ventilated room; i.e. minimum of 6 to 12 air changes per hour in facilities with a mechanically ventilated room and at least 60 liters/second/patient in facilities with natural ventilation Limit the number of persons present in the room to the absolute minimum required for the person's care and support Perform hand hygiene before and after contact with the person and his or her surroundings and after PPE removal. The duration of infectivity is also unknown so it is unclear how long people must be isolated, but current recommendations are for 24 hours after resolution of symptoms. In the SARS outbreak the virus was not cultured from people after the resolution of their symptoms. It is believed that the existing SARS research may provide a useful template for developing vaccines and therapeutics against a MERS-CoV infection. As of March 2020 there was one ( DNA based ) MERS vaccine which completed phase I clinical trials in humans, and three others in progress all of which are viral vectored vaccines, two adenoviral vectored ( ChAdOx1 -MERS, BVRS-GamVac ) and one MVA vectored (MVA-MERS-S ). As of 2020, there is no specific vaccine or treatment for the disease. Using extra-corporeal membrane oxygenation (ECMO) seems to improve outcomes significantly. Neither the combination of antivirals and interferons ( ribavirin + interferon alfa-2a or interferon alfa-2b) nor corticosteroids improved outcomes. MERS has had a relatively low population-wide reproduction number in previous outbreaks, but such outbreaks have occurred due to superspreading events. Total laboratory-confirmed cases of MERS world-wide per year have been as follows: MERS was also implicated in an outbreak in April 2014 in Saudi Arabia , where MERS has infected 688 people and 282 MERS-related deaths have been reported since 2012. In response to newly reported cases and deaths, and the resignation of four doctors at Jeddah's King Fahd Hospital who refused to treat MERS patients for fear of infection, the government removed the Minister of Health and set up three MERS treatment centers. Eighteen more cases were reported in early May. In June 2014, Saudi Arabia announced 113 previously unreported cases of MERS, revising the death toll to 282. [ citation needed ] A hospital-related outbreak in Riyadh in the summer of 2015 increased fears of an epidemic occurring during the annual Hajj pilgrimage that was to begin in late September. After a period of few cases, cases began increasing in the middle of the summer. The CDC placed the travel health alert to level 2, which calls for taking enhanced precautions. In May 2019, 14 cases of MERS were reported to the World Health Organization (WHO) by Saudi authorities, of which five were fatal. All those who died had comorbidities and other relatively serious health problems ranging from only diabetes mellitus in one person (aged 35) to complicated combinations of diabetes mellitus, hypertension and ischemic heart disease in two (65 and 80 years old) and diabetes mellitus, hypertension and nephropathy in another one who was 73 years old. Another patient who died and was 64 years old, had diabetes mellitus and hypertension. All those who died were males and three of them were reported to have had contact with, and exposure to, camels. Among the nine persons who survived were two females who were believed to have had contact with a person infected with MERS, one being a 23-year-old healthcare worker. Of the total 14 cases, four were females and 10 were males. All females survived. Reports of fatal cases were from Riyadh, Jeddah, Madinah and Najran. WHO did not recommend screening of travelers upon arrival or traveling restrictions. On 2 May 2014, the Centers for Disease Control and Prevention (CDC) confirmed the first diagnosis of MERS in the United States at Community Hospital in Munster, Indiana . The man diagnosed was a health care worker who had been in Saudi Arabia a week earlier, and was reported to be in good condition. A second patient who also traveled from Saudi Arabia was reported in Orlando, Florida on 12 May 2014. On 14 May 2014, officials in the Netherlands reported the first case had appeared. In May 2015, the first case in South Korea was confirmed in a man who had visited Saudi Arabia, United Arab Emirates and Bahrain. Another man from South Korea, who was travelling to China, was diagnosed as the first case in China. So far, no Chinese citizen has been found infected. As of 27 June 2015, 19 people in South Korea have died from this outbreak , with 184 confirmed cases of infection. There have been at least 6508 quarantined. [ excessive citations ] In 2018 a case was found in South Korea; the patient had recently returned from Kuwait (via Dubai). One study found that severe cases of illness had higher viral loads than milder cases, and that concentrations peaked in the second week of illness. In April 2014, MERS emerged in the Philippines with a suspected case of a home-bound Overseas Filipino Worker (OFW). Several suspected cases involving individuals who were on the same flight as the initial suspected case are being tracked but are believed to have dispersed throughout the country. Another suspected MERS-involved death in Sultan Kudarat province caused the Department of Health (DOH) to put out an alert. On 6 July 2015 the DOH confirmed the second case of MERS in the Philippines. A 36-year-old male foreigner from the Middle East was tested positive. On 27 July 2015, the accident and emergency department at Manchester Royal Infirmary closed after two patients were treated for suspected MERS infection. The facility was reopened later that evening, and it was later confirmed by Public Health England that the two patients had tested negative for the disease. In January 2016, a larger outbreak of MERS among camels in Kenya was reported. By 5 February 2016 more than 500 camels had died of the disease. On 12 February 2016, the disease was reported to be MERS. No human cases were identified, although one study found antibodies in healthy humans in Kenya. The table above provides a comparison between the 2014 Saudi Arabia outbreak and the South Korean outbreak in 2015 of the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) infection. MERS was also implicated in an outbreak in April 2014 in Saudi Arabia , where MERS has infected 688 people and 282 MERS-related deaths have been reported since 2012. In response to newly reported cases and deaths, and the resignation of four doctors at Jeddah's King Fahd Hospital who refused to treat MERS patients for fear of infection, the government removed the Minister of Health and set up three MERS treatment centers. Eighteen more cases were reported in early May. In June 2014, Saudi Arabia announced 113 previously unreported cases of MERS, revising the death toll to 282. [ citation needed ] A hospital-related outbreak in Riyadh in the summer of 2015 increased fears of an epidemic occurring during the annual Hajj pilgrimage that was to begin in late September. After a period of few cases, cases began increasing in the middle of the summer. The CDC placed the travel health alert to level 2, which calls for taking enhanced precautions. In May 2019, 14 cases of MERS were reported to the World Health Organization (WHO) by Saudi authorities, of which five were fatal. All those who died had comorbidities and other relatively serious health problems ranging from only diabetes mellitus in one person (aged 35) to complicated combinations of diabetes mellitus, hypertension and ischemic heart disease in two (65 and 80 years old) and diabetes mellitus, hypertension and nephropathy in another one who was 73 years old. Another patient who died and was 64 years old, had diabetes mellitus and hypertension. All those who died were males and three of them were reported to have had contact with, and exposure to, camels. Among the nine persons who survived were two females who were believed to have had contact with a person infected with MERS, one being a 23-year-old healthcare worker. Of the total 14 cases, four were females and 10 were males. All females survived. Reports of fatal cases were from Riyadh, Jeddah, Madinah and Najran. WHO did not recommend screening of travelers upon arrival or traveling restrictions. On 2 May 2014, the Centers for Disease Control and Prevention (CDC) confirmed the first diagnosis of MERS in the United States at Community Hospital in Munster, Indiana . The man diagnosed was a health care worker who had been in Saudi Arabia a week earlier, and was reported to be in good condition. A second patient who also traveled from Saudi Arabia was reported in Orlando, Florida on 12 May 2014. On 14 May 2014, officials in the Netherlands reported the first case had appeared. In May 2015, the first case in South Korea was confirmed in a man who had visited Saudi Arabia, United Arab Emirates and Bahrain. Another man from South Korea, who was travelling to China, was diagnosed as the first case in China. So far, no Chinese citizen has been found infected. As of 27 June 2015, 19 people in South Korea have died from this outbreak , with 184 confirmed cases of infection. There have been at least 6508 quarantined. [ excessive citations ] In 2018 a case was found in South Korea; the patient had recently returned from Kuwait (via Dubai). One study found that severe cases of illness had higher viral loads than milder cases, and that concentrations peaked in the second week of illness. In April 2014, MERS emerged in the Philippines with a suspected case of a home-bound Overseas Filipino Worker (OFW). Several suspected cases involving individuals who were on the same flight as the initial suspected case are being tracked but are believed to have dispersed throughout the country. Another suspected MERS-involved death in Sultan Kudarat province caused the Department of Health (DOH) to put out an alert. On 6 July 2015 the DOH confirmed the second case of MERS in the Philippines. A 36-year-old male foreigner from the Middle East was tested positive. On 27 July 2015, the accident and emergency department at Manchester Royal Infirmary closed after two patients were treated for suspected MERS infection. The facility was reopened later that evening, and it was later confirmed by Public Health England that the two patients had tested negative for the disease. In January 2016, a larger outbreak of MERS among camels in Kenya was reported. By 5 February 2016 more than 500 camels had died of the disease. On 12 February 2016, the disease was reported to be MERS. No human cases were identified, although one study found antibodies in healthy humans in Kenya. The table above provides a comparison between the 2014 Saudi Arabia outbreak and the South Korean outbreak in 2015 of the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) infection. Collaborative efforts were used in the identification of the MERS-CoV. Egyptian virologist Dr. Ali Mohamed Zaki isolated and identified a previously unknown coronavirus from the lungs of a 60-year-old Saudi Arabian man with pneumonia and acute kidney injury . After routine diagnostics failed to identify the causative agent, Zaki contacted Ron Fouchier, a leading virologist at the Erasmus Medical Center (EMC) in Rotterdam, the Netherlands, for advice. Fouchier sequenced the virus from a sample sent by Zaki. Fouchier used a broad-spectrum "pan-coronavirus" real-time reverse-transcription polymerase chain reaction (RT-qPCR) method to test for distinguishing features of a number of known coronaviruses (such as OC43, 229E, NL63, and SARS-CoV ), as well as for RNA-dependent RNA polymerase (RdRp), a gene conserved in all coronaviruses known to infect humans. While the screens for known coronaviruses were all negative, the RdRp screen was positive. On 15 September 2012, Dr. Zaki's findings were posted on ProMED-mail , the Program for Monitoring Emerging Diseases, a public health on-line forum. The United Kingdom's Health Protection Agency (HPA) confirmed the diagnosis of severe respiratory illness associated with a new type of coronavirus in a second patient, a 49-year-old Qatari man who had recently been flown into the UK. He died from an acute, serious respiratory illness in a London hospital. In September 2012, the UK HPA named it the London1 novel CoV/2012 and produced the virus' preliminary phylogenetic tree, the genetic sequence of the virus based on the virus's RNA obtained from the Qatari case. On 25 September 2012, the WHO announced that it was "engaged in further characterizing the novel coronavirus" and that it had "immediately alerted all its Member States about the virus and has been leading the coordination and providing guidance to health authorities and technical health agencies". The Erasmus Medical Center (EMC) in Rotterdam "tested, sequenced and identified" a sample provided to EMC virologist Ron Fouchier by Ali Mohamed Zaki in November 2012. On 8 November 2012, in an article published in the New England Journal of Medicine , Dr. Zaki and co-authors from the Erasmus Medical Center published more details, including a tentative name, Human Coronavirus-Erasmus Medical Center (HCoV-EMC), the virus's genetic makeup, and closest relatives (including SARS). In May 2013, the Coronavirus Study Group of the International Committee on Taxonomy of Viruses adopted the official designation, the Middle East Respiratory Syndrome Coronavirus (MERS-CoV), which was adopted by WHO to "provide uniformity and facilitate communication about the disease". Prior to the designation, WHO had used the non-specific designation 'Novel coronavirus 2012' or simply 'the novel coronavirus'. When rhesus macaques were given interferon-α2b and ribavirin and exposed to MERS, they developed less pneumonia than control animals. Five critically ill people with MERS in Saudi Arabia with acute respiratory distress syndrome (ARDS) and on ventilators were given interferon-α2b and ribavirin but all ended up dying of the disease. The treatment was started late in their disease (a mean of 19 days after hospital admission) and they had already failed trials of steroids so it remains to be seen whether it may have benefit earlier in the course of disease. Another proposed therapy is inhibition of viral protease or kinase enzymes. Researchers are investigating a number of medications, including using interferon, chloroquine , chlorpromazine , loperamide , lopinavir , remdesivir and galidesivir as well as other agents such as mycophenolic acid , camostat and nitazoxanide .

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Rift Valley fever

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Pappataci fever

Pappataci fever (also known as Phlebotomus fever and, somewhat confusingly, sandfly fever and three-day fever ) is a vector-borne febrile arboviral infection caused by three serotypes of Phlebovirus . It occurs in subtropical regions of the Eastern Hemisphere . The name, pappataci fever, comes from the Italian word for sandfly ; it is the union of the words pappa (usually this is used as a generic name for food, but in this case it is a verb meaning "eating") and taci (silent), distinguishing these insects from blood-feeding mosquitoes, which produce a typical noise while flying.A few days after the infective bite, a feeling of lassitude, abdominal distress and chills develop followed by fever of 39 to 40 °C (102 to 104 °F) , severe frontal headaches, muscle and joint aches, flushing of the face and a fast heart rate . After two days the fever begins to subside and the temperature returns to normal. Fatigue, a slow heart rate and low blood pressure may persist from a few days to several weeks but complete recovery is the rule. Three serotypes of Phlebovirus are known as the causative agents: Naples virus , Sicilian virus and Toscana virus . [ citation needed ]Although commercial tests are not readily available, diagnosis can be confirmed by serology-based assays or quantitative PCR by laboratories that have developed assays to perform such identification. [ citation needed ]Prevention of sandfly bites, and control of sandflies and their breeding grounds with insecticides are the principal methods for prevention. Mosquito nets may not be sufficient to prevent sandfly bites. [ citation needed ]There is no specific treatment for the disease. Pain killers and fluid replacement may be useful. Pappataci fever is prevalent in the subtropical zone of the Eastern Hemisphere between 20°N and 45°N, particularly in Southern Europe , North Africa , the Balkans , Eastern Mediterranean , Iraq , Iran , Pakistan , Afghanistan and India . The disease is transmitted by the bites of phlebotomine sandflies of the Genus Phlebotomus , in particular, Phlebotomus papatasi , Phlebotomus perniciosus and Phlebotomus perfiliewi . The sandfly becomes infected when biting an infected human in the period between 48 hours before the onset of fever and 24 hours after the end of the fever, and remains infected for its lifetime. Besides this horizontal virus transmission from man to sandfly, the virus can be transmitted in insects transovarially , from an infected female sandfly to its offspring. Pappataci fever is seldom recognised in endemic populations because it is mixed with other febrile illnesses of childhood, but it is more well known among immigrants and military personnel from non-endemic regions.

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Rift Valley fever

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1967 Marburg virus outbreak

The 1967 Marburg virus outbreak was the first recorded outbreak of Marburg virus disease . It started in early August 1967 when 30 people became ill in the West German towns of Marburg and Frankfurt and later two in Belgrade , Yugoslavia (now Serbia ). The infections were traced back to three laboratories in the separate locations which received a shared shipment of infected African green monkeys . The outbreak involved 25 primary Marburg virus infections and seven deaths, and six non-lethal secondary cases. In early August 1967, patients with unusual symptoms indicating an infectious disease were admitted to the university hospitals in Marburg and Frankfurt . The first patients were treated in their homes for up to 10 days, even though the illness was described as beginning suddenly with extreme malaise , myalgia , headache , and a rapid increase in body temperature to as high as 39 °C (102.2 °F) or more. Although the clinical symptoms were not very alarming during the first 3–4 days, additional symptoms and signs appeared at the end of the first week. The patients were therefore admitted to a hospital. In some cases, patients died from severe hemorrhagic shock on the day after hospital admission. Severe hemorrhagic shock occurred in about 25% of patients. All patients who died had hemorrhagic shock. The first infections occurred in laboratory workers who were conducting necropsies on imported African green monkeys. The incubation time of Marburg virus disease could only be estimated retrospectively, after the source of infection and the date of exposure were known. Incubation ranged from 5 to 9 days, with an average of 8 days. The ratio of primary to secondary infections was 21:3 in Marburg, 4:2 in Frankfurt, and 1:1 in Belgrade. Three cases of secondary infection resulted from inadvertent needle-stick inoculations; in one case, a pathology technician cut himself on the forearm with a knife during a postmortem examination. Airborne transmission between humans did not occur, as indicated, for example, by the instance of a young man who slept in the same bed with his brother only a couple of days before he died; the brother did not develop disease and was seronegative for Marburg virus disease six months later. The origin of the outbreaks was investigated at the same time as the microbiological studies. Early on in the investigation, it was realized that the patients in Marburg were employees of Behringwerke , a producer of sera and vaccines. The patients in Frankfurt were employees of Paul Ehrlich Institute , a control institute of sera and vaccines. The primary case in Belgrade was an employee involved in testing of live vaccines. All the patients at the three locations had contact with blood, organs, and cell cultures from African green monkeys ( Cercopithecus aethiops ). The monkeys' organs were used to make kidney cell culture for the production and safety testing of vaccines. The separate outbreaks were traced back to a shared shipment of infected green monkeys. Generally, shipments of green monkeys went directly from Uganda to Frankfurt. However, because of the Six Day War (5–10 June 1967), this shipment of monkeys was rerouted through London, where they were placed in animal storage because of a strike at the airport. After a two day delay, the monkeys were shipped to Frankfurt, and then to the laboratories in Frankfurt, Marburg, and Belgrade in June and July. The subsequent processing of the monkeys for cell culture at the three locations led to the laboratory-related outbreaks. The monkeys were believed to have been infected in Uganda, although infection from other animals in storage in London was also possible. The Marburg virus disease made reappearances in other countries in 1975, 1980, 1987, 1990, 1998–2000, 2004–05, 2007, 2008, 2017, 2021, 2022 and 2023. The seven deaths out of the 31 initially diagnosed infections during the 1967 Marburg virus outbreak represent a case fatality rate of 23%. The 32nd case was diagnosed retroactively via serology.

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SARI

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Sari

A sari (sometimes also saree or shari ) [note 1] is a women's garment from the Indian subcontinent , that consists of an un-stitched stretch of woven fabric arranged over the body as a robe , with one end attached to the waist, while the other end rests over one shoulder as a stole (shawl) , sometimes baring a part of the midriff . It may vary from 4.1 to 8.2 metres (4.5 to 9 yards) in length, and 60 to 120 centimetres (24 to 47 inches) in breadth, and is form of ethnic wear in India , Sri Lanka , Nepal , Bangladesh and Pakistan . There are various names and styles of sari manufacture and draping, the most common being the Nivi style. The sari is worn with a fitted bodice also called a choli ( ravike or kuppasa in southern India, and cholo in Nepal) and a petticoat called ghagra , parkar , or ul-pavadai . It remains fashionable in the Indian subcontinent today. The Hindustani word sāṛī ( साड़ी , ساڑھی ), described in Sanskrit śāṭī which means 'strip of cloth' and शाडी śāḍī or साडी sāḍī in Pali , ಸೀರೆ or sīre in Kannada and which evolved to sāṛī in modern Indian languages. The word śāṭika is mentioned as describing women's dharmic attire in Sanskrit literature and Buddhist literature called Jatakas . This could be equivalent to the modern day sari. The term for female bodice , the choli evolved from ancient stanapaṭṭa . Rajatarangini , a tenth-century literary work by Kalhana , states that the choli from the Deccan was introduced under the royal order in Kashmir. The petticoat is called sāyā ( साया , سایہ ) in Hindi-Urdu , parkar ( परकर ) in Marathi , ulpavadai ( உள்பாவாடை ) in Tamil ( pavada in other parts of South India: Malayalam : പാവാട , romanized : pāvāṭa , Telugu : పావడ , romanized : pāvaḍa , Kannada : ಪಾವುಡೆ , romanized: pāvuḍe ), sāẏā ( সায়া ) in Bengali and eastern India, and sāya ( සාය ) in Sinhalese . Apart from the standard "petticoat", it may also be called "inner skirt" or an inskirt.The history of sari-like drapery can be traced back to the Indus Valley civilisation , which flourished during 2800–1800 BCE around the northwestern part of the Indian subcontinent . Cotton was first cultivated and woven on the Indian subcontinent around the 5th millennium BCE. Dyes used during this period are still in use, particularly indigo , lac , red madder and turmeric . Silk was woven around 2450 BCE and 2000 BCE. The word sari evolved from śāṭikā ( Sanskrit : शाटिका ) mentioned in early Hindu literature as women's attire. The sari or śāṭikā evolved from a three-piece ensemble comprising the antarīya , the lower garment; the uttarīya ; a veil worn over the shoulder or the head; and the stanapatta , a chestband. This ensemble is mentioned in Sanskrit literature and Buddhist Pali literature during the 6th century BCE. Ancient antariya closely resembled the dhoti wrap in the "fishtail" version which was passed through the legs, covered the legs loosely and then flowed into long, decorative pleats at front of the legs. It further evolved into Bhairnivasani skirt, today known as ghagri and lehenga . Uttariya was a shawl-like veil worn over the shoulder or head. It evolved into what is known today known as dupatta and ghoonghat . Likewise, the stanapaṭṭa evolved into the choli by the 1st century CE. The ancient Sanskrit work Kadambari by Banabhatta and ancient Tamil poetry, such as the Silappadhikaram , describes women in exquisite drapery or sari. In ancient India, although women wore saris that bared the midriff, the Dharmasastra writers stated that women should be dressed such that the navel would never become visible, which may have led to a taboo on navel exposure at some times and places. It is generally accepted that wrapped sari-like garments for lower body and sometimes shawls or scarf like garment called 'uttariya' for upper body, have been worn by Indian women for a long time, and that they have been worn in their current form for hundreds of years. In ancient couture the lower garment was called ' nivi ' or 'nivi bandha', while the upper body was mostly left bare. The works of Kalidasa mention the kūrpāsaka , a form of tight fitting breast band that simply covered the breasts. It was also sometimes referred to as an uttarāsaṠga or stanapaṭṭa . Poetic references from works like Silappadikaram indicate that during the Sangam period in ancient Tamil Nadu in southern India, a single piece of clothing served as both lower garment and head covering, leaving the midriff completely uncovered. Similar styles of the sari are recorded paintings by Raja Ravi Varma in Kerala. Numerous sources say that everyday costume in ancient India until recent times in Kerala consisted of a pleated dhoti or ( sarong ) wrap, combined with a breast band called kūrpāsaka or stanapaṭṭa and occasionally a wrap called uttarīya that could at times be used to cover the upper body or head. The two-piece Kerala mundum neryathum (mundu, a dhoti or sarong, neryath, a shawl, in Malayalam ) is a survival of ancient clothing styles. The one-piece sari in Kerala is derived from neighbouring Tamil Nadu or Deccan during medieval period based on its appearance on various temple murals in medieval Kerala. Early Sanskrit literature has a wide vocabulary of terms for the veiling used by women, such as Avagunthana (oguntheti/oguṇthikā), meaning cloak-veil, Uttariya meaning shoulder-veil, Mukha-pata meaning face-veil and Sirovas-tra meaning head-veil. In the Pratimānātaka , a play by Bhāsa describes in context of Avagunthana veil that " ladies may be seen without any blame (for the parties concerned) in a religious session, in marriage festivities, during a calamity and in a forest ". The same sentiment is more generically expressed in later Sanskrit literature. Śūdraka , the author of Mṛcchakatika set in fifth century BCE says that the Avagaunthaha was not used by women everyday and at every time. He says that a married lady was expected to put on a veil while moving in the public. This may indicate that it was not necessary for unmarried females to put on a veil. This form of veiling by married women is still prevalent in Hindi-speaking areas, and is known as ghoonghat where the loose end of a sari is pulled over the head to act as a facial veil. Based on sculptures and paintings, tight bodices or cholis are believed to have evolved between the 2nd century BCE to 6th century CE in various regional styles. Early cholis were front covering tied at the back; this style was more common in parts of ancient northern India. This ancient form of bodice or choli are still common in the state of Rajasthan today. Varies styles of decorative traditional embroidery like gota patti, mochi, pakko, kharak, suf, kathi, phulkari and gamthi are done on cholis . In Southern parts of India, choli is known as ravikie which is tied at the front instead of back, kasuti is traditional form of embroidery used for cholis in this region. In Nepal, choli is known as cholo or chaubandi cholo and is traditionally tied at the front. Red is the most favoured colour for wedding saris , which are the traditional garment choice for brides in Hindu wedding . Women traditionally wore various types of regional handloom saris made of silk, cotton, ikkat, block-print, embroidery and tie-dye textiles. Most sought after brocade silk saris are Banasari, Kanchipuram, Gadwal, Paithani, Mysore, Uppada, Bagalpuri, Balchuri, Maheshwari, Chanderi, Mekhela, Ghicha, Narayan pet and Eri etc. are traditionally worn for festive and formal occasions. Silk Ikat and cotton saris known as Patola, Pochampally, Bomkai, Khandua, Sambalpuri, Gadwal, Berhampuri, Bargarh, Jamdani, Tant, Mangalagiri, Guntur, Narayan pet, Chanderi, Maheshwari, Nuapatn, Tussar, Ilkal, Kotpad and Manipuri were worn for both festive and everyday attire. Tie-dyed and block-print saris known as Bandhani, Leheria/Leheriya, Bagru, Ajrakh, Sungudi, Kota Dabu/Dabu print, Bagh and Kalamkari were traditionally worn during monsoon season. Gota Patti is popular form of traditional embroidery used on saris for formal occasions, various other types of traditional folk embroidery such mochi, pakko, kharak, suf, kathi, phulkari and gamthi are also commonly used for both informal and formal occasion. Today, modern fabrics like polyester, georgette and charmeuse are also commonly used. There are more than 80 recorded ways to wear a sari. The most common style is for the sari to be wrapped around the waist, with the loose end of the drape to be worn over the shoulder, baring the midriff. However, the sari can be draped in several different styles, though some styles do require a sari of a particular length or form. Ṛta Kapur Chishti , a sari historian and recognised textile scholar, has documented 108 ways of wearing a sari in her book, 'Saris: Tradition and Beyond'. The book documents the sari drapes across fourteen states of Gujarat , Maharashtra , Goa , Karnataka , Kerala , Tamil Nadu , Andhra Pradesh , Odisha , West Bengal , Jharkhand , Bihar , Chhattisgarh , Madhya Pradesh , and Uttar Pradesh . The Sari Series, a non-profit project created in 2017 is a digital anthology documenting India's regional sari drapes providing over 80 short films on how-to-drape the various styles. The French cultural anthropologist and sari researcher Chantal Boulanger categorised sari drapes into the following families: The Nivi is the most common style of sari worn today. It originated in the Deccan region. In the Deccan region, the Nivi existed in two styles, a style similar to modern Nivi and the second style worn with front pleats of Nivi tucked in the back. The increased interactions during colonial era saw most women from royal families come out of purdah in the 1900s. This necessitated a change of dress. Maharani Indira Devi of Cooch Behar popularised the chiffon sari. She was widowed early in life and followed the convention of abandoning her richly woven Baroda shalus in favour of the unadorned mourning white as per tradition. Characteristically, she transformed her " mourning " clothes into high fashion. She had saris woven in France to her personal specifications, in white chiffon, and introduced the silk chiffon sari to the royal fashion repertoire. Under colonial rule, petticoat was adopted, along with Victorian styles of puffed-sleeved blouses, which was commonly seen among the elites in Bombay presidency and Bengal presidency . Nivi drape starts with one end of the sari tucked into the waistband of the petticoat , usually a plain skirt . The cloth is wrapped around the lower body once, then hand-gathered into even pleats below the navel. The pleats are tucked into the waistband of the petticoat. They create a graceful, decorative effect which poets have likened to the petals of a flower. After one more turn around the waist, the loose end is draped over the shoulder. The loose end is called the aanchal , pallu , pallav , seragu , or paita depending on the language. It is draped diagonally in front of the torso. It is worn across the right hip to over the left shoulder, partly baring the midriff. The navel can be revealed or concealed by the wearer by adjusting the pallu , depending on the social setting. The long end of the pallu hanging from the back of the shoulder is often intricately decorated. The pallu may be hanging freely, tucked in at the waist, used to cover the head, or used to cover the neck, by draping it across the right shoulder as well. Some Nivi styles are worn with the pallu draped from the back towards the front, coming from the back over the right shoulder with one corner tucked by the left hip, covering the torso/waist. The Nivi sari was popularised through the paintings of Raja Ravi Varma . In one of his paintings, the Indian subcontinent was shown as a mother wearing a flowing Nivi sari. The ornaments sometimes worn in the midriff region on top of a sari are waist chains . They are sometimes worn as a part of bridal jewellery. The Nivi is the most common style of sari worn today. It originated in the Deccan region. In the Deccan region, the Nivi existed in two styles, a style similar to modern Nivi and the second style worn with front pleats of Nivi tucked in the back. The increased interactions during colonial era saw most women from royal families come out of purdah in the 1900s. This necessitated a change of dress. Maharani Indira Devi of Cooch Behar popularised the chiffon sari. She was widowed early in life and followed the convention of abandoning her richly woven Baroda shalus in favour of the unadorned mourning white as per tradition. Characteristically, she transformed her " mourning " clothes into high fashion. She had saris woven in France to her personal specifications, in white chiffon, and introduced the silk chiffon sari to the royal fashion repertoire. Under colonial rule, petticoat was adopted, along with Victorian styles of puffed-sleeved blouses, which was commonly seen among the elites in Bombay presidency and Bengal presidency . Nivi drape starts with one end of the sari tucked into the waistband of the petticoat , usually a plain skirt . The cloth is wrapped around the lower body once, then hand-gathered into even pleats below the navel. The pleats are tucked into the waistband of the petticoat. They create a graceful, decorative effect which poets have likened to the petals of a flower. After one more turn around the waist, the loose end is draped over the shoulder. The loose end is called the aanchal , pallu , pallav , seragu , or paita depending on the language. It is draped diagonally in front of the torso. It is worn across the right hip to over the left shoulder, partly baring the midriff. The navel can be revealed or concealed by the wearer by adjusting the pallu , depending on the social setting. The long end of the pallu hanging from the back of the shoulder is often intricately decorated. The pallu may be hanging freely, tucked in at the waist, used to cover the head, or used to cover the neck, by draping it across the right shoulder as well. Some Nivi styles are worn with the pallu draped from the back towards the front, coming from the back over the right shoulder with one corner tucked by the left hip, covering the torso/waist. The Nivi sari was popularised through the paintings of Raja Ravi Varma . In one of his paintings, the Indian subcontinent was shown as a mother wearing a flowing Nivi sari. The ornaments sometimes worn in the midriff region on top of a sari are waist chains . They are sometimes worn as a part of bridal jewellery. Because of the harsh extremes in temperature on the Indian subcontinent, the sari fills a practical role as well as a decorative one. It is not only warming in winter and cooling in summer, but its loose-fitting tailoring is preferred by women who must be free to move as their duties require. For this reason, [ citation needed ] it is the uniform of Biman Bangladesh Airlines and Air India uniform for air hostesses . An air hostess-style sari is draped in similar manner to a traditional sari, but most of the pleats are pinned to keep them in place. Bangladeshi female newsreaders and anchors also drape their sari in this particular style. Saris are worn as uniforms by the female hotel staff of many five-star luxury hotels in India , Sri Lanka , and Bangladesh as the symbol of Indian , Sri Lankan , and Bangladeshi culture , respectively. Similarly, the female politicians of all three countries wear the sari in a professional manner. Bangladeshi politicians usually wear saris with long sleeve blouse while covering their midriff. Some politicians pair up saris with hijabs or shawls for more coverage. The women of the Nehru–Gandhi family like Indira Gandhi and Sonia Gandhi have worn a special blouse for the campaign trail which is longer than usual and is tucked in to prevent any midriff showing while waving to the crowds. Stylist Prasad Bidapa has to say, "I think Sonia Gandhi is the country's most stylish politician. But that's because she's inherited the best collection of saris from her mother-in-law. I'm also happy that she supports the Indian handloom industry with her selection." Most female MPs in the Sri Lankan Parliament wear a Kandyan osari. This includes prominent women in politics, the first female premier in the world, Sirimavo Bandaranaike and President Chandrika Bandaranaike Kumaratunga . Contemporary examples include Pavithra Wanniarachchi , the sitting health minister in Cabinet . The adoption of the sari is not exclusive to Sinhalese politicians; Muslim MP Ferial Ashraff combined a hijab with her sari while in Parliament.Sari is the national attire for women in Bangladesh , Although Dhakai Jamdani (hand made sari) is worldwide known and most famous to all women who wear sari but there are also many variety of saris in Bangladesh. There are many regional variations of them in both silk and cotton. There are many regional variations of saris in both silk and cotton. e.g., Dhakai Banarasi sari , Rajshahi silk , Tangail sari , Tant sari , Tassar silk sari, Manipuri sari and Katan sari. The sari is reserved as the dress of choice for important occasions and events. In 2013, the traditional art of weaving jamdani was declared a UNESCO Intangible Cultural Heritage of Humanity . In 2016, Bangladesh received geographical indication (GI) status for Jamdani sari. Sri Lankan women wear saris in many styles. Two ways of draping the sari are popular and tend to dominate: the Indian style (classic nivi drape) and the Kandyan style (or Osariya in Sinhala). The Kandyan style is generally more popular in the hill country region of Kandy from which the style gets its name. Though local preferences play a role, most women decide on style depending on personal preference or what is perceived to be most flattering for their figure. The traditional Kandyan (Osariya) style consists of a full blouse which covers the midriff completely and is partially tucked in at the front. However, the modern intermingling of styles has led to most wearers baring the midriff. The final tail of the sari is neatly pleated rather than free-flowing. This is rather similar to the pleated rosette used in the Pin Kosuvam style noted earlier in the article. The Kandyan style is considered the national dress of Sinhalese women. It is the uniform of the air hostesses of SriLankan Airlines . During the 1960s, the mini sari known as 'hipster' sari created a wrinkle in Sri Lankan fashion, since it was worn below the navel and barely above the line of prosecution for indecent exposure. The conservative people described the 'hipster' as " an absolute travesty of a beautiful costume almost a desecration " and " a hideous and purposeless garment ". The sari is the most commonly worn women's clothing in Nepal where a special style of sari draping is called haku patasihh . The sari is draped around the waist and a shawl is worn covering the upper half of the sari, which is used in place of a pallu .In Pakistan, the saris are still popular and worn on special occasions. The Shalwar kameez , however, is worn throughout the country on a daily basis. The sari nevertheless remains a popular garment among the middle and upper class for many formal functions. Saris can be seen worn commonly in metropolitan cities such as Karachi and Islamabad and are worn regularly for weddings and other business types of functions. Saris are also worn by many Muslim women in Sindh to show their status or to enhance their beauty. Phulkari , Kota doria , banarasi , Ajrak are the most worn. The sari is worn as daily wear by Pakistani Hindus , by elderly Muslim women who were used to wearing it in pre-partition India and by some of the new generation who have reintroduced the interest in saris. Black Sari Day, is an celebration of Iqbal Bano a woman who fought in a Black sari in Lahore against Zia. She sang Hum Dekhenge . Although this event is to bring family closer and to enjoy the day of Iqbal Bano.While the sari is typical traditional wear for women in the Indian subcontinent, clothing worn by women in Southeast Asian countries like Myanmar , Malaysia , Indonesia , the Philippines , Cambodia , Thailand and Laos resemble it, where a long rectangular piece of cloth is draped around the body. These are different from the sari as they are wrapped around the lower-half of body as a skirt, worn with a shirt/blouse and resemble a sarong , as seen in the Burmese longyi ( Burmese : လုံချည် ; MLCTS : lum hkyany ; IPA: [ lòʊɰ̃dʑì ] ), Filipino malong and tapis , Laotian xout lao ( Lao : ຊຸດລາວ ; IPA: [ sut.láːw ] ), Laotian and Thai suea pat ( Lao : ເສື້ອປັດ ; pronounced [ sɯ̏a.pát ] ) and sinh ( Lao : ສິ້ນ , IPA: [ sȉn ] ; Thai : ซิ่น , RTGS : sin , IPA: [ sîn ] ), Cambodian sbai ( Khmer : ស្បៃ ) and sampot ( Khmer : សំពត់ , saṃbát , IPA: [ sɑmpʊət ] ) and Timorese tais . Saris, worn predominantly in the Indian subcontinent are usually draped with one end of the cloth fastened around the waist, and the other end placed over the shoulder baring the midriff. Saris are woven with one plain end (the end that is concealed inside the wrap), two long decorative borders running the length of the sari, and a one to three-foot section at the other end which continues and elaborates the length-wise decoration. This end is called the pallu ; it is the part thrown over the shoulder in the nivi style of draping. In past times, saris were woven of silk or cotton. The rich could afford finely woven, diaphanous silk saris that, according to folklore , could be passed through a finger ring . The poor wore coarsely woven cotton saris. All saris were handwoven and represented a considerable investment of time or money. Simple hand-woven villagers' saris are often decorated with checks or stripes woven into the cloth. Inexpensive saris were also decorated with block printing using carved wooden blocks and vegetable dyes, or tie-dyeing , known in India as bhandani work. More expensive saris had elaborate geometric, floral, or figurative ornaments or brocades created on the loom , as part of the fabric. Sometimes warp and weft threads were tie-dyed and then woven, creating ikat patterns. Sometimes threads of different colours were woven into the base fabric in patterns; an ornamented border, an elaborate pallu , and often, small repeated accents in the cloth itself. These accents are called buttis or bhuttis (spellings vary). For fancy saris, these patterns could be woven with gold or silver thread , which is called zari work. Sometimes the saris were further decorated, after weaving, with various sorts of embroidery. Resham work is embroidery done with coloured silk thread. Zardozi embroidery uses gold and silver thread, and sometimes pearls and precious stones . Cheap modern versions of zardozi use synthetic metallic thread and imitation stones, such as fake pearls and Swarovski crystals. In modern times, saris are increasingly woven on mechanical looms and made of artificial fibres, such as polyester , nylon, or rayon , which do not require starching or ironing . They are printed by machine, or woven in simple patterns made with floats across the back of the sari. This can create an elaborate appearance on the front, while looking ugly on the back. The punchra work is imitated with inexpensive machine-made tassel trim. Fashion designer Aaditya Sharma declared, "I can drape a sari in 54 different styles". Hand-woven, hand-decorated saris are naturally much more expensive than the machine imitations. While the overall market for handweaving has plummeted (leading to much distress among Indian handweavers), hand-woven saris are still popular for weddings and other grand social occasions.The traditional sari made an impact in the United States during the 1970s. Eugene Novack who ran the New York store, Royal Sari House commented that he had initially been selling mainly to Indian women in the New York area. However, many American business women and housewives soon became his customers, favouring styles resembling western attire such as gowns. He also said that men appeared intrigued by the fragility and the femininity it confers on the wearer. Newcomers to the sari report that it is comfortable to wear, requiring no girdles or stockings and that the flowing garb feels so feminine with unusual grace. The sari has gained its popularity internationally because of the growth of Indian fashion trends globally. Many Bollywood celebrities, like Aishwarya Rai , have worn it at international events representing India's cultural heritage . In 2010, Bollywood actress Deepika Padukone wanted to represent her country at an international event, wearing the national costume. On her very first red carpet appearance at the Cannes International Film Festival , she stepped out on the red carpet in a Rohit Bal sari. Many foreign celebrities have worn traditional sari attire designed by Indian fashion designers . American actress Pamela Anderson made a surprise guest appearance on Bigg Boss , the Indian version of Big Brother , dressed in a sari that was specially designed for her by Mumbai-based fashion designer Ashley Rebello. Ashley Judd donned a purple sari at the YouthAIDS Benefit Gala in November 2007 at the Ritz Carlton in Mclean, Virginia. There was an Indian flavour to the red carpet at the annual Fashion Rocks concert in New York, with designer Rocky S walking the ramp along with Jessica, Ashley, Nicole, Kimberly and Melody – the Pussycat Dolls – dressed in saris. in 2014, American singer Selena Gomez was seen in a sari for an UNICEF charity event at Nepal. In the United States , the sari has recently become politicised with the digital-movement, "Sari, Not Sorry". Tanya Rawal-Jindia , a gender studies professor at UC Riverside , initiated this anti-xenophobia fashion-campaign on Instagram. While an international image of the modern style sari may have been popularised by airline flight attendants , each region in the Indian subcontinent has developed, over the centuries, its own unique sari style. Following are other well-known varieties, distinct on the basis of fabric, weaving style, or motif, in the Indian subcontinent.Handloom sari weaving is one of India's cottage industries . The handloom weaving process requires several stages in order to produce the final product. Traditionally the processes of dyeing (during the yarn, fabric, or garment stage), warping , sizing, attaching the warp, weft winding and weaving were done by weavers and local specialists around weaving towns and villages. Paithanpattu – Maharashtra Yeola sari – Maharashtra Peshwai shalu – Maharashtra Mahalsa sari – Maharashtra Narayanpeth – Maharashtra Khun fabric – Maharashtra Karvati tussar sari – MaharashtraPaithanpattu – Maharashtra Yeola sari – Maharashtra Peshwai shalu – Maharashtra Mahalsa sari – Maharashtra Narayanpeth – Maharashtra Khun fabric – Maharashtra Karvati tussar sari – Maharashtra

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Sari (disambiguation)

A sari is a female garment in the Indian subcontinent. Sari may also refer to:

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Sari-sari store

A sari-sari store , anglicized as neighborhood sundry store , is a convenience store found in the Philippines . The word sari-sari is Tagalog meaning "variety" or "sundry". Such stores occupy an important economic and social location in a Filipino community and are ubiquitous in neighborhoods and along streets. Sari-sari stores tend to be family-run and privately owned operating within the shopkeeper's residence. Commodities are displayed in a large screen-covered or metal-barred window in front of the shop. Candies in recycled jars, canned goods , and cigarettes are displayed while cooking oil , salt , and sugar are stored at the back of the shop. Prepaid mobile phone credits are provided. The sari-sari store operates with a small revolving fund , and it generally does not offer perishable goods requiring refrigeration. The few that do have refrigerators carry soft drinks , beers, and bottled water. Sari-sari stores are an integral part of the ecosystem of society and contribute to the grassroots micro-economy. According to the Magna Kultura Foundation, the network of sari-sari stores nationwide accounts for almost seventy percent (70%) of sales of manufactured consumer food products, which makes it a valuable part of the economy and an important conduit for making vital goods available to Filipino neighborhoods. Sari-sari stores are the backbone of the grassroots economy. An estimated 800,000 sari-sari stores hold a significant portion of the domestic retail market and the country's GDP. 13 percent or Php 1.3 trillion of the Philippines GDP of Php 9.7 trillion in the year 2011 came from retail, which is composed largely of micro, small, and medium-sized enterprises (MSMEs) or small businesses like sari-sari stores. [ citation needed ] Often sari-sari store owners apply a markup of about 10% on average, compared to the 20% average markup of the 24/7 convenience store alternatives such as 7-11, so most Filipinos tend to buy at sari-sari stores when possible. Sari-sari stores have higher prices when compared to supermarkets but provide several benefits to their customers. The sari-sari store provides easy access to basic commodities at low cost. Without them, villagers must go to the nearest market town, which may be quite far from the village itself. In the Philippines, following the concept of tingi or retail, a customer can buy 'units' of the product rather than a whole package. For example, one can buy a single cigarette for (5) five pesos (0.10 US dollars) rather than a whole pack. This is convenient for those who cannot buy the whole package or do not need much of it, although it is cumulatively more expensive. The sari-sari store saves customers from paying extra transportation costs, especially in rural areas, since some towns can be very far from the nearest market or grocery. The store may also allow purchases on credit. The stores act as trading centers in rural areas. Farmers and fishermen may directly trade their products to the sari-sari store in return for basic articles, fuel, and other supplies. The owners can buy grocery commodities in bulk, and then sell them in-store at a mark-up. Trucks deliver LPG and soft drinks directly to the store. The store requires little investment since the products are cheap and only a few modifications on one side of the house are needed to convert it to a sari-sari store. The sari-sari store also allows credit purchases from its "suki" (repeat customers known to the store owners). They usually keep a record of their customers' outstanding balances on a school notebook and demand payments on paydays. The lifespan of sari-sari stores is highly variable, with many closing after a few weeks due to insufficient income or management mishandling by owners who have limited formal schooling. The Magna Kultura Foundation notes that the sari-sari store is part of Philippine culture, and it has become an integral part of every Filipino's life. It is a constant feature of residential neighborhoods in the Philippines, both in rural and urban areas, proliferating even in the poorest communities. About ninety-three percent (93%) of all sari-sari stores nationwide are located in residential communities. The neighborhood sari-sari store (variety or general) is part and parcel of daily life for the average Filipino. Any essential household good that might be missing from one's pantry – from basic food items like sugar, coffee, and cooking condiments, to other necessities like soap or shampoo, is most conveniently purchased from the nearby sari-sari store at economically sized quantities that are affordable to common citizens. The sari-sari store offers a place where people can meet. The benches provided in front of the store are usually occupied by local people; some men spend time drinking there while women discuss the latest local news, youths also use the place to hang out and children also rest there in the afternoons after playing and buy soft drinks and snacks.

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Sari-Sari Channel

Sari-Sari Channel (visually rendered in all capital letters as SARI SARI CHANNEL ) is a 24-hour general entertainment channel under a joint-venture between Cignal TV and Viva Communications . Named after the Philippine Sari-sari store , it offers a smorgasbord of shows from the portfolios of Viva TV and TV5. The channel's content include archive shows and movies from Viva Television and Viva Films , original movies from Studio5, the film production arm of TV5 Network and in-house original productions in partnership of the latter's talents. In 2015, Sari-Sari Channel was delegated as the official production outfit to handle all entertainment programs of TV5 after Viva Communications chief Vicente "Vic" del Rosario, Jr. was appointed as the network's entertainment head, replacing Wilma Galvante , following the retrenchment on TV5's main entertainment department. Starting October 21, 2017, selected original serials from the channel is broadcast on TV5 under the Sari-Sari Weekend on TV5 block. It is also carried over to its overseas counterpart Kapatid Channel since 2018. Since 2020, after Cignal TV took over the TV5 Network's management and operations, most episodes of Cignal-TV5-Viva produced shows are currently aired on this channel the next day after being shown on TV5.Bawat Sandali Dalawang Gabi Frenemies in Love Kuya and Me Mariposa (2016) My Only Love Sa Bawat Patak ng Ulan (2016) #ParangNormal Activity 10 Signatures to Bargain With God [lower-alpha 1] 1000 Heartbeats: Pintig Pinoy (2021) 2 1/2 Daddies A Not-So-Fake Love Story (2019) Alabang Girls Ang Kwarto Sa May Hagdanan [lower-alpha 1] Barrio Kulimlim (2016) Beh Buti Nga (2019) Born to Be a Star (2016, 2021) Blue Jeans (2018) Brush (2018) Challenge Accepted Class 3-C Has A Secret (2019) [lower-alpha 1] Cuerpo Y Alma Dalawang Gabi (2016) Dear Heart Destiny Guard (2019) Di Na Muli (2021) Diary of a 30 Something (2017) Encounter (2021) For the Love (2023) Frenemies in Love (2016) From the Beautiful Country (2016) [lower-alpha 1] Ghost Adventures Glamorosa Ha-pi House (2017) [lower-alpha 1] Hourglass [lower-alpha 1] Job Order (2018) Kagat ng Dilim (2020–2021) Kalye Kweens (2022) Kalye Wars (2018) Kurdapya (2023) Kuya and Me (2018) Lokomoko High Mac and Chiz Masked Singer Pilipinas Mga Kuwentong Epik (2022–2023) Midnight DJ Minsan pa Nating Hagkan ang Nakaraan (2023) My Only Love (2016) Nandito Ako Never Say Goodbye Operation Break the Casanova's Heart [lower-alpha 1] Pag-Ibig Hanggang Kamatayan Puto (2021) Red Envelope Rolling in It Philippines (2021–2022) Sa Ngalan ng Anak (2016) Sinugatang Puso Studio 5 Original Movies (2016) Tabi Po (2016) Taddy Taddy Po Takot Ka Ba Sa Dilim? Tasya Fantasya Team A (2023) The Feb 15 Club (2016) The Kasambahays 1&2 The Last Woman Standing The Legal Mistress (2018) The Mysterious Case of Ana Madrigal (2016) The Wall Philippines (2021) Tukhang {{efn|name=fn1} Viva Drama Specials Where is Franco? [lower-alpha 1] Will You Marry Me (2019) Wives of House of No. 2 (2016) [lower-alpha 1] Sari-Saring SineBawat Sandali Dalawang Gabi Frenemies in Love Kuya and Me Mariposa (2016) My Only Love Sa Bawat Patak ng Ulan (2016)#ParangNormal Activity 10 Signatures to Bargain With God [lower-alpha 1] 1000 Heartbeats: Pintig Pinoy (2021) 2 1/2 Daddies A Not-So-Fake Love Story (2019) Alabang Girls Ang Kwarto Sa May Hagdanan [lower-alpha 1] Barrio Kulimlim (2016) Beh Buti Nga (2019) Born to Be a Star (2016, 2021) Blue Jeans (2018) Brush (2018) Challenge Accepted Class 3-C Has A Secret (2019) [lower-alpha 1] Cuerpo Y Alma Dalawang Gabi (2016) Dear Heart Destiny Guard (2019) Di Na Muli (2021) Diary of a 30 Something (2017) Encounter (2021) For the Love (2023) Frenemies in Love (2016) From the Beautiful Country (2016) [lower-alpha 1] Ghost Adventures Glamorosa Ha-pi House (2017) [lower-alpha 1] Hourglass [lower-alpha 1] Job Order (2018) Kagat ng Dilim (2020–2021) Kalye Kweens (2022) Kalye Wars (2018) Kurdapya (2023) Kuya and Me (2018) Lokomoko High Mac and Chiz Masked Singer Pilipinas Mga Kuwentong Epik (2022–2023) Midnight DJ Minsan pa Nating Hagkan ang Nakaraan (2023) My Only Love (2016) Nandito Ako Never Say Goodbye Operation Break the Casanova's Heart [lower-alpha 1] Pag-Ibig Hanggang Kamatayan Puto (2021) Red Envelope Rolling in It Philippines (2021–2022) Sa Ngalan ng Anak (2016) Sinugatang Puso Studio 5 Original Movies (2016) Tabi Po (2016) Taddy Taddy Po Takot Ka Ba Sa Dilim? Tasya Fantasya Team A (2023) The Feb 15 Club (2016) The Kasambahays 1&2 The Last Woman Standing The Legal Mistress (2018) The Mysterious Case of Ana Madrigal (2016) The Wall Philippines (2021) Tukhang {{efn|name=fn1} Viva Drama Specials Where is Franco? [lower-alpha 1] Will You Marry Me (2019) Wives of House of No. 2 (2016) [lower-alpha 1]Sari-Saring Sine

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Serotonin antagonist and reuptake inhibitor

Serotonin antagonist and reuptake inhibitors ( SARIs ) are a class of drugs used mainly as antidepressants , but also as anxiolytics and hypnotics . They act by antagonizing serotonin receptors such as 5-HT 2A and inhibiting the reuptake of serotonin , norepinephrine , and/or dopamine . Additionally, most also antagonize α 1 -adrenergic receptors . The majority of the currently marketed SARIs belong to the phenylpiperazine class of compounds.The binding profiles of SARIs and some metabolites in terms of their affinities ( K i , nM ) for various receptors and transporters are as follows: These drugs act as antagonists or inverse agonists of the 5-HT 2A , α 1 -adrenergic, and H 1 receptors, as partial agonists of the 5-HT 1A receptor, and as inhibitors of the transporters. mCPP is an antagonist of the 5-HT 2B receptor, an agonist of the 5-HT 1A , 5-HT 2C , and 5-HT 3 receptors, and acts as a partial agonist of the human 5-HT 2A and 5-HT 2C receptors. The binding profiles of SARIs and some metabolites in terms of their affinities ( K i , nM ) for various receptors and transporters are as follows: These drugs act as antagonists or inverse agonists of the 5-HT 2A , α 1 -adrenergic, and H 1 receptors, as partial agonists of the 5-HT 1A receptor, and as inhibitors of the transporters. mCPP is an antagonist of the 5-HT 2B receptor, an agonist of the 5-HT 1A , 5-HT 2C , and 5-HT 3 receptors, and acts as a partial agonist of the human 5-HT 2A and 5-HT 2C receptors.

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SARI

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Sari, Iran

Sari ( Persian : ساری ; [ sɒːˈɾiː ] ⓘ ); also Romanized as Sâri and Sārī ; also known as Shahr-e-Tajan and Shari-e-Tajan , is a city in the Central District of Sari County , Mazandaran province, Iran , serving as capital of the province, the county and the district. Sari was the former capital of Iran for a short period and is in the north of the country, between the northern slopes of the Alborz Mountains and southern coast of the Caspian Sea . Sari is the largest and most populous city of Mazandaran.Excavations in the Hutto cave present evidence for the existence of settlements around Sari as far back as the 70th millennium BCE. The Muslim historian Hamdollah Mostowfi attributes the foundation of Sari to king Tahmoures Divband of the Pishdadian Dynasty . Ferdowsi mentions the name of the city in Shahnameh , at the time of Fereydun and Manuchehr , when Manuchehr is returning to Fereydun's capital, Tamisheh in Mazandaran , after the victory over Salm and Tur : ز دریای گیلان (٠ازندران) چون ابر سیاه / د٠اد٠به ساری رسید آن سپاه / چو آ٠د به نزدیک شاه آن سپاه / فریدون پذیره بیا٠د به راه the city's name was also Zadracarta in 658 B.C to 225 A.D. Coming from this and other similar evidence in the Shahnameh , native people of Sari have a folklore that the city was populated when the blacksmith Kaveh (a native of the city) revolted against the tyranny of Zahak . After that success, Fereydun of Pishdadi (from Tamishan) feeling indebted to Kaveh, chose this city so as to live near him until his death. For this reason, when Touraj and Salam murdered Iraj (son of Fereydun), they buried him here. Espahbod Tous-e Nouzar (great-grandson of Fereydun) systematically founded it to remain as family monument. Sari may be synonymous with the city of Zadracarta mentioned by Ancient Greek sources as early as the 6th century BCE ( Achaemenid dynasty ). However, other sources suggest that modern Gorgan is located closer to, or on, the site of Zadracarta. According to Arrian , this was the largest city of Hyrcania . The term means "the yellow city" and it was given to it because of the great number of orange, lemon, and other fruit trees that grew in the outskirts of that city. Hence it is by D'Anville, Rochette, and other geographers, identified Saru, which Pietro Della Valle says in his "Travels" means "the yellow city". It is probable that Zadracarta and Saru are the same with the Syringis of Polybius, taken from Arsaces II by Antiochus the Great , in his vain attempt to reunite the revolted provinces of Hyrcania and Parthia to the Syrian crown. Han Way, who visited Saru in 1734, makes mention of four ancient Magian temples as still standing then, built in the form of several rotundas, each thirty feet in diameter, and about 120 in height. However Sir William Ouseley , who had travelled to the site in 1811, has speculated that these to be masses of brick masonry of the Mohammedan age. Out of four, one of the rotunda is still standing since the rest were overturned by an earthquake. This and other remains of similar buildings, bear the names of Fereydun, Salm, Tur, and other mythical figures, whose celebrity had been established about 2000 years prior to their erection. One of them Avas called the tomb of Kaus, and was supposed to contain the ashes of Cyrus the Great . Sir William Ouseley thinks it was that of Kabus, or Kaus, the son of Washmakin, who governed Mazanderan in the fourth century of the Hejira. It was at Saru that the ashes of the youthful hero, Sohraub , were deposited by his father, Roostum , after he had unwittingly slayed Sohrab in a hand-to-hand battle. Saru is celebrated for its abundance of gardens, which emit a pleasing fragrance in the vernal and summer months. An oriental proverb declares that the "gates of paradise derive sweetness from the air of Sari and the flowers of Eden receive their fragrance from its soil". The city was again a regional capital in the Sassanid dynasty era. In the seventh century, Farrukhan the Great of the Dabuyid dynasty reconstructed the city, and because his son's name was "Saruyeh", he called it by this name. Sari once again became the capital of Tabaristan during that century ( Amol was the capital previously ). After invasions by the successors of Mongols , Timur of Uzbeks , Turcoman , and Tatars the city lost its high status and was periodically burnt to ashes. Because Shah Abbas I 's mother was from Behshahr (Ashraf), he founded Farahabad as his alternate capital of Persia in the north of the city and created the gardens in Ashraf. Mazandaran alongside neighboring Gilan were subsequently settled during Abbas' reign by large numbers of Georgians , Circassians , Armenians and other peoples of the Caucasus , whose descendants still live across Mazandaran. Still many towns, villages and neighbourhoods in Mazandaran bear the name "Gorji" (i.e. Georgian) in them, although most of the Georgians are already assimilated into the mainstream Mazanderanis. After the Safavid dynasty fell and until the rise of Agha Mohammad Khan to power there, is no evidence of any notable events in Sari. Major developments took place after the Qajar dynasty . During the reign of Reza Shah Pahlavi , the face of the town was changed drastically. Sari Rail Station and most of the streets and governmental buildings date from that era. During World War II the Soviet army occupied the city, but left it after the war.Excavations in the Hutto cave present evidence for the existence of settlements around Sari as far back as the 70th millennium BCE. The Muslim historian Hamdollah Mostowfi attributes the foundation of Sari to king Tahmoures Divband of the Pishdadian Dynasty . Ferdowsi mentions the name of the city in Shahnameh , at the time of Fereydun and Manuchehr , when Manuchehr is returning to Fereydun's capital, Tamisheh in Mazandaran , after the victory over Salm and Tur : ز دریای گیلان (٠ازندران) چون ابر سیاه / د٠اد٠به ساری رسید آن سپاه / چو آ٠د به نزدیک شاه آن سپاه / فریدون پذیره بیا٠د به راه the city's name was also Zadracarta in 658 B.C to 225 A.D. Coming from this and other similar evidence in the Shahnameh , native people of Sari have a folklore that the city was populated when the blacksmith Kaveh (a native of the city) revolted against the tyranny of Zahak . After that success, Fereydun of Pishdadi (from Tamishan) feeling indebted to Kaveh, chose this city so as to live near him until his death. For this reason, when Touraj and Salam murdered Iraj (son of Fereydun), they buried him here. Espahbod Tous-e Nouzar (great-grandson of Fereydun) systematically founded it to remain as family monument. Sari may be synonymous with the city of Zadracarta mentioned by Ancient Greek sources as early as the 6th century BCE ( Achaemenid dynasty ). However, other sources suggest that modern Gorgan is located closer to, or on, the site of Zadracarta. According to Arrian , this was the largest city of Hyrcania . The term means "the yellow city" and it was given to it because of the great number of orange, lemon, and other fruit trees that grew in the outskirts of that city. Hence it is by D'Anville, Rochette, and other geographers, identified Saru, which Pietro Della Valle says in his "Travels" means "the yellow city". It is probable that Zadracarta and Saru are the same with the Syringis of Polybius, taken from Arsaces II by Antiochus the Great , in his vain attempt to reunite the revolted provinces of Hyrcania and Parthia to the Syrian crown. Han Way, who visited Saru in 1734, makes mention of four ancient Magian temples as still standing then, built in the form of several rotundas, each thirty feet in diameter, and about 120 in height. However Sir William Ouseley , who had travelled to the site in 1811, has speculated that these to be masses of brick masonry of the Mohammedan age. Out of four, one of the rotunda is still standing since the rest were overturned by an earthquake. This and other remains of similar buildings, bear the names of Fereydun, Salm, Tur, and other mythical figures, whose celebrity had been established about 2000 years prior to their erection. One of them Avas called the tomb of Kaus, and was supposed to contain the ashes of Cyrus the Great . Sir William Ouseley thinks it was that of Kabus, or Kaus, the son of Washmakin, who governed Mazanderan in the fourth century of the Hejira. It was at Saru that the ashes of the youthful hero, Sohraub , were deposited by his father, Roostum , after he had unwittingly slayed Sohrab in a hand-to-hand battle. Saru is celebrated for its abundance of gardens, which emit a pleasing fragrance in the vernal and summer months. An oriental proverb declares that the "gates of paradise derive sweetness from the air of Sari and the flowers of Eden receive their fragrance from its soil". The city was again a regional capital in the Sassanid dynasty era. In the seventh century, Farrukhan the Great of the Dabuyid dynasty reconstructed the city, and because his son's name was "Saruyeh", he called it by this name. Sari once again became the capital of Tabaristan during that century ( Amol was the capital previously ). After invasions by the successors of Mongols , Timur of Uzbeks , Turcoman , and Tatars the city lost its high status and was periodically burnt to ashes.Because Shah Abbas I 's mother was from Behshahr (Ashraf), he founded Farahabad as his alternate capital of Persia in the north of the city and created the gardens in Ashraf. Mazandaran alongside neighboring Gilan were subsequently settled during Abbas' reign by large numbers of Georgians , Circassians , Armenians and other peoples of the Caucasus , whose descendants still live across Mazandaran. Still many towns, villages and neighbourhoods in Mazandaran bear the name "Gorji" (i.e. Georgian) in them, although most of the Georgians are already assimilated into the mainstream Mazanderanis. After the Safavid dynasty fell and until the rise of Agha Mohammad Khan to power there, is no evidence of any notable events in Sari.Major developments took place after the Qajar dynasty . During the reign of Reza Shah Pahlavi , the face of the town was changed drastically. Sari Rail Station and most of the streets and governmental buildings date from that era. During World War II the Soviet army occupied the city, but left it after the war.The coastline north of Sari fronts onto the Mazandaran Sea ; north-east of the city lies Neka . Qa'emshahr (formerly known as Shahi) is to its south-west, Juybar is to its north-west, and Kiasar , Damghan , and Semnan are cities located to the south. Sari has a humid subtropical climate ( Köppen : Cfa , Trewartha : Cf ) that borders on a Mediterranean climate ( Csa ). Winters are cool and rainy whilst summers are hot and humid. Sari's 2005–2006 statistical weather information, in comparison with that of other Mazandaran cities, shows that Sari has an average climate, but it is somewhat sunnier and has more spring rain. However, recent rainfall in Sari has declined. Extremes for the Mahdasht Station: Highest recorded temperature: 44.0 °C (111.2 °F) on 4 June 1980 Lowest recorded temperature: −5.0 °C (23.0 °F) on 17 February 1993 Sari has a humid subtropical climate ( Köppen : Cfa , Trewartha : Cf ) that borders on a Mediterranean climate ( Csa ). Winters are cool and rainy whilst summers are hot and humid. Sari's 2005–2006 statistical weather information, in comparison with that of other Mazandaran cities, shows that Sari has an average climate, but it is somewhat sunnier and has more spring rain. However, recent rainfall in Sari has declined. Extremes for the Mahdasht Station: Highest recorded temperature: 44.0 °C (111.2 °F) on 4 June 1980 Lowest recorded temperature: −5.0 °C (23.0 °F) on 17 February 1993 The Clock Tower, in the Clock Square (Meydan-e-Sa'at) located in downtown Sari, attracts visitors and has become a local landmark. Mohammad Ali Hamidi built the clock tower in 1930. Sari also contains the tombs of the Muslim cleric leaders Yahya and Zayn Al-Abedin, Emamzade-ye Abbas, and Shazdeh Hussein the architecture of which are from the 15th century. [ citation needed ]The economy of Sari is based on food production such as milled rice, dairy products, canned meat and cookies. Sari is a major citrus fruits producer, especially oranges, tangerines and lemons. [ citation needed ] Oil seeds such as soybean and grape being cultivated in vast lands around villages for producing of vegetable ghee and cooking oil. During the 1950s to 1970s, a factory of MM company was the city's largest industrial complex and one of the country's biggest vegetable oil producers. [ citation needed ] After the 1979 revolution , the company was nationalized but got bankrupt and closed later on. [ better source needed ] Other sources of the economy include, but are not limited to, paper, wood, fabrics and construction materials. Mazandaran Wood and Paper Industries, the biggest factory of its kind in the middle east, is situated in a 2000-acre ground on Semnan Road. Mazpaper is presently producing more than 20% of country's paper requirements and is a major economical entity not only for the city but also for the province. [ citation needed ] The MWPI's major subsidiary is the NEKA CHOUB Co., that is manufacturing plywood and chipboard. The city is served by Refah Chain Stores Co. , Iran Hyper Star , Isfahan City Center , Shahrvand Chain Stores Inc. , Ofoq Kourosh chain store .Sari's major districts are: Mirzazamani, Azad Goleh, Bagher Abad, Booali & Posht-e-Hotel (both located in Pasdaran Blvd.), Barbari Mahalleh, Bazaar-e Nargesiyeh, Bazaar-e Rooz, Chenar-Bon, Gol-Afshan, Golma, Kooy-e Azadi, Kooy-e DadGostari, Kooy-e Daneshgah, Kooy-e Djahad, Kooy-e Golha, Kooy-e-Karmandan, Kooy-e Mahyar, Kooy-e MirSarorozeh, Kooy-e Qelich, Lesani, Mehdi-Abad, Na'l-Bandan, No-Tekiyeh, Peyvandi, Pir Tekiyeh, Pol-e Gardan, Posht-e Nim-e Shaban, Posht-e Zendan, Rahband-e Dokhaniyat, Dokhaniyat, Kooy-e Etehad, Rahband-e Sangtarashan, Sang, Sari Kenar, Sarvineh Bagh, Seyyed AlShohada, Shafa, Shahband, Shazdeh Hossein, Shekar Abad, Tabarestan, Tavakkoli, Torki Mahalleh, Torkmen Mahalleh, etc.Sari's old city structure changed in the first Pahlavi era. New avenues and streets in the city center date from that period. In the Qajar dynasty, Sari's neighborhoods included: Afghoun Mahalleh, Bahar Abad, Balouchi Kheyl, Balouchi Mahalleh, Birameter (Bahram-Ottor), Chaleh Bagh, Dar Masdjed, Isfahouni Mahalleh, Kohneh Baq Shah, Kurd Mahalleh, Mir Mashad Mahalleh, Mir Sar Rozeh, Na'l Bandan, Naqareh Khaneh, Ossanlou Mahalleh, Paay-e Chenar, QelichLi Mahalleh, Sabzeh Meydan, Shazdeh Hossein, Shepesh Koshan, Shishehgar Mahalleh.The population density of some neighborhoods in downtown (for example: Mirzazamani, Peyvandi, Sang) is greater than 20,000 per square kilometer. Note that before 1950, the population of the city during the summer was less than in winter. This influenced estimations, such that an estimate done in summer might be inaccurate. 1808 = 21,000 est. 1827 = 19,000 est. 1832 = 20,000 est. 1850 = 15,000 est. 1856 = 9,000 est. 1872 = 15,500 est. 1874 = 16,000 est. 1883 = 16,100 est. 1905 = 25,000 est. 1923 = 35,000 est. 1956 = 26,278 cen. 1966 = 44,547 cen. 1976 = 70,753 cen. 1986 = 141,020 cen. 1996 = 195,882 cen. At the 2006 National Census, its population was 259,084 in 71,522 households. The following census in 2011 counted 296,417 people in 90,798 households. The 2016 census showed a population of 309,820 people in 101,932 households. Most Sari people speak the Mazandarani language Tabari as a mother tongue; however, Persian is the most common language spoken in Iran and the lingua franca . Zoroastrians from Sari who fled to India in the 10th century founded there a city which they named "Navu Sari" (English: "New Sari"), a name which was by now shortened to Navsari ; the town is still a center of the Zoroastrian Parsi community of India.Sari is served by Dasht-e Naz International Airport, which is located in the north-eastern part of the city. List of arrival and departure flights can be found in the Airport's website. The city is connected to Gorgan and Tehran by the Shomal Railway route. That is a major branch of Iran's Railroad . The port of Amir Abad is located on the southern coast of the Caspian Sea . Local highways have been well developed after the Iran–Iraq War. road 22 connects Sari to several cities in the province such as Qaemshahr , Neka and Babol , as well as major cities outside the province such as Gorgan and Mashhad . There are five bus terminals, but one, Terminal-e Dowlat, is the most used. The others serve cities that are located within 150 kilometers from Sari: Gorgan, Nowshahr, Chaloos, and Kiyasar are within this range. * indicates that destination is actually nearer than the figure shown The layout of the city renders occasional use of taxis. There is a wide choice of taxi systems including limousines, wireless radio taxis, airport or rail station taxis, and telephone taxis. City buses are also common because they connect Sari's suburbs to the center of city, providing a low cost and convenient means of transportation to and from the town for people living in those neighborhoods. Although Sari is considered a safe city for pedestrians even at night, nevertheless care should be taken when walking around. [ citation needed ]Sari is served by Dasht-e Naz International Airport, which is located in the north-eastern part of the city. List of arrival and departure flights can be found in the Airport's website. The city is connected to Gorgan and Tehran by the Shomal Railway route. That is a major branch of Iran's Railroad . The port of Amir Abad is located on the southern coast of the Caspian Sea . Local highways have been well developed after the Iran–Iraq War. road 22 connects Sari to several cities in the province such as Qaemshahr , Neka and Babol , as well as major cities outside the province such as Gorgan and Mashhad . There are five bus terminals, but one, Terminal-e Dowlat, is the most used. The others serve cities that are located within 150 kilometers from Sari: Gorgan, Nowshahr, Chaloos, and Kiyasar are within this range. * indicates that destination is actually nearer than the figure shownSari is served by Dasht-e Naz International Airport, which is located in the north-eastern part of the city. List of arrival and departure flights can be found in the Airport's website. The city is connected to Gorgan and Tehran by the Shomal Railway route. That is a major branch of Iran's Railroad .The port of Amir Abad is located on the southern coast of the Caspian Sea .Local highways have been well developed after the Iran–Iraq War. road 22 connects Sari to several cities in the province such as Qaemshahr , Neka and Babol , as well as major cities outside the province such as Gorgan and Mashhad . There are five bus terminals, but one, Terminal-e Dowlat, is the most used. The others serve cities that are located within 150 kilometers from Sari: Gorgan, Nowshahr, Chaloos, and Kiyasar are within this range. * indicates that destination is actually nearer than the figure shownThe layout of the city renders occasional use of taxis. There is a wide choice of taxi systems including limousines, wireless radio taxis, airport or rail station taxis, and telephone taxis. City buses are also common because they connect Sari's suburbs to the center of city, providing a low cost and convenient means of transportation to and from the town for people living in those neighborhoods. Although Sari is considered a safe city for pedestrians even at night, nevertheless care should be taken when walking around. [ citation needed ]Places of interest in the area include: Farah Abad Coast Gohar Baran Coast Dehkadeh Aramesh Tourist Village Tajan River Park Melal park (It is located on the western side of Tajan River. Melal Park has a Biking track and an Artificial Island) Zare' Forest Park Salardareh Forest Park Dasht-E-Naaz National Park Pol-e-Gardan hiking trail Nemashoun Lake Lak-Dasht Lake Soleyman-Tangeh Lake (A dam lake 45km Southwest of Sari) Bam-e-Shahr Hill (Offers a great panoramic view of the city) Qor-Maraz (Natural spa, Neka) Jamaloddin kola (Damaneh kohe shahdezh)In the course of history, Sari was once one of the most cultured cities in the history of Iran. The scientific knowledge of Saravis were noted throughout history and recorded by Pietro Della Valle and other visitors. Today, the universities are as follows: University of Agricultural Science and Natural Resources Mazandaran University of Medical Sciences (MazUMS) University of Natural Science Islamic Azad University of Sari Imam Mohammad Bagher University of Technology Sarian University of Art & Architecture Payam-e-Noor University University of Tech & Engineering (Khalil Moqadam) University of Tarbiyat-e Moallem Sama Technology Faculty of Azad University Rouzbehan University Science and Research Branch Islamic azad university Hadaf UniversityMany sport complexes are in Sari, including: Jahan-Pahlavan Takhti Sports Complex, located on Farhang Street; Hashemi-Nassab Sports Complex, located on the railway side of the autobahn; Montazeri Sports complex, located in Shahband neighborhood. Sari's Mottaqi football stadium is one of the oldest sports field in the country but nowadays it is seldom used in major soccer matches. Sari is the birthplace of several wrestlers and athletes. Notable wrestlers from Sari include Asgari Mohammadian , Majid Torkan and Morad Mohammadi . The town was the host and scene of 2006 Wrestling World Cup Competitions.Sari is the birthplace of several wrestlers and athletes. Notable wrestlers from Sari include Asgari Mohammadian , Majid Torkan and Morad Mohammadi . The town was the host and scene of 2006 Wrestling World Cup Competitions.Although Sari is the most important cultural place in the north of Iran, earthquakes and other causes destroyed most of its cultural heritage and ancient monuments. Still, Sari has been described as Safa City (City of Curvet). Notable are Famous Houses such as Kolbadi House and Amir Divan House (Ramedani House); also the Resket Tower from the House of Karen era and the Farahabad Palace Complex from the Safavid era and historical Sari Central Mosque and tomb tower Imamzadeh Abbas . Khosrow Sinai (born 19 January 1941 in Sari) a renowned film director of the country was the first Iranian film director to win an international prize after the Islamic revolution in Iran . He is also known as an Iranian scholar and has been awarded the prestigious Knight's Cross of the Order of Merit of the Republic of Poland . Seyed Abdolhossein Mokhtabad -Amrei (born 1966 in Sari) is an Iranian composer and singer of Persian Classical music. He received his vocal training under supervision of renowned and legendary maestros and since his professional debut inاارا 1991, has performed numerous concerts in Iran and abroad, including most European Countries, South East Asia and Northern America "Canada & United States" and produced more than 20 sets of music albums. Sari has raised many authors and poets. Mina Assadi is probably the most famous one. She was born and raised in Sari but then moved to Tehran to study journalism and work as a journalist at newspapers like Kayhan . Today Mina Assadi lives in exile in Stockholm , Sweden. Mohsen Emadi (born 29 October 1976 in Sari) is another Persian poet and translator.Seyed Abdolhossein Mokhtabad -Amrei (born 1966 in Sari) is an Iranian composer and singer of Persian Classical music. He received his vocal training under supervision of renowned and legendary maestros and since his professional debut inاارا 1991, has performed numerous concerts in Iran and abroad, including most European Countries, South East Asia and Northern America "Canada & United States" and produced more than 20 sets of music albums.Sari has raised many authors and poets. Mina Assadi is probably the most famous one. She was born and raised in Sari but then moved to Tehran to study journalism and work as a journalist at newspapers like Kayhan . Today Mina Assadi lives in exile in Stockholm , Sweden. Mohsen Emadi (born 29 October 1976 in Sari) is another Persian poet and translator.

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SARI

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Sarı

Sarı ( IPA: [ ˈsaɾɯ ] ) is the Turkish word for "yellow" or "blond". It may refer to:

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SARI

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Canang sari

Canang sari ( Balinese : ᬘᬦᬂᬲᬭᬶ ) is one of the daily offerings made by Balinese Hindus to thank the Sang Hyang Widhi Wasa in praise and prayer. Canang sari will be seen in the Balinese temples ( pura ), on small shrines in houses, and on the ground or as a part of a larger offering. The phrase canang sari is derived from the Balinese words sari (essence) and canang (a small palm-leaf basket as the tray). Canang itself consists of two syllables from the Kawi language : ca (beautiful) and nang (purpose).Canang sari has some parts; there are peporosan , ceper , raka-raka , and sampian urasari . Peporosan or the core material is made from betel leaf , banana leaf , lime , gambier , prestige, tobacco and betel nuts . Material of peporosan symbolizes the Trimurti , the three major Hindu Gods. Shiva is symbolized by lime, Vishnu is symbolized by betel nut, and Brahma is symbolized by gambier. Canang sari are covered by ceper (a tray made from palm leaf) as a symbol of Ardha Candra . Raka-raka is topped with sampian urasari , which are in turn overlaid by flowers placed in a specific direction. Each direction symbolizes a Hindu God ( deva ): A canang sari is completed by placing on top of the canang an amount of kepeng (the coin money ) or paper money , which is said to make up the essence (the "sari") of the offering. Canang sari is offered every day to Sang Hyang Widhi Wasa as a form of thanking for the peace given to the world; it is the simplest daily household offering. The philosophy behind the offering is self-sacrifice in that they take time and effort to prepare. Canang sari is not offered when there is a death in the community or family. Canang sari is also used on certain days, such as: Kliwon , Purnama, and Tilem.

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SARI

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Yusuf Sarı

Yusuf Sarı (born 20 November 1998) is a Turkish professional footballer who plays as a winger for Turkish Süper Lig club Adana Demirspor . Born in France, he plays for the Turkey national team .Sarı made his professional debut for Marseille in a 2–0 Ligue 1 win over Toulouse FC on 24 September 2017. He also made two appearances as right-winger domestic cup. One against SAS Epinal and another against Bourg-en-Bresse, where he obtained a penalty kick at the end of the game. The penalty kick was scored by his teammate Clinton N'Jie . On 29 August 2018, Sarı was loaned to Ligue 2 side Clermont Foot until the end of the season. But he come back to Marseille in January 2019. Sarı did not get enough chances at Marseille and decided to move to Turkish Süper Lig club Trabzonspor . The deal was confirmed on 18 June 2019 where he signed a 3-year contract. On 31 May 2022, Adana Demirspor signed Sarı to a three-year contract. Sarı made his professional debut for Marseille in a 2–0 Ligue 1 win over Toulouse FC on 24 September 2017. He also made two appearances as right-winger domestic cup. One against SAS Epinal and another against Bourg-en-Bresse, where he obtained a penalty kick at the end of the game. The penalty kick was scored by his teammate Clinton N'Jie .On 29 August 2018, Sarı was loaned to Ligue 2 side Clermont Foot until the end of the season. But he come back to Marseille in January 2019. Sarı did not get enough chances at Marseille and decided to move to Turkish Süper Lig club Trabzonspor . The deal was confirmed on 18 June 2019 where he signed a 3-year contract. On 31 May 2022, Adana Demirspor signed Sarı to a three-year contract. Sarı was born in France and is of Turkish descent. He debuted for the Turkey U21s in a 3–0 2019 UEFA European Under-21 Championship qualification loss to the Sweden U21s on 23 March 2018. Sarı was called up to the senior Turkey national team for a UEFA Euro 2024 qualifying match and friendly in September 2023. On 12 September, he made his full international debut in a 4–2 friendly loss to Japan . On 18 November, he scored his first goal for Turkey – the winning goal from a penalty kick in a 3–2 friendly win over Germany in Berlin.

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SARI

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Shantipuri sari

Shantipuri sari ( Bengali : শান্তিপুরী শাড়ি ) is a traditional handwoven cotton sari of West Bengal. It is produced in the Shantipur city and surrounding area of Nadia district, West Bengal . Shantipuri handloom sari (or fabrics) is famous for the novelty of designs, hand spinning method with extra weft, different color patterns and the thin finesse of the fabric. The fine Shantipuri sari is a highly demanded commodity all over the world. Shantipuri Sari got geographical indications tag in 2009. The specialty of Shantipur Sari is that it is marketed in a simple traditional fold form known as Guti Bhanj . Textile weaving started in Shantipur from the first decade of the fifteenth century. Centuries ago, textile weaving was spread around Shantipur. Saris were one of the textiles that were woven here. Later the saris made in Shantipur came to be known as Shantipuri Sari . The word "Shantipuri" is derived from the textile center Shantipur. In the early fifteenth century, Weavers first settled in Shantipur during the reign of Raja Ganesha of Gauḍa in Bengal. The oldest date of Shantipur sari goes back to 1409 AD. According to records, the first saris were woven in Shantipur in 1409 AD during the reign of Gaur king Ganesh Danu Sadhandeb. The weaving tradition of Shantipur is recorded in the biographical manuscript of Sri Advaity Acharya (1460–1558) as Advaitya Mangal . During the reign of Nadia Raj Rudra Roy (1683–94) and during the Mughal rule handloom weaving of Shantipur emerged as a traditional industry. During the reign of Raja Rudra Raya (1683–94) of Nadia, the work of the weavers gained great acclaim and fame. At that time sarees were exported to Arabia , Greece , Turkey , Iran and Afghanistan . Thereafter, the industry came under the control of the East India Company until the Governor General came into existence. The products were mainly sari and dhoti , but specialty of Shantipur was in sari making. The weavers and sari of Shantipur were so famous that they actually found a place in Bengali folk literature . The famous poet, lyricist and writer of the pre-independence age Dwijendralal Roy has also immortalized the beauty of Shantipuri Tant Sari ( Bengali : শান্তিপুরের তাঁতের শাড়ি ) in his poem. ওই পরনে তার ডুরে শাড়ি মিহী শান্তিপুরে ওই শান্তিপুরে ডুরে রে ভাই শান্তিপুরের ডুরে। There she wears the fine Dure of Shantipur, The Striking Semblance of Dure of Shantipur, Look Brother – That's the Dure of Shantipur. In the early stages, the handloom fabrics produced in Shantipur consisted of handspun cotton yarn and was woven on throw-shuttle pit loom, the use of millspun yarn beginning in late 1824 AD. The barrel dobby was introduced by Darga Das Kastha during 1920–1925 AD and the throw shuttles were converted into fly shuttles. Devendranath Mukhopadhyay introduced the Jacquard machine, which widened the scope of designing from simple to complex and varied. Biren Kumar Basak , a weaver of Shantipur, received the Padma Shri in 2021 for his work. The process of weaving such a fine wonder saree starts from a very basic level of yarn cutting. The artisans take extreme care from the beginning to the end of the production process, as producing high quality sarees requires extra care. Materials used in Shantipuri saris are mainly cotton and silk . Cotton is first made into yarn by a spinning wheel. It is the main raw material of the sari. The best quality yarn is taken, and is first steamrolled and ironed before being dyed in different colours. Then it is gradually expanded using a large wheel. Only after the weaver is fully satisfied about the quality of yarn does he proceed to use it on his loom by rolling it up in a multitude of bobbins. The bobbins are fitted in the loom in a sequential alternating pattern to achieve the variety of color patterns that is desired, but not the pattern of the anchal . The specialty of Shantipuri sari is that it uses 120-180 threads per inch and hence the textiles have a unique feel. The weaver begins his work after arranged the yarn in the loom; he uses a standard jacquard loom. The earliest looms used in Shantipur for saree weaving were vertical warp-weighted looms, but today most looms are foot treadle floor looms. The process of weaving such a fine wonder saree starts from a very basic level of yarn cutting. The artisans take extreme care from the beginning to the end of the production process, as producing high quality sarees requires extra care. Materials used in Shantipuri saris are mainly cotton and silk . Cotton is first made into yarn by a spinning wheel. It is the main raw material of the sari. The best quality yarn is taken, and is first steamrolled and ironed before being dyed in different colours. Then it is gradually expanded using a large wheel. Only after the weaver is fully satisfied about the quality of yarn does he proceed to use it on his loom by rolling it up in a multitude of bobbins. The bobbins are fitted in the loom in a sequential alternating pattern to achieve the variety of color patterns that is desired, but not the pattern of the anchal . The specialty of Shantipuri sari is that it uses 120-180 threads per inch and hence the textiles have a unique feel. The weaver begins his work after arranged the yarn in the loom; he uses a standard jacquard loom. The earliest looms used in Shantipur for saree weaving were vertical warp-weighted looms, but today most looms are foot treadle floor looms. Shantipur saree has several Specialties, which make it unique from all other saris. The unique quality of doubling the number of threads through the reed (sana) – resulting in a unique tube mark on the saree. The thread count can be increased anywhere from 2-9 threads, with a higher thread count indicating a softer and shinier finish. Shantipuri saris maintain the standard of 100x100 thread; this thread quality is rare in saris from anywhere else. Shantipur's weavers discourage the removal of reed marks from their products during the process of giving the finishing touches to their products; this is the essential difference between Shantipuri and Phulia saris and creates a separate niche in the market for Shantipuri loom saris. Apart from the three weaving Specialties mentioned above, there are several other design features. Namely - (a) the anchal (fall edge of the saree) of the sari is decorated with ribbons of varying thickness. These stripes, called Sajanshoi , have colors that complement the colors used in the borders. Some saris even include silver colored star patterns embroidered on the border, giving it a night sky look. (b) In fact this is why these saris have a very smooth texture and give the wearer a touch of sophistication, designs like the so-called 'diamond' section are still popular among rich and prestigious customers. (c) The weavers of Shantipur still work without any electrical tools and their secret lies in the manner they spread out the threads after making the textile, which gives it a characteristic identity. Shantipuri saris have multiple variations, and according to these variations the saris have different names. Depending on the design, color, pattern Shantipuri saris are named Nilambari , Ganga-jmuna , Benkipar , Bhomra , Rajmahal , Chandmalla , Anshpar , Brindavani Mour Par , Dorookha .

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Handloom sari

Handloom saris are a traditional textile art of Bangladesh and India . The production of handloom saris is important for economic development in rural India. Completion of a single sari takes two to three days of work. Several regions have their own traditional styles of weaving handloom saris. [ citation needed ]A handloom sari is often woven on a shuttle-pit loom made from ropes, wooden beams and poles. The shuttle is thrown from side-to-side by the weaver. Other weavers use a fly-shuttle loom which can produce different types of patterns. The saris can vary in size and quality. Handloom sari weaving is generally a family business and is one of India's cottage industries . The handloom saris are made from silk or cotton threads. The handloom weaving process requires several stages in order to produce the final product. Traditionally the processes of dyeing (during the yarn, fabric, or garment stage), warping , sizing, attaching the warp, weft winding and weaving were done by weavers and local specialists around weaving villages. However, currently most of the activities are outsourced. [ citation needed ]Weaving takes place in many regions of India. Each region follows traditions for the motifs , designs and colours. Handloom weaving takes place in villages supporting lakhs (hundred thousands) of families for their livelihoods .Tant sari is a traditional sari of Bangladesh . "Tant" means "Handloom" in Bengali language . Handloom industry of Tangail is famous for its Tangail saris which are also a type of Tant sari . Some of the well-known Indian handloom saris are Kanchipuram silk saris , Maheshwari saris, Bagh print saris, Chanderi silk saris , Tussar silk saris , Banarasi silk saris , Baluchuri saris, Sambalpuri saris , Kantha stitch saris , Bandhani saris and Munga saris. Some handloom saris are made out of high-quality silk fabric, which is valued for its lustre. Tant saris are one of the earliest sari weaving techniques. It is the most common cloth used by Bengali women . Bengal Tant handlooms especially thrived during the Mughal period in Dhaka and Sonargaon , where it received immense support from the royalty with muslin and jamdani which are now a Intangible cultural heritage as well as Gi products of Bangladesh . Tangail weaving stands as one of Bangladesh 's oldest cottage industries, with Tangail weave sarees gaining global appreciation.The immensely popular Handloom sarees from, Tangail, Bangladesh are known for their finer count and intricate designs, with extra warp designs using coloured yarn. The designs on Baluchari saris feature mythology stories that can be seen in the temples of Bishnupur & Bankura of West Bengal . The pallus and borders showcase elaborate designs of flowers, animals and royal court scenes. Some feature scenes from the Ramayana and Mahabharata . The most popular colours of Baluchari saris are green, red, white and yellow. A master weaver usually takes 20–25 days to complete weaving of a Baluchari sari. The quality of zari used in weaving Kanchipuram saris in Tamil Nadu is viewed as high quality and attracts foreign visitors. The zaris used are generally gold and silver . Tussar sari are soft to touch and are woven in areas of Chhattisgarh , Jharkhand and Bhagalpur . The bright colour combinations and the breathable nature of the fabric make it unique. Banarasi saris have been a valuable possession for brides . Woven by craftsmen of Uttar Pradesh , they feature intricately woven designs with golden and silver threads. These saris are usually heavy and are traditionally worn in festivals as well as at weddings.Tant saris are one of the earliest sari weaving techniques. It is the most common cloth used by Bengali women . Bengal Tant handlooms especially thrived during the Mughal period in Dhaka and Sonargaon , where it received immense support from the royalty with muslin and jamdani which are now a Intangible cultural heritage as well as Gi products of Bangladesh . Tangail weaving stands as one of Bangladesh 's oldest cottage industries, with Tangail weave sarees gaining global appreciation.The immensely popular Handloom sarees from, Tangail, Bangladesh are known for their finer count and intricate designs, with extra warp designs using coloured yarn. The designs on Baluchari saris feature mythology stories that can be seen in the temples of Bishnupur & Bankura of West Bengal . The pallus and borders showcase elaborate designs of flowers, animals and royal court scenes. Some feature scenes from the Ramayana and Mahabharata . The most popular colours of Baluchari saris are green, red, white and yellow. A master weaver usually takes 20–25 days to complete weaving of a Baluchari sari.The quality of zari used in weaving Kanchipuram saris in Tamil Nadu is viewed as high quality and attracts foreign visitors. The zaris used are generally gold and silver .Tussar sari are soft to touch and are woven in areas of Chhattisgarh , Jharkhand and Bhagalpur . The bright colour combinations and the breathable nature of the fabric make it unique.Banarasi saris have been a valuable possession for brides . Woven by craftsmen of Uttar Pradesh , they feature intricately woven designs with golden and silver threads. These saris are usually heavy and are traditionally worn in festivals as well as at weddings.The handloom sector plays a vital role in India's economy. It is responsible for nearly 22% of the cloth produced in the country. The handloom sector is the second largest economic activity after agriculture, employing nearly 30 lakh (three hundred thousand) weavers and 4.33 million people in all, according to the Handloom Census of 2009–2010. In the 2010 census, 4.4 million families were engaged in hand weaving. In December 2011, the handloom industry wove 6.9 billion square metres (74.3 billion square feet) of cloth. The economic policy in India aims to advance the handloom industry from the pre-independence period. The Textile Policy 1985 emphasized the promotion of handloom garments. Andhra Pradesh is said to be the home of 359,212 weaver families who work in primary cooperative handloom societies. Primary Handloom Weavers Cooperatives (PWCS) includes weavers within certain specific geographical limits and provides production work to the members. The cooperatives also ensure that the weavers receive fair wages and conduct various welfare measures.

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Sari cancer

Sari cancer is a very rare type of skin cancer that occurs along the waistline in females wearing the sari , caused by constant irritation which can result in scaling and changes in pigmentation of the skin. It is a rare type of cancer and have been found in the Indian subcontinent , where saris are commonly worn by girls and women throughout their lives. Although, it has more to do with hygiene and not taking care of one's skin. It involves chronic inflammation .The foremost symptoms of sari cancer are the constant irritation with scaling and pigmentation change at the waistline; gradually, over the course of many years, these become chronic. The person may have non-healing ulcer or a hyper- or hypopigmented patch or a growth-like lesion over the waistline. The lesion may be associated with serous discharge with foul smell. [ citation needed ]The sari is common female attire in the Indian subcontinent. It is a piece of long (generally 5.5 metres or 18 feet ) cloth which can be made of various materials: cotton , silk , nylon , chiffon or synthetic fabric . It is worn over an inner skirt (petticoat) which is tightened around the waist by a thick cotton cord. This is the traditional costume of most Indian women. The sari is attached to the waist throughout the day in the hot and humid climate. The waist is often soiled with dust and sweat and remains without proper cleaning. This causes changes in pigmentation and mild scaling over the waist. This, in turn, causes chronic irritation and gradually malignancy may develop in the skin at the waistline. Excision biopsy is required to confirm the diagnosis of sari cancer. In many cases local excision with skin grafting is considered the appropriate treatment. Different ways of wearing the petticoat may help sari-wearers to prevent sari cancer. Some such strategies are: Loosening the petticoat Changing the usual rope-like belt to broader ones that reduce pressure on the area Continuously changing the level at which the petticoat is tied In 1945 physicians Khanolkar and Suryabai described a new type of skin cancer with hypopigmented and thickened scars which were more likely to progress into malignant lesions. They termed it "dhoti cancer", the dhoti being a traditional male costume of India which like the sari is wrapped around the waist. The term "sari cancer" was first used by a group of doctors led by Dr. A. S. Patil from Bombay Hospital, India, in the Bombay Hospital Journal . The dermatological problem in the waist of Indian women wearing saris had been recognised before by some other researchers. This type of cancer is related to Marjolin's ulcer , the malignant degeneration of a chronic wound which was described by Jean-Nicolas Marjolin in 1828. [ citation needed ]

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Baluchari sari

Baluchari Sari ( Bengali : বালুচরী শাড়ি) is a type of sari , a garment worn by women in the Indian states of West Bengal , Tripura and Assam and the country of Bangladesh . This particular type of sari originated in West Bengal and is known for depictions of mythological scenes on the anchal of the sari. It used to be produced in Murshidabad but presently Bishnupur and its surrounding areas of West Bengal are the only place where authentic Baluchari saris are produced. It takes approximately one week to produce one such sari. In 2011, the Baluchari Sari was granted the status of Geographical Indication for West Bengal in India. In the history of textiles in Bengal, Baluchari came much after muslin. Two hundred years ago Baluchari was practiced in a small village called Baluchar in Murshidabad district, from where it got its name. In the eighteenth century, Murshidkuli Khan, Nawab of Bengal patronized its rich weaving tradition and brought the craft of making this sari from Dhaka to the Baluchar village in Murshidabad and encouraged the industry to flourish. After a flood of the Ganga river and the subsequent submerging of the village, the industry moved to Bishnupur village in Bankura district. Baluchari Sari made of tassar silk and a thousand years old when the Jagat Malla king rule in Mallabhum . This flourishing trend later declined, especially during British rule, due to political and financial reasons. It became a dying craft as most of the weavers were compelled to give up the profession. In the first half of twentieth century, Subho Thakur, a famous artist, felt the need to recultivate the rich tradition of Baluchari craft. Though Bishnupur was always famous for its silk, he invited Akshay Kumar Das, a master weaver of Bishnupur, to his center to learn the technique of jacquard weaving. Sri Das then went back to Bishnupur and worked hard to weave Baluchari on their looms with the financial and moral support of Sri Hanuman Das Sarda of Silk Khadi Seva Mandal. According to Maniklal Sinha , Baluchari saree in the post independent year, government of India tried to recover. In obedience to the government of its then Sri Shyamadas babu this extinct Baluchari Tat-Veteran renowned artist 'Akshay Kumar Das (Potranga) and his subtle artwork discovered its weaving process by feeling. In this regard, he is completely helped by Nikhil Bharat Khadi and Village Development Commission certified by Bishupur . Silk Khadi Seva Mandal Local Director Hanuman Das Sarada. Thus 'Akshay Babur a renaissance of the Baluchari saree has been heralded through sheer hard work and a touch of innovative ingenuity. Once Bishnupur was the capital of Malla dynasty and different kinds of crafts flourished during their period under the patronage of Malla kings. Temples made of terracotta bricks were one achievement of these rulers. A major influence of these temples can be seen in Baluchari sarees. Mythological stories taken from the walls of temples and woven on Baluchari sarees is a common feature in Bishnupur. The production process of Baluchari can be divided into several parts: Cultivation of cocoons: Since the discovery so many years ago that the fibre or filament composing the cocoon of the silkworm can be constructed into a beautiful and durable fabric, silkworms have been bred for the sole purpose of producing raw silk. Processing of yarns: To make the yarn soft, it is boiled in a solution of soda and soap and then dyed in acid colour, according to the requirement of the sari. The yarn is stretched from both the sides in opposite directions putting some force with both palms. This process is needed to make the yarn crisper. Motif making: Making of the motifs for 'pallavs' and other part of Baluchari is in itself an intricate process. The design is drawn on a graph paper, it is coloured and punching is done using cards. After punching, these cards are sewed in order and fixed in the jacquard machine. Weaving: After the jacquard loom has been introduced, the weaving of a Baluchari sari takes five to six days. Two weavers work on a shifting basis. Baluchari thus prepared becomes a sign of aristocracy, the attire of status. Maintenance of quality of Baluchari sari is taken care of precisely. The quality is checked from the stage of dying of the yarn to the packaging of the sari. Baluchari saris, or locally called Baluchari saris, today often have depictions from scenes of Mahabharat and Ramayana. During the Mughal and British eras, they had a square design in the pallu with paisley motifs in them, and depicted scenes from the lives of the Nawab of Bengal featuring women smoking hookahs, nawabs driving horse carriages, and even European officers of the East India Company. It would take two craftsmen working for almost a week to produce one sari. The main material used is silk and the sari is polished after weaving. Baluchari saris illustrate Hindu mythological scenes, nature , folklore , legends, historical events, and abstract designs . They showcase gods, heroes, nature elements, love stories, battles , and contemporary patterns. While there isn't a lot of variation in the method of weaving used today, balucharis can be broadly categorized based on the threads used in weaving the patterns: Baluchari (resham): The simplest balucharis have resham threads in a single colour to weave the entire pattern Baluchari (meenakari): These balucharis have threads in two or more colours with attractive meenakari work that further brightens the patterns Swarnachari (baluchari in gold): They are the most gorgeous balucharis, woven with gold (swarna) or silver coloured threads (often with meenakari work in another colour), which is called Zari. That illuminate the patterns to a much larger extent.These saris were mostly worn by women from upper class and Zamindar households in Bengal during festive occasions and weddings.With the changing times, the Baluchari sari has had a makeover and a touch of eco-friendliness in terms of the used yarns and colours. Cotton Kapas is spun with fibres of banana plants and bamboo shoots and the dyes are extracts of fruits, flowers, leaves, and vegetables such as pomegranate, jamun, neem fruits and leaves, basil leaves, turmeric, marigold flowers, mangoes and others. The organic baluchari cotton sarees were displayed in the sari fair organised by Rang Mahal, a forum of weavers from Nadia district in West Bengal. However, with the GI certification of Baluchari sarees with reference to Bankura district of West Bengal in India, it is now not permitted to use the term Baluchari for any other similar product based on cotton or any other material. The Baluchari sari was one of the award winners for the main weaving styles amongst 34 National Awards for the years 2009 and 2010 presented by the Hon. President Pranab Mukherjee . The Baluchari sari of Bankura was showcased at the India International Trade Fair organised at New Delhi . The pavilion of West Bengal prominently displayed those products of handicrafts and handloom sector which were recognised for their unique nature keeping the theme "Skilling India" in view.

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Banarasi sari

A Banarasi sari is a sari made in Varanasi , an ancient city which is also called Benares (Banaras). The saris are among the finest saris in India and are known for their gold and silver brocade or zari , fine silk and opulent embroidery. The saris are made of finely woven silk and are decorated with intricate designs, and, because of these engravings, are relatively heavy. Their special characteristics include intricate intertwining floral and foliate motifs, kalga and bel , a string of upright leaves called jhallar at the outer, edge of border is a characteristic of these saris. Other features are gold work, compact weaving, figures with small details, metallic visual effects, pallus, jal (a net like pattern), and mina work. The saris are often part of an Indian bride's trousseau . Depending on the intricacy of its designs and patterns, a sari can take from 15 days to a month and sometimes up to six months to complete. Banarasi saris are mostly worn by Indian women on important occasions such as when attending a wedding and are expected to be complemented by the woman's best jewellery.Ralph Fitch (1583–1591) describes Banaras as a thriving sector of the cotton textile industry. The earliest mention of the brocade and Zari textiles of Banaras is found in the 19th century. With the migration of silk weavers from Gujarat during the famine of 1603, it is likely that silk brocade weaving started in Banaras in the seventeenth century and developed in excellence during the 18th and 19th century. During the Mughal period , around the 14th century, weaving of brocades with intricate designs using gold and silver threads became the specialty of Banaras. The traditional Banarasi sari is done with cottage industry for about 1.2 million people associated directly or indirectly with the handloom silk industry of the region around Varanasi encompassing Gorakhpur , Chandauli , Bhadohi , Jaunpur and Azamgarh districts . In the last few years, a variety of independent, Varanasi-based brands have emerged to revive the Banarasi sari and bring them directly to mainstream consumers, including Ekaya, Tilfi Banaras, HKV Benaras among others. Over the years, the Banarasi silk handloom industry has been incurring huge losses because of competition from mechanised units producing the Varanasi silk saris at a faster rate and at cheaper cost, another source of competition has been saris made of cheaper synthetic alternatives to silk. In 2009, after two years of wait, weaver associations in Uttar Pradesh, secured Geographical Indication (GI) rights for the 'Banaras Brocades and saris'. GI is an intellectual property right, which identifies a good as originating in a certain region where a given quality, reputation or other characteristic of the product is essentially attributable to its geographical origin. As per the GI certificate, Banarasi products fall under four classes (23–26), namely silk brocades, textile goods, silk sari, dress material and silk embroidery. Most importantly this means that no sari or brocade made outside the six identified districts of Uttar Pradesh , that is, Varanasi , Mirzapur , Chandauli , Bhadohi , Jaunpur and Azamgarh districts , can be legally sold under the name of Banaras sari and brocade. Prior to this, in July 2007, nine organizations, Banaras Bunkar Samiti, Human Welfare Association (HWA), joint director industries (eastern zone), director of handlooms and textiles Uttar Pradesh Handloom Fabrics Marketing Cooperative Federation, Eastern UP Exporters Association (EUPEA), Banarasi Vastra Udyog Sangh, Banaras Hath Kargha Vikas Samiti and Adarsh Silk Bunkar Sahkari Samiti,had applied to the Chennai-based Geographical Indication Registry of the Government of India , in a move that was supported by United Nations Conference on Trade and Development (UNCTAD). There are four main varieties of Banarasi sari, which includes pure silk (Katan), Organza (Kora) with Zari and silk ; Georgette , and Shattir, and according to design process, they are divided into categories like, Jangla, Tanchoi, Vaskat, Cutwork , Tissue and ButidarSince a large number of silk dyeing units in the trade use chemical dyes, which cause pollution in the Ganges River , a move is on to shift to natural dyes . A research team from the Indian Institute of Technology, Banaras Hindu University (IIT-BHU) used the technique of solvent extraction and enzymatic extraction to develop natural colours from plants, flowers and fruits including accaccia , butea ( palash ), madder, marigold and pomegranate (anar) The increasingly errant and erratic electric power supply, which leads to the electric powered looms sitting idle for greater parts of the day, has made it difficult for the weavers to complete the saris in short time; consequently their earnings are affected. Also, increasing quantities of look-alike Banarasi saris are flooding the market. These saris are mass-produced in China on massive looms and therefore retail at very low prices.The increasingly errant and erratic electric power supply, which leads to the electric powered looms sitting idle for greater parts of the day, has made it difficult for the weavers to complete the saris in short time; consequently their earnings are affected. Also, increasing quantities of look-alike Banarasi saris are flooding the market. These saris are mass-produced in China on massive looms and therefore retail at very low prices.

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Sarı Saltık

Part of a series on Nizari - Ismāʿīli Batiniyya , Hurufiyya , Kaysanites and Twelver Shī'ism Sarı Saltık (also spelled Sarı Saltuk , "the blonde", Ottoman Turkish : صارى صالتق , romanized : Ṣarı̊ Ṣaltı̊q ; also referred as Sari Saltuk Baba or Dede ) (died 1297/98) was a 13th-century Alevi Turkish dervish , venerated as a saint by the Bektashi Sufi Muslims in the Balkans and parts of Middle East as well as the mainstream Sunni Muslim community.According to 14th-century Moroccan traveller Ibn Battuta , Saltik was an "ecstatic devotee", although "things are told of him that are reproved by the Divine Law ". He is considered by various sources a disciple of Mahmud Hayran, of Haji Bektash Veli , or of one of the successors of Ahmed ar-Rifa'i . According to the 17th-century traveller Evliya Çelebi , his real name was Mehmed, and he was from Bukhara . Early 20th-century historian Frederick Hasluck considered him a saint of a Tatar tribe from Crimea , which had brought his cult into Dobruja , from where it was spread by the Bektashis. According to the 15th-century Oghuzname narrative, in 1261 he accompanied a group of Anatolia Turkomans into Dobruja , where they were settled by the Byzantine Emperor Michael VIII to protect the northern frontier of the empire. However, Dobruja was occupied by Tatars in the same period. The same source places him in Crimea after 1265, along the Turkomans transferred there by Tatar khan Berke , and after 1280 mentions him leading the nomads back to Dobruja. After the death of Sari Saltik, some of the Turkomans returned to Anatolia, while other remained and became Christians, becoming the ancestors of the Gagauz people . This migration has characteristics of a folk epic destan , and its historicity is doubted by some scholars. The town of Babadag (Turkish, Babadağ, Mountain of the Baba ), in the Romanian Dobruja , identified with the town of Baba Saltuq visited in 1331/1332 by Ibn Battuta, is said to be named after him. The oldest sources about Sari Saltik available place his tomb in the area of the future town. This tomb was visited in 1484/1485 by Ottoman Sultan Bayezid II during a military campaign, and, after reporting an important victory, he ordered the building of a religious and educational complex here (including a mausoleum to Saltik, finished in 1488), around which the town developed. According to Evliya Çelebi, a marble sarcophagus was found during the construction, with a Tatar inscription attesting it was the tomb of the saint. However this miraculous discovery is not mentioned in other sources talking about the sultan's passage through the town. Babadag became an important place of pilgrimage, visited in 1538 by Suleiman the Magnificent , and the most important urban centre in 16th-century Dobruja. The town however decayed during the frequent wars that ravaged the region during the 17th century, and was eventually burned down, along with the mausoleum to Saltik, during the Russo-Turkish Wars . A simple domed türbe was rebuilt over the grave of the saint in 1828. The mausoleum in Babadag remains of relative importance even nowadays, and was recently renovated, being reinaugurated in 2007 by the then- Turkish prime-minister Recep Tayyip Erdoğan . The town of Babadag (Turkish, Babadağ, Mountain of the Baba ), in the Romanian Dobruja , identified with the town of Baba Saltuq visited in 1331/1332 by Ibn Battuta, is said to be named after him. The oldest sources about Sari Saltik available place his tomb in the area of the future town. This tomb was visited in 1484/1485 by Ottoman Sultan Bayezid II during a military campaign, and, after reporting an important victory, he ordered the building of a religious and educational complex here (including a mausoleum to Saltik, finished in 1488), around which the town developed. According to Evliya Çelebi, a marble sarcophagus was found during the construction, with a Tatar inscription attesting it was the tomb of the saint. However this miraculous discovery is not mentioned in other sources talking about the sultan's passage through the town. Babadag became an important place of pilgrimage, visited in 1538 by Suleiman the Magnificent , and the most important urban centre in 16th-century Dobruja. The town however decayed during the frequent wars that ravaged the region during the 17th century, and was eventually burned down, along with the mausoleum to Saltik, during the Russo-Turkish Wars . A simple domed türbe was rebuilt over the grave of the saint in 1828. The mausoleum in Babadag remains of relative importance even nowadays, and was recently renovated, being reinaugurated in 2007 by the then- Turkish prime-minister Recep Tayyip Erdoğan . In various Orthodox Christian legends, he is identified with saints such as Saint George , Elijah , Saint Nicholas , Saint Simeon , Saint Naum or Saint Spyridon . According to a local legend, his body was buried in seven coffins, in remote towns and villages within the lands of the Infidels . Nowadays, alleged tombs ( türbe ) of his, are found all over the Balkans ( Blagaj, Mostar , Krujë , Kaliakra ) and western Anatolia ( İznik ).

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SARI

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Sari Lennick

Sari (Wagner) Lennick (born August 4, 1975) is an American actress. She is known for her film roles as Judith Gopnik in the Coen Brothers' movie A Serious Man (2010 Best Picture Oscar nominee and Robert Altman Independent Spirit Award winner) and Evelyn in Woody Allen 's Café Society , which opened the 2016 Cannes Film Festival and was theatrically released in the U.S. on July 15, 2016. Sari Lennick was born and raised in Miami, Florida . She graduated from the University of Southern California with a bachelor's degree majoring in theatre and philosophy . Following USC, she moved to New York City and earned a Master of Fine Arts in Acting from the Actors Studio Drama School at New School University. She currently resides in Los Angeles and is married to financial services executive Alan T. Lennick. They have a son, Dylan, born in August 2007.

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SARI

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Sari (film)

5 May 2023 ( 2023-05-05 ) Sari is a 2023 Indian Marathi -language romantic drama film written and directed by K. S. Ashoka , and produced by Suresh Nagpal and Akash Nagpal. The movie is an official remake of the movie Dia . The film stars Ajinkya Raut, Ritika Shrotri and Pruthvi Ambaar with a music score by B. Ajaneesh Loknath Amitraj and Arijit Chakraborty. Ajinkya Raut as Rohit Ritika Shrotri as Dia Pruthvi Ambaar as Adi Mrinal Kulkarni as Dr. Lakshmi "Lucky", Adi's mother Sanjay Khapre as Dia's father Pankaj Vishnu as Dia's father's friend Jyothi Rai as Rohit's sister Chandan Ravandur N as Auto Driver Gokul Chakravarthy as a passenger on a train Vishal Asha as Auto Driver Anand N Kumar as Rohit's friendThe music is composed by B. Ajaneesh Loknath (in his debut in Marathi cinema ), Amitraj and Arijit Chakraborty. The film was theatrically released on 5 May 2023 India and released in UK and Ireland on 19 May 2023. The film was made available to stream on OTT platform Amazon Prime . The film was theatrically released on 5 May 2023 India and released in UK and Ireland on 19 May 2023. The film was made available to stream on OTT platform Amazon Prime . A reviewer from The Times of India gave 2.0/5 stars and stated that there are many loopholes in the plot and many times the film seems overdramatic. Pratibha Joy of OTTPlay gave the same rating and gave praise to the original film stating: the Kannada original was far more appealing and tugged at one's heartstrings. A reviewer from Maharashtra Times wrote 'Anything can happen in life', definitely comes from watching this movie.

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SARI

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Sari Gelin

Sari Gelin ( Azerbaijani : Sarı Gəlin , سارؽ گلین ; Persian : دا٠ن کشان , romanized : Dâman Kešân ) or Sari Aghjik ( Armenian : Սարի Õ¡Õ²Õ»Õ«Õ¯ , romanized : Sāri Āγčīk ) is the name for a number of folk songs popular among the people of Iran , the southern Caucasus (most prominently present-day Azerbaijan and Armenia ) and in eastern Anatolia in present-day Turkey . All versions of the song use the same melody and are written in the Bayati makam or mode , but are sung with different lyrics. The consensus about its country of origin is contested. Sari Gelin is either a blond bride or a girl from the mountains, depending on the respective lyric language. What the versions have in common, is a boy complaining to/about a girl he loves but cannot achieve. In Armenian , the song is known as Sari Aghjik , where the word sari ( սարի ) means "of the mountain", and the word "aghjik", with an equal syllable number, means "girl". Together they mean "girl/bride from the mountains". In Azerbaijani and Turkish the song is known as Sari Gelin, sarı as a Turkic adjective means "yellow". The word gelin or gəlin means someone who comes to the family (i.e. a bride). Thus Sarı Gelin can mean "golden/blond/fair-skinned bride." All versions of Sari Gelin-Sari Aghjik use the same melody and are written in the literary genre known as Bayati , which is one of the most popular forms of poetry in most of the Middle East. Bayati poetry is known for its reflective and introspective prose. Generally, Bayati poetry consists of lines of seven syllables written in a simple rhythm. However, There are many different lyrical interpretations of Sari Gelin among Armenians , Azerbaijanis , Georgians , Persians , and Turks . The song is a subject of contention and accusations of plagiarism among the countries where it is popular. At the moment, there is no consensus about its country of origin. The Sari Aghjik (Mountain Girl) version uses the same melody with the Armenian word for the girl ( aghjik Õ¡Õ²Õ»Õ«Õ¯ ) as in the song Vard Siretsi ("I loved a rose"). Both Armenian versions, are about the boy complaining that the unkind girl has rejected him. In Armenian Sari Aghjik , the girl has chosen someone else over him. The lyrics translate to: Գնաց, ուրիշին Õ¡Õ¼Õ¡Õ¾ ... Ա՜խ, մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ, Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Գնաց, ուրիշին Õ¡Õ¼Õ¡Õ¾, Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. She left and chose someone else, Akh! let your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. She left and chose someone else My heart yaman! Leyli dear beloved (Persian-Armenian) Թույն Õ´Õ« Õ¡Õ®Õ¡ Õ©Õ¥Õª վերքիս ... Ա՜խ մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ ... Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Թույն Õ´Õ« Õ¡Õ®Õ¡ Õ©Õ¥Õª վերքիս ... Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. Don't pour poison into (salt on) my wound. Akh! let your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. Don't pour poison into my wound My heart yaman! Leyli dear beloved. Տիրել Õ¥Õ½ խելք ու մտքիս ... Ա՜խ մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ ... Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Տիրել Õ¥Õ½ խելք ու մտքիս ... Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. You have possessed my thoughts and my mind. Akh, may your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. You have possessed my thoughts and my mind. My heart yaman! Leyli dear beloved The phrase "Don't pour poison into (salt on) my wound" is an idiom that means "don't make my troubles worse". In Azerbaijan, Sarı Gəlin (Blond Maiden) is a legend that symbolizes the love between a Muslim Azerbaijani and a Christian Armenian girl who are kept apart. Saçın ucun hörməzlər, gülü sulu dərməzlər, Sarı Gəlin. You don't braid the end of your hair, you don't pick a dewy flower. yellow (blond, fair) bride bu sevda nə sevdadır, səni mənə verməzlər; neynim aman, aman, (×2) Sarı Gəlin. What a love is this love! they will not give you to me. what can I do? aman! (secure me! / help! / please!) aman! (×2) yellow bride bu dərənin uzunu, çoban qaytar quzunu, Sarı Gəlin. The tallest of this valley, shepherd, return the lamb, yellow bride. nə ola bir gün görəm, nazlı yarın üzünü; neynim aman, aman, (×2) Sarı Gəlin. I wish that one day I could see the face of my playful love what can I do? aman! aman! (×2) yellow bride. Gün ola mən bir görəydim Nazlı yarımın üzünü Neynim aman, aman (×2) Sarı gəlin Could there be a day I would see (correct translation?) the face of my playful love what can I do? aman! aman! (×2) yellow bride. The Azerbaijani version of the song was processed [ clarification needed ] and pitched by Azerbaijani composer Asaf Zeynally (1909–1932). The text of the song in the Azerbaijani language was published in 1982 in Baku under the edition of Hamid Arasly . In 2001 the Azerbaijani text of the song was published by Rafik Babayev . DayIrMan sings a longer Azerbaijani version, which translates to: Don't pluck the flower while it's young, yellow bride. Don't braid the end of your hair, Don't pluck the flower while it's young, yellow bride. You were born for love with me; / We were born to love each other; You are the only one; on earth, in life, in the sky. You are my sunshine, my fire. I fell in love with you on a moonlit night The sun, a man and yellow bride; The only star, land and your breath, I love life, life is you. My eyes that see you are full of eagerness, You came into my dream like a ray, yellow bride. What kind of love is this? They won't let me marry you. What should I do, what should I do, yellow bride? What kind of love is this? They won't give you to me. It's me, looking for you among the stars. Answer me, don't break my heart! I will breathe with your warm breath, I will remember you all my life, Enough! dry your tears, don't cry! Don't keep the fire in your heart too long, Your destined happiness is written on your forehead. Pure love within one night. But this is only a dream and you are in my dream, You are my yellow bride among my wishes. What kind of love is this? They won't let us marry. What should I do, what should I do, yellow bride? What kind of love is this? They won't give you to me. It's us, only us and the sky, You came to me in this utter night. The light woke me up, And we got separated among the stars. Oh, God, hear my crying, I felt this sharp pain in my heart, Love is a game and I was winning, I couldn't imagine such an end. But you wanted death, You achieved your goal in the end, yellow bride. What kind of love is this? They won't let me marry you. What should I do, what should I do, yellow bride? You are my yellow bride, You are my yellow bride. Along this valley, Give the lamb back to me, shepherd ... You are my yellow bride ... İçinde bir kız gezer, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. A girl is walking around, oh, may your grandma die! my yellow bride, aman! (×3) my tall beautiful dear. Dertlere derman yazar, / Katlime ferman yazar , ay! nenen ölsün, Sarı gelin aman! (×3) suna yarim. She writes the prescription for my pains, / She writes the sentence to my assassination , oh, may your grandma die! my yellow bride aman, (×3) my tall beautiful dear. Kanadında gümüş var, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. It (She) has silver in its wings, oh, may your grandma die! my yellow bride, aman! (×3) my tall beautiful dear. Altı mor sümbüllü bağ ay nenen ölsün sarı gelin aman! (×3) suna yarim. Underneath has garden with purple hyacinth, oh, may your grandma die! my yellow bride aman! (×3) my tall beautiful dear. Niceki bu halimse, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. Till I am well (alive), oh, may your grandma die! my yellow bride, aman! (×2) My tall beautiful dear. There are versions of this song in Sorani , the Kurdish language that is predominantly spoken in Iran and Iraqi Kurdistan . One of these versions was performed by Mohammad Mamle , a well-known Kurdish singer. Yar bo min bê wefa bû Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim My boyfriend was not faithful for me He put his head on her thigh until the morning She was my lover's (new) guest Dostî namîhrebanî Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim He is not a merciful lover He put his head on her thigh until the morning She was my lover's (new) guest Zorim hewll legel da Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim I've tried so hard with him He put his head on her thigh until the morning She was my lover's (new) guest Bê xeber bûm nemzanî Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim I didn't know about it He put his head on her thigh until the morning She was my lover's (new) guest The Persian version is entitled Dāman Kešān ( دا٠ن کشان ) or Sāqi e Mey Xārān ( ساقی ٠ی خواران ). ،دا٠ن کشان ،ساقی ٠ی خواران ،از کنار یاران ،٠ست و گیسو افشان .٠ی گریزد Dragging her skirt, The cup-bearer of wine drinkers, past her suitors/friends, inebriated and with flowing hair, flees. ،در جا٠٠ی ،از شرنگ دوری ،وز غ٠٠هجوری ،چون شرابی جوشان .٠ی بریزد In the goblet of wine, from the sorrow of separation, and from the grief of parting, like boiling wine, she pours. دار٠قلبی لرزان ز غ٠ش؛ .دیده شد نگران ،ساقی ٠ی خواران ،از کنار یاران ،٠ست و گیسو افشان .٠ی گریزد I have a heart trembling because of her sorrow; my eyes have become distressed. The cup-bearer of wine drinkers, past her suitors/friends, inebriated and with flowing hair, flees. دار٠چش٠ی گریان ز رهش؛ .روز و شب بش٠ار٠تا بیاید I have an eye crying before her way; I count days and nights until she comes. آزرده دل ،از جفای یاری ،بی وفا دلداری ،٠اه افسونکاری .شب نخفت٠Heartbroken from the anguish of a sweetheart, a disloyal beloved, a charming moonlike beauty, I didn't sleep at night. با یادش تا ،دا٠ن از کف داد٠،شد جهان از یاد٠.راز عشقش در دل تا نهفت٠With her memory, as I lost control, I forgot the world, while I hid the secret of her love in my heart. ز چش٠انش ریزد به دل٠.شور عشق و ا٠ید ،دا٠ن از کف داد٠،شد جهان از یاد٠.راز عشقش در دل تا نهفت٠From her eyes she pours into my heart the sensation of love and hope. I lost control, I forgot the world, while I hid the secret of her love in my heart. دار٠چش٠ی گریان ز رهش؛ .روز و شب بش٠ار٠تا بیاید I have an eye crying before her way; I count day and night until she comes. The composer of the music is anonymous. The Greek lyrics were written by Christos C. Papadopoulos. The Sari Aghjik (Mountain Girl) version uses the same melody with the Armenian word for the girl ( aghjik Õ¡Õ²Õ»Õ«Õ¯ ) as in the song Vard Siretsi ("I loved a rose"). Both Armenian versions, are about the boy complaining that the unkind girl has rejected him. In Armenian Sari Aghjik , the girl has chosen someone else over him. The lyrics translate to: Գնաց, ուրիշին Õ¡Õ¼Õ¡Õ¾ ... Ա՜խ, մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ, Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Գնաց, ուրիշին Õ¡Õ¼Õ¡Õ¾, Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. She left and chose someone else, Akh! let your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. She left and chose someone else My heart yaman! Leyli dear beloved (Persian-Armenian) Թույն Õ´Õ« Õ¡Õ®Õ¡ Õ©Õ¥Õª վերքիս ... Ա՜խ մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ ... Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Թույն Õ´Õ« Õ¡Õ®Õ¡ Õ©Õ¥Õª վերքիս ... Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. Don't pour poison into (salt on) my wound. Akh! let your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. Don't pour poison into my wound My heart yaman! Leyli dear beloved. Տիրել Õ¥Õ½ խելք ու մտքիս ... Ա՜խ մերըդ Õ´Õ¥Õ¼Õ¶Õ«, սարի Õ¡Õ²Õ»Õ«Õ¯, Ö ÕœÕµ, Ö ÕœÕµ ... Քարի Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Քար սիրտ Õ¡Õ²Õ»Õ«Õ¯, Ö Õµ, Ö Õµ, Չար սիրտ Õ¡Õ²Õ»Õ«Õ¯: Տիրել Õ¥Õ½ խելք ու մտքիս ... Ô´Õ¬Õ¥ ÕµÕ¡Õ´Õ¡Õ¶, Õ¬Õ¥ÕµÕ¬Õ« յար Õ»Õ¡Õ¶. You have possessed my thoughts and my mind. Akh, may your mother die! You mountain girl, oy oy you stone girl, oy oy, you stone-hearted girl, oy oy, you wicked-hearted girl. You have possessed my thoughts and my mind. My heart yaman! Leyli dear beloved The phrase "Don't pour poison into (salt on) my wound" is an idiom that means "don't make my troubles worse".In Azerbaijan, Sarı Gəlin (Blond Maiden) is a legend that symbolizes the love between a Muslim Azerbaijani and a Christian Armenian girl who are kept apart. Saçın ucun hörməzlər, gülü sulu dərməzlər, Sarı Gəlin. You don't braid the end of your hair, you don't pick a dewy flower. yellow (blond, fair) bride bu sevda nə sevdadır, səni mənə verməzlər; neynim aman, aman, (×2) Sarı Gəlin. What a love is this love! they will not give you to me. what can I do? aman! (secure me! / help! / please!) aman! (×2) yellow bride bu dərənin uzunu, çoban qaytar quzunu, Sarı Gəlin. The tallest of this valley, shepherd, return the lamb, yellow bride. nə ola bir gün görəm, nazlı yarın üzünü; neynim aman, aman, (×2) Sarı Gəlin. I wish that one day I could see the face of my playful love what can I do? aman! aman! (×2) yellow bride. Gün ola mən bir görəydim Nazlı yarımın üzünü Neynim aman, aman (×2) Sarı gəlin Could there be a day I would see (correct translation?) the face of my playful love what can I do? aman! aman! (×2) yellow bride. The Azerbaijani version of the song was processed [ clarification needed ] and pitched by Azerbaijani composer Asaf Zeynally (1909–1932). The text of the song in the Azerbaijani language was published in 1982 in Baku under the edition of Hamid Arasly . In 2001 the Azerbaijani text of the song was published by Rafik Babayev . DayIrMan sings a longer Azerbaijani version, which translates to: Don't pluck the flower while it's young, yellow bride. Don't braid the end of your hair, Don't pluck the flower while it's young, yellow bride. You were born for love with me; / We were born to love each other; You are the only one; on earth, in life, in the sky. You are my sunshine, my fire. I fell in love with you on a moonlit night The sun, a man and yellow bride; The only star, land and your breath, I love life, life is you. My eyes that see you are full of eagerness, You came into my dream like a ray, yellow bride. What kind of love is this? They won't let me marry you. What should I do, what should I do, yellow bride? What kind of love is this? They won't give you to me. It's me, looking for you among the stars. Answer me, don't break my heart! I will breathe with your warm breath, I will remember you all my life, Enough! dry your tears, don't cry! Don't keep the fire in your heart too long, Your destined happiness is written on your forehead. Pure love within one night. But this is only a dream and you are in my dream, You are my yellow bride among my wishes. What kind of love is this? They won't let us marry. What should I do, what should I do, yellow bride? What kind of love is this? They won't give you to me. It's us, only us and the sky, You came to me in this utter night. The light woke me up, And we got separated among the stars. Oh, God, hear my crying, I felt this sharp pain in my heart, Love is a game and I was winning, I couldn't imagine such an end. But you wanted death, You achieved your goal in the end, yellow bride. What kind of love is this? They won't let me marry you. What should I do, what should I do, yellow bride? You are my yellow bride, You are my yellow bride. Along this valley, Give the lamb back to me, shepherd ... You are my yellow bride ...İçinde bir kız gezer, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. A girl is walking around, oh, may your grandma die! my yellow bride, aman! (×3) my tall beautiful dear. Dertlere derman yazar, / Katlime ferman yazar , ay! nenen ölsün, Sarı gelin aman! (×3) suna yarim. She writes the prescription for my pains, / She writes the sentence to my assassination , oh, may your grandma die! my yellow bride aman, (×3) my tall beautiful dear. Kanadında gümüş var, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. It (She) has silver in its wings, oh, may your grandma die! my yellow bride, aman! (×3) my tall beautiful dear. Altı mor sümbüllü bağ ay nenen ölsün sarı gelin aman! (×3) suna yarim. Underneath has garden with purple hyacinth, oh, may your grandma die! my yellow bride aman! (×3) my tall beautiful dear. Niceki bu halimse, ay! nenen ölsün, sarı gelin aman! (×3) suna yarim. Till I am well (alive), oh, may your grandma die! my yellow bride, aman! (×2) My tall beautiful dear.There are versions of this song in Sorani , the Kurdish language that is predominantly spoken in Iran and Iraqi Kurdistan . One of these versions was performed by Mohammad Mamle , a well-known Kurdish singer. Yar bo min bê wefa bû Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim My boyfriend was not faithful for me He put his head on her thigh until the morning She was my lover's (new) guest Dostî namîhrebanî Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim He is not a merciful lover He put his head on her thigh until the morning She was my lover's (new) guest Zorim hewll legel da Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim I've tried so hard with him He put his head on her thigh until the morning She was my lover's (new) guest Bê xeber bûm nemzanî Ser leser rranî, taku beyanî Bûn be mîwanî nazenînim I didn't know about it He put his head on her thigh until the morning She was my lover's (new) guestThe Persian version is entitled Dāman Kešān ( دا٠ن کشان ) or Sāqi e Mey Xārān ( ساقی ٠ی خواران ). ،دا٠ن کشان ،ساقی ٠ی خواران ،از کنار یاران ،٠ست و گیسو افشان .٠ی گریزد Dragging her skirt, The cup-bearer of wine drinkers, past her suitors/friends, inebriated and with flowing hair, flees. ،در جا٠٠ی ،از شرنگ دوری ،وز غ٠٠هجوری ،چون شرابی جوشان .٠ی بریزد In the goblet of wine, from the sorrow of separation, and from the grief of parting, like boiling wine, she pours. دار٠قلبی لرزان ز غ٠ش؛ .دیده شد نگران ،ساقی ٠ی خواران ،از کنار یاران ،٠ست و گیسو افشان .٠ی گریزد I have a heart trembling because of her sorrow; my eyes have become distressed. The cup-bearer of wine drinkers, past her suitors/friends, inebriated and with flowing hair, flees. دار٠چش٠ی گریان ز رهش؛ .روز و شب بش٠ار٠تا بیاید I have an eye crying before her way; I count days and nights until she comes. آزرده دل ،از جفای یاری ،بی وفا دلداری ،٠اه افسونکاری .شب نخفت٠Heartbroken from the anguish of a sweetheart, a disloyal beloved, a charming moonlike beauty, I didn't sleep at night. با یادش تا ،دا٠ن از کف داد٠،شد جهان از یاد٠.راز عشقش در دل تا نهفت٠With her memory, as I lost control, I forgot the world, while I hid the secret of her love in my heart. ز چش٠انش ریزد به دل٠.شور عشق و ا٠ید ،دا٠ن از کف داد٠،شد جهان از یاد٠.راز عشقش در دل تا نهفت٠From her eyes she pours into my heart the sensation of love and hope. I lost control, I forgot the world, while I hid the secret of her love in my heart. دار٠چش٠ی گریان ز رهش؛ .روز و شب بش٠ار٠تا بیاید I have an eye crying before her way; I count day and night until she comes.The composer of the music is anonymous. The Greek lyrics were written by Christos C. Papadopoulos. While the Persian version is completely different, there are notable similarities between Armenian, Azerbaijani and Turkish version: If the statements are taken as complementary rather than just similar, the Muslim Turk (language of both Azerbaijan and Turkey) boy has fallen in love with a Christian Armenian/Kipchak blond maiden from the mountains and valleys, probably close to Palandöken ; But they are kept apart, and the unkind girl is taken away, causing the boy to lament and curse frequently.In Armenia In Azerbaijan In Iran In Turkey International

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Chanderi sari

The Chanderi sari is a traditional Koli sari made in Chanderi , Madhya Pradesh , India . The weaving culture of Chanderi emerged between the 2nd and 7th centuries. It is situated on the boundary of two cultural regions of the state, Malwa and Bundelkhand . The people of the Vindhyachal Ranges have a wide range of traditions. In the 11th century the trade locations Malwa, Medwa, central India and south Gujarat increased the region's importance. The Chanderi sari tradition began in the 13th century Around 1350 by Koli weavers. Chanderi saris are produced from three kinds of fabric: pure silk, Chanderi cotton and silk cotton. [ clarification needed ] Traditional coin, floral art, peacocks and modern geometric designs are woven into different Chanderi patterns. The saris are among the finest in India and are known for their gold and silver brocade or zari , fine silk, and opulent embroidery.

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Kanchipuram silk sari

The Kanchipuram silk sari is a type of silk sari made in the Kanchipuram region in Tamil Nadu , India . These saris are worn as bridal & special occasion saris by most women in Tamil Nadu, Kerala, Karnataka & Andhra Pradesh. It has been recognized as a Geographical indication by the Government of India in 2005 – 2006. As of 2008, an estimated 5,000 families were involved in sari production. There are 25 silk and cotton yarn industries and 60 dyeing units in the region. The saris are woven from pure mulberry silk thread. The pure mulberry silk and the Zari used in the making of Kanchipuram saris comes from South India. To weave a Kanchipuram sari three shuttles are used. While the weaver works on the right side, his aide works on the left side shuttle. The border colour and design are usually quite different from the body. If the mundhi (the hanging end of the sari) has to be woven in a different shade, it is first separately woven and then delicately joined to the Sari. The part where the body meets the mundhi is often denoted by a zigzag line. In a genuine Kanchipuram Silk Sari, body and border are woven separately and then interlocked together. The joint is woven so strongly that even if the saris tears, the border will not detach. That differentiates the kanchivaram silk saris from the others. Saris are distinguished by their wide contrast borders. Temple borders, checks, stripes and floral (buttas) are traditional designs found on a Kanchipuram saris. The patterns and designs in the kanchipuram saris were inspired with images and scriptures in South Indian temples or natural features like leaves, birds and animals. These are saris with rich woven mundhi showing paintings of Raja Ravi Varma and epics of Mahabharata and Ramayana . Kanchipuram saris vary widely in cost depending upon the intricacy of work, colours, pattern, material used like zari (gold thread) etc. The silk is also known for its quality and craftsmanship, which has helped earn its name. Kanchipuram saris woven with heavy silk and gold cloth are considered to be special and are worn on occasions and festivities. In 2005, the Government of Tamil Nadu applied for Geographical Indication for Kanchipuram saris. The Government of India recognized it as a Geographical indication officially since the year 2005-06. The Tamil film Kanchivaram released in 2008 depicts the struggles of silk weavers in Kanchipuram.

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Gadwal sari

Gadwal sari is a handcrafted woven sari style in Gadwal of Jogulamba Gadwal district in the Indian state of Telangana . It was registered as one of the geographical indication from Telangana by the Geographical Indications of Goods (Registration and Protection) Act, 1999 . They are most notable for the Zari on the saris. The sari consists of a cotton body , silk border, and zari pallu. with silk pallu which is also given a new name Sico saris . The weave is so light that the saree can be packed in a matchbox. The Brahmotsavas of Tirupati begins with the deity's idol being adorned with Gadwal Saree.Gadwal Handloom Centre , established in 1946 by the late Ratan Babu Rao, was mainly responsible for the widespread knowledge and detail regarding the Gadwal Sari.

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Kasta sari

The Kaashtha sari ( Marathi : नऊवारी साड़ी ) is a Koli style of sari draping very similar to the way the Maharashtrian dhoti is worn. The word Kaashtha refers to the sari being tucked at the back. Since this sari is usually worn by using a single nine yard cloth, it is also referred to as Nauvari, which means Nine Yards . Sakachcha sari is another term commonly used to refer to this style of sari. It is referred to as Akanda Vastra, which means it doesn't need any other attire to support it. In fact, this attire holds utmost importance as women across different walks of life have worn it. It is not just worn at religious and cultural events, but women have fought wars in the past and still work in farmlands wearing this. It is the traditional Marathi style of sari which is worn without a petticoat. This style of sari draping is common among all the castes but the way of draping differs according to the region and topography as well. For example, Brahmin women wear it in a particular way (called brahmni on the other side), while Aagri people from the Raigad district wear it in a knee-length fashion called 'adwa patal', whereas with a small variation the kunbi or the farmer women of the Raigad district and some parts of Ratnagiri as well wear nineyard ( called "uprati") .The name uprati means upside down, which is because of some folds draping the sari are upside down. One of the special features of adwa patal and uprati arethat is that these saris are draped without tying knots, though the sari is still very tightly draped. On the contrary, women from rural Puñe and Satara Ahmed Nagar or Kolhapur wear it to the ankle length which is very popular. Also, Brahmins wear it in a particular way where the border of the sari is displayed on the front side as well, similar to the kashta on the back side. Some details are given below as well. This sari is draped so that its center is neatly placed at the back of the waist and the ends are tied securely in the front, and then the two ends are wrapped around the legs. The decorative ends are then draped over the shoulder and the upper body or torso. Sayali Badade, an HR executive said, " A woman who wore a Nauvari was always looked upon with respect. The reason was that both shoulders of women were covered, and it made for a completely traditional wear. The style was originally started and popularised during the Peshwai reign. " Women of the Koli tribe also wear this style of sari but cut into two pieces. One piece is worn around the waist while the other piece is used to cover the upper part of the body. It is taken on the head over the left shoulder in the Maratha fashion. The Koli women are decorative with both dress and ornament and this sari of nine yards of cotton fabric is draped adeptly over the hips so that the figure is graceful in movement. It is the traditional Marathi style of sari which is worn without a petticoat. This style of sari draping is common among all the castes but the way of draping differs according to the region and topography as well. For example, Brahmin women wear it in a particular way (called brahmni on the other side), while Aagri people from the Raigad district wear it in a knee-length fashion called 'adwa patal', whereas with a small variation the kunbi or the farmer women of the Raigad district and some parts of Ratnagiri as well wear nineyard ( called "uprati") .The name uprati means upside down, which is because of some folds draping the sari are upside down. One of the special features of adwa patal and uprati arethat is that these saris are draped without tying knots, though the sari is still very tightly draped. On the contrary, women from rural Puñe and Satara Ahmed Nagar or Kolhapur wear it to the ankle length which is very popular. Also, Brahmins wear it in a particular way where the border of the sari is displayed on the front side as well, similar to the kashta on the back side. Some details are given below as well. This sari is draped so that its center is neatly placed at the back of the waist and the ends are tied securely in the front, and then the two ends are wrapped around the legs. The decorative ends are then draped over the shoulder and the upper body or torso. Sayali Badade, an HR executive said, " A woman who wore a Nauvari was always looked upon with respect. The reason was that both shoulders of women were covered, and it made for a completely traditional wear. The style was originally started and popularised during the Peshwai reign. " Women of the Koli tribe also wear this style of sari but cut into two pieces. One piece is worn around the waist while the other piece is used to cover the upper part of the body. It is taken on the head over the left shoulder in the Maratha fashion. The Koli women are decorative with both dress and ornament and this sari of nine yards of cotton fabric is draped adeptly over the hips so that the figure is graceful in movement. The traditional 'nauvari' retains its charm even in the modern age. Also known as 'Lugada', this sari is now regularly worn mostly by elderly Maharashtrian women. However, in contemporary fashion, the trend of wearing nine-yard Kasta sari is picking up fast among the younger lot that wants to keep the age-old Marathi tradition alive. It requires perfect technique, practice and perfection to wear a nine-yard sari. Mostly worn in dance competitions (" lavani ") and Maharashtrian folk dance, the Kasta sari has surely made a great come back in the fashion industry. Prashant Shalgar, a nine-yard Kasta sari seller, said, " It has always been in demand. Though earlier only elder generation women would pick them up, now many young girls choose them for their elegant looks. Prashant Kolhe, a management executive, said, " My grandmother used to wear a nine-yard sari. It would look great on her. She used to carry it very well. I guess Indian saris are the best fashion wear available on the globe. You cannot look graceful, trendy and comfortable in any other dress." Women dabbawalas in Mumbai are dressed in nauvari saris. To make the wearing more easy and comfortable, the market is all set to sell stitched Kasta sari for those who love drape it. Sandhya Kenjale, another Kasta sari seller, says, " I started stitching nineyard saris because I could never drape it properly. For draping a nineyard sari, you should have some guidance for it is a technique to wear it. There are many occasions when women choose to wear nine-yard saris but the drawback is they do not know the technique. Ready-to-wear nine-yard sari is the perfect solution for such problems. Just wear it like a salwar , put the pallu over the shoulder, and you are dressed in few minutes. Also, teen-aged girls are seen wearing it in their school or college gatherings. Many brides are now taking help of such ready-to-wear nine-yard saris. With a wide range of them available in the market, buyers have a lot of choice. Available in Bangalore silk, Belgaum silk, pure silk, Orissa silk, nine-yard saris are priced reasonably. "Prashant Shalgar added, " Marathi movies are responsible for keeping the traditional wear alive. To make it easy, these saris are now stitched and sold in the market. " Stylist Pradnya Bhalekar stated, " You can wear a stitched Nauvari like a salwar. It is as simple as wearing your favourite pair of denims. Besides, you don't have to worry that the drape might come off. " Shobhaa De told in her blog that she suggested to Mukesh Ambani that the cheerleaders of Mumbai Indians wear the traditional nine yard kasta sari and perform dance routines for the local lavani. On the contrary, some consider the Kasta sari has fallen out of favour currently. It is considered far too revealing. It is rarely seen in the cities. This type of sari is regularly made fun of in films, portrayed as some sort of "sexy" garment, meant to titillate. In reality, the Kasta sari embodies freedom for women. In a way it is similar to the dhoti as it allows leg movement and the ankles are left free. But today the Kasta sari will only be considered decent if distorted to hide every inch of a woman's body. The traditional 'nauvari' retains its charm even in the modern age. Also known as 'Lugada', this sari is now regularly worn mostly by elderly Maharashtrian women. However, in contemporary fashion, the trend of wearing nine-yard Kasta sari is picking up fast among the younger lot that wants to keep the age-old Marathi tradition alive. It requires perfect technique, practice and perfection to wear a nine-yard sari. Mostly worn in dance competitions (" lavani ") and Maharashtrian folk dance, the Kasta sari has surely made a great come back in the fashion industry. Prashant Shalgar, a nine-yard Kasta sari seller, said, " It has always been in demand. Though earlier only elder generation women would pick them up, now many young girls choose them for their elegant looks. Prashant Kolhe, a management executive, said, " My grandmother used to wear a nine-yard sari. It would look great on her. She used to carry it very well. I guess Indian saris are the best fashion wear available on the globe. You cannot look graceful, trendy and comfortable in any other dress." Women dabbawalas in Mumbai are dressed in nauvari saris.To make the wearing more easy and comfortable, the market is all set to sell stitched Kasta sari for those who love drape it. Sandhya Kenjale, another Kasta sari seller, says, " I started stitching nineyard saris because I could never drape it properly. For draping a nineyard sari, you should have some guidance for it is a technique to wear it. There are many occasions when women choose to wear nine-yard saris but the drawback is they do not know the technique. Ready-to-wear nine-yard sari is the perfect solution for such problems. Just wear it like a salwar , put the pallu over the shoulder, and you are dressed in few minutes. Also, teen-aged girls are seen wearing it in their school or college gatherings. Many brides are now taking help of such ready-to-wear nine-yard saris. With a wide range of them available in the market, buyers have a lot of choice. Available in Bangalore silk, Belgaum silk, pure silk, Orissa silk, nine-yard saris are priced reasonably. "Prashant Shalgar added, " Marathi movies are responsible for keeping the traditional wear alive. To make it easy, these saris are now stitched and sold in the market. " Stylist Pradnya Bhalekar stated, " You can wear a stitched Nauvari like a salwar. It is as simple as wearing your favourite pair of denims. Besides, you don't have to worry that the drape might come off. " Shobhaa De told in her blog that she suggested to Mukesh Ambani that the cheerleaders of Mumbai Indians wear the traditional nine yard kasta sari and perform dance routines for the local lavani. On the contrary, some consider the Kasta sari has fallen out of favour currently. It is considered far too revealing. It is rarely seen in the cities. This type of sari is regularly made fun of in films, portrayed as some sort of "sexy" garment, meant to titillate. In reality, the Kasta sari embodies freedom for women. In a way it is similar to the dhoti as it allows leg movement and the ankles are left free. But today the Kasta sari will only be considered decent if distorted to hide every inch of a woman's body. Women adorning kasta saris are seen in some Bollywood films, although they are mostly worn in song sequences. Generally, in modern Bollywood fashion, the pallu is fully wrapped around the waist rather than on the shoulder and to cover the blouse or choli folded chunri of contrast color is pinned up. Also, the hairstyle on is step-cut up to shoulder length with smart nose ring or Nath and Chandrakor Bindi. The most famous example of Kasta sari in Bollywood is the song sequence of "Humko Aaj Kal Hai Intezaar" in the film Sailaab (1990) featuring Madhuri Dixit in a yellow and green Kasta sari. Another recent example is of Kim Sharma in the film Tom, Dick, and Harry (2006). She played the role of Bijlee, a fisherwoman, for which she appeared in Kasta saris of different color throughout the entire film. The first look and promos of Agneepath , the 2012 remake of the 1990 Hindi film of the same name was released which featured actress Katrina Kaif dancing for an item song " Chikni Chameli " in a yellow kasta sari. Actress Vidya Balan dressed in a red kasta sari along with lavani dancers performed live on stage her latest item number "Mala Jau De" for the audience, from Vidhu Vinod Chopra's upcoming film Ferrari Ki Sawaari . She told she was inspired from Madhuri Dixit's performance from Sailaab. In 2015, actresses Deepika Padukone and Priyanka Chopra featured in nauvari saris for a dance sequence in the film Bajirao Mastani . Anju Modi, the costume designer for the film stated, "I do hope that after this movie, the nauvari sari makes a comeback."

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Kerala sari

Kerala sari (Set-sari) ( Malayalam : കേരള സാരി ) is a clothing of women in the Indian state of Kerala .It is worn as a garment that closely resembles the mundum neriyathum though it is not considered a true mundum neriyathum by classic definition. Traditional mundum neriyathum consists of a two-piece cloth, while Kerala sari is worn in a way to resemble navi drape using two-piece mundum neiyathum. Otherwise, the Kerala sari closely resembles the mundum neriyathum and is often worn by Malayali women as a quasi mundum neriyathum. Surviving medieval Kerala mural paintings depict existence of three-styles of clothing worn by women, these include one-piece mundum, single-piece sari with over-lapping pleats resembling nivi-drape worn today by Mohiniyattam dancers and two-piece mundam-neryathum attire which evolved into Kerala sari. Balaramapuram, Chendamangalam and Kuthampully are the three major sari weaving centres in Kerala, these clusters have been given a Geographical Indication Tag by the Indian Government and all three are famous for the weaving of Kasavu saris notable for its white cotton or silk textile with golden borders. The Balaramapuram cluster weavers traditionally weave Kasavu saris and mundu. The Balaramapuram cluster is known for having a simple gold border and it is woven out of cotton and silk yarn. Chendamangalam, the second cluster, is known for weaving saris with cotton and silk and striped golden borders. They are similar to Balaramapuram but with lesser emphasis on the golden border. Weaving in Chedamangalam was introduced by the Paliam royal family . Paliath Achans, who were the Rajas of Chendamangalam and the hereditary prime ministers to the Maharaja of Kochi have been associated with Chendamangalam from the 16th century onwards. The Devanga Chettiars settled in this region at their behest to serve the family's sartorial needs. The Kuthampully cluster is based in Thrissur District, their history dates back 500 years when their forefathers came to Kerala from Mysore . The weavers of Kuthampully came under the patronage of the Kochi royal family, and had woven fabrics for the royal family. The saris by Kuthampully weavers are quite different from the other two clusters as they include more patterns, borders and motifs. Kerala sari is regarded as the cultural costume of women of the Malayali community. The grace and appeal of the golden borders contrasting with the otherwise plain white mundum neryathum of Keralite women has come to symbolize Malayali women. The sari is a hot favorite during the time of Onam , not just in Kerala but in other parts of India as well. Both the traditional and modern styles of the mundum neryathum are depicted in the paintings of the Indian painter Raja Ravi Varma . The mundum neriyathum was modified in several paintings depicting shakuntala from the mahabharatha to a style of draping now popularly known as the 'nivi saree' or 'national drape'. In one of his paintings, the Indian subcontinent was shown as a mother wearing a flowing nivi saree.

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Sári Fedák

Sári Fedák (born Sarolta Klára Mária Fedák ; 27 September 1879, in Beregszász , Hungary (now Berehove, Ukraine – 5 May 1955, in Budapest , Hungary ) was a Hungarian actress and singer, one of the most well-known prima donnas of her time. According to American journalist and non-fiction writer Richard Traubner , Fedák and Sári Petráss remain "the two best-remembered Hungarian female operetta stars of all time" . She studied acting with Szidi Rákosi until 1899, beginning her career the same year with the Magyar Színház theatre company. Beginning in 1900 she played in Pozsony (now Bratislava ), and in several theatres in Budapest, including Népszínház , Király Színház , and Vígszínház . Following World War I , she spoke out against the Austro-Hungarian monarchy . Later, during the era of the Hungarian Soviet Republic she agitated for joining the Red Army. [ clarification needed ] After the fall of the Republic, Fedák fled to Vienna , but was captured and held in prison at Wiener Neustadt for a short time. As she supported the Republic, she could play in only Vienna from 1920-21. She made appearances in Berlin and Paris in 1921 and 1925. In 1934, she toured several American cities. [ clarification needed ]In 1922 she married writer Ferenc Molnár , after a six-year relationship. The couple divorced in 1925 or 1926, after "he had accused her of intimacy with 42 gentlemen, and she had replied in kind with a list of 142 ladies". In 1923, she became a member of the Fővárosi Operettszínház theatre. Starting in 1940, she was the leading actress in the Új Magyar Színház theatre. In 1944, working at the Donausender radio station in Vienna, she rallied for Hungary to continue the fight in World War II on the side of Nazi Germany and was sentenced to eight months in prison after the war. She was also banned from playing in theatres for three years. She never appeared on stage again. [ citation needed ] After being released from prison, she moved to Nyáregyháza , retiring from active life. She died in 1955, aged 75, and was interred in Budapest 's Farkasréti Cemetery .

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Patola sari

A Patola sari is a double ikat woven sari, usually made from silk , made in Patan , Gujarat , India . The word patola is the plural form; the singular is patolu. These saris are made using silk threads that are first dyed with natural colors and then woven together to create the intricate patterns and designs. They are usually worn for special occasions, such as weddings and formal events.To create a patola sari, both the warp and weft threads are wrapped to resist the dye according to the desired pattern of the final woven fabric. This tying is repeated for each colour that is to be included in the finished cloth. The technique of dyeing the warp and weft before weaving is called double ikat . The bundles of thread are strategically knotted before dyeing. Silk weavers of the Salvi caste from the state of Maharashtra chose Gujarat as the home for their renowned patola fabric. It is believed that salvis went to Gujarat in the 12th century with the intention of acquiring the patronage of the Chaulukyas Rajputs , who ruled all of Gujarat and parts of Malva and south Rajasthan at the time, with Anahiwad Patan as the capital. Legend says that over 700 patola weavers came to the palace of Raja Kumarpal , on the personal request of king himself. The Solanki (Chalukya) rulers used to dress in patola silk themselves on special occasions. [ citation needed ] It is broadly accepted belief that these Salvis originally belonged to the region, which now lies at the middle of the present day Marathawada and Vidarbha divisions of Maharashtra state. The art of Patola weaving is an ancient one. According to some historians, the art of Patola weaving was known also in the 4th century in "Ajanta" caves, which resembles the tie-dyes technique of patola. Ajanta Caves were patronized by the Vatsagulma branch of the Vakataka dynasty, which controlled a vast area of Deccan during the 3rd, 4th & 5th centuries A.D. Vatsagulma is presently the 'Washim' district of the Vidarbha Division of Maharashtra. After the decline of Solanki empire, salvis founded a rich trade in Gujarat. Patola saris quickly became a sign of social status among Gujarati women and girls, especially as part of stridhan , items that a woman can claim as her. These art of patan is more than 850 years old. Patola has had a huge importance as status clothes in Southeast Asia where it was imported from at least the Middle Ages. Local elites in far eastern locations such as Timor and Maluku Islands strove to acquire patola or patola imitations, which were often provided by European merchants in the early-modern era. Patola motifs were frequently taken over by indigenous weaving traditions. There are four distinct patterns which are woven primarily in Gujarat by the Salvi community. In Jain and Hindu communities, double ikat saris with entire designs of parrots, flowers, elephant and dancing figures are generally used. In Muslim communities, saris with geometric designs and flower patterns are typical, being worn mostly for weddings and other special occasions. Maharashtrian Brahmins wear saris woven with plain, dark coloured borders and body and a bird design called Nari Kunj.

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Venkatagiri Sari

Venkatagiri Sari is a sari style woven in Venkatagiri of Tirupati district in the Indian state of Andhra Pradesh . It was registered as one of the geographical indication from Andhra Pradesh by Geographical Indications of Goods (Registration and Protection) Act, 1999 . Venkatagiri saris are known for their fine weaving. These style of saris can also be found in the villages of Sengunthapuram , Variyankaval , Elaiyur, Kallathur, Andimadam and Marudhur villages. The history of the sari dates back to the early 1700s during the rule of Venkatagiri. They were encouraged by the Velugoti dynasty of Nellore and also by the Bobbili and Pithapuram dynasties. In those days, they were mostly weaved for queens, royal women and Zamindaris . The production of the Venkatagiri sari includes different stages which includes: The Venkatagiri sari has different varieties like, Venkatagiri 100 , Venkatagiri-putta and Venkatagiri-silk , with the Venkatagiri 100 being popular of all. The saris are made from fine cotton and the most significant is the use of zari . The power looms have effected the sari making by the local artisans. Department of Handicrafts under Ministry of Textiles (India) oversees the issues and promotes the artisans .

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Ritu Kala Samskaram

Half sari function or Langa Voni Telugu : లంగా ఓణి, Pavadai Dhavani Tamil : பாவாடை தாவணி, Langa Davani Kannada : ಲಂಗ ದಾವಣಿ. In South Indian Hindu tradition, the Ritu Kala Samskara ceremony or Ritushuddhi is a ceremony performed when a girl wears a sari for the first time. It is the celebration of a girl's rite of passage after menarche (first menstruation) or period, and she is deemed a young woman both physically and spiritually. Langa voni is traditional clothing for unmarried girls in South India . [ citation needed ]Ritusuddhi , also called as Ritu Kala Samskara , is the coming of age ceremony for girls, after menarche or first menstruation or simply, first period. This milestone in a girl's life is observed by her family and friends, with gifts and her wearing a sari for the ritual. The rite of passage is celebrated, in modern times, as a "half-saree party" or half-sari function, where the female relatives and friends of the girl gather, and she receives and wears a half-saree and other gifts. Thereafter, at ceremonious events, she wears the half-sarees, until her marriage when she puts on a full sari. In South India coming of age ceremony or rites of passage is celebrated when a girl reaches puberty. She wears a new langa voni during the first part of the ceremony and then she is gifted her first sari by her maternal uncle , which she wears during the second half of the ceremony. This marks her transition into womanhood The tradition of presenting a langa voni begins with the girl's first naming ceremony Namakaran and her first rice feeding ceremony called Annaprashana . She receives her last one at her coming of age ceremony . In Shaktism the Earth's menstruation is celebrated during the Ambubachi Mela , an annual fertility festival held in June, in Assam , India . During Ambubachi, the annual menstruation course of the goddess Kamakhya is worshipped in the Kamakhya Temple .

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Zsa Zsa Gabor

Hungary Turkey (1935–1949) United States Actress socialite Zsa Zsa Gabor ( / ˌ ʒ ɑː ʒ ɑː ˈ ɡ ɑː b ɔːr / , Hungarian: [ ˈɡaːbor ˈʒɒʒɒ ] ; born Sári Gábor [ ˈɡaːbor ˈʃaːri ] ; February 6, 1917 – December 18, 2016) was a Hungarian-American socialite and actress. Her sisters were actresses Eva Gabor and Magda Gabor . Gabor competed in the 1933 Miss Hungary pageant, where she placed as second runner-up, and began her stage career in Vienna the following year. She emigrated from Hungary to the United States in 1941, and became a sought-after actress with "European flair and style." She was considered to have a personality that "exuded charm and grace". Her first film role was a supporting role in Lovely to Look At , released in 1952. The same year, she appeared in We're Not Married! , and played one of her few leading roles in Moulin Rouge , directed by John Huston . Huston later described Gabor as a "creditable" actress. Outside her acting career, Gabor was known for her extravagant Hollywood lifestyle, her glamorous personality, and her many marriages. In total, Gabor had nine husbands, including hotel magnate Conrad Hilton and actor George Sanders . She once stated, "Men have always liked me and I have always liked men. But I like a mannish man, a man who knows how to talk to and treat a woman—not just a man with muscles." Zsa Zsa Gabor was born Sári Gábor on February 6, 1917, [lower-alpha 1] in Budapest , Hungary, then part of the Austro-Hungarian Empire . The middle of three daughters, her parents were Jolie (née Janszieka Tillemann) and Vilmos Gábor (né Grün), owner of a jewelry store in Budapest, a Royal Hungarian Army officer. Her parents were both of Jewish ancestry. Gabor was named after Sári Fedák , an actress. Gabor was called ZsaZsa because, as a little girl, she couldn't pronounce her own name. In 1941, Gabor left Hungary for the United States . During a layover at Eppley Airfield in Omaha, Nebraska en route to Hollywood , she made headlines by telling the Associated Press that she had danced with Adolf Hitler twice. [lower-alpha 2] On July 8, 1944, aided by Gabor's husband, Conrad Hilton , Gabor's parents fled Budapest during the Nazi invasion and occupation of Hungary . Gabor's elder sister, Magda , later became an American socialite and her younger sister, Eva , became an American actress and businesswoman. The Gabor sisters were first cousins of Annette Lantos, wife of California Congressman Tom Lantos (D-CA). In January 1933, following her time as a student at a Swiss boarding school, Gabor placed second runner-up in the fifth Miss Hungary pageant, behind Lilly Radó and crown winner Júlia Gál. On August 31, 1934, she sang the soubrette role in Richard Tauber 's operetta , Der singende Traum ( The Singing Dream ), at the Theater an der Wien in Vienna . This would mark her first stage appearance. In 1944, she co-wrote a novel with writer Victoria Wolf entitled Every Man For Himself . According to Gabor, the fictional story was derived, in small part, from Gabor's life experiences. The book was subsequently bought by an American magazine. In 1949, Gabor declined an offer to play the leading role in a film version of the classic book Lady Chatterley's Lover . According to the Cedar Rapids Gazette , she turned down the role of Lady Chatterley due to the story's controversial theme. Her more serious film acting credits include Moulin Rouge , Lovely to Look At , and We're Not Married! , all from 1952, and 1953's Lili . In 1958, she ran the gamut of moviemaking, from Touch of Evil to the camp oddity Queen of Outer Space . Later, she appeared in such films as Won Ton Ton, the Dog Who Saved Hollywood (1976) and Frankenstein's Great Aunt Tillie (1984). She did cameos for A Nightmare on Elm Street 3: Dream Warriors (1987), The Beverly Hillbillies (1993), and A Very Brady Sequel (1996), as well as voicing a character in the animated Happily Ever After (1990). [ citation needed ] She was also a regular guest on television shows, appearing with Milton Berle , Jack Paar , Johnny Carson , Howard Stern , David Frost , Arsenio Hall , Phil Donahue , and Joan Rivers . She was a guest on the Bob Hope specials, the Dean Martin Roasts, Hollywood Squares , Rowan & Martin's Laugh-In , and It's Garry Shandling's Show . In 1968, she appeared in the role of Minerva on an episode of Batman , becoming the show's final "special guest villain" before it was cancelled. In 1973, she was the guest roastee on The Dean Martin Celebrity Roast . She appeared on Late Night with David Letterman in 1987, where she told host David Letterman about her blind date with Henry Kissinger , which was arranged by Richard Nixon . Author Gerold Frank , who helped Gabor write her autobiography in 1960, described his impressions of her: Zsa Zsa is unique. She's a woman from the court of Louis XV who has somehow managed to live in the 20th century, undamaged by the PTA ... She says she wants to be all the Pompadours and Du Barrys of history rolled into one, but she also says, "I always goof. I pay all my own bills. ... I want to choose the man. I do not permit men to choose me." In his autobiography, television host Merv Griffin , who was known to spend time with Gabor's younger sister Eva socially, wrote of the Gabor sisters' arrival in New York and Hollywood: All these years later, it's hard to describe the phenomenon of the three glamorous Gabor girls and their ubiquitous mother. They burst onto the society pages and into the gossip columns so suddenly, and with such force, it was as if they'd been dropped out of the sky. In 1998, film historian Neal Gabler called her kind of celebrity "The Zsa Zsa Factor". Gabor was married nine times. She was divorced seven times, and one marriage was annulled . She wrote in her autobiography, All in all — I love being married ... I love the companionship, I love cooking for a man (simple things like chicken soup and my special Dracula's goulash from Hungary), and spending all my time with a man. Of course I love being in love — but it is marriage that really fulfills me. But not in every case. Her husbands, in chronological order, were: Gabor's divorces inspired her to make numerous quotable puns and innuendos about her marital and extramarital history. She commented: "I am a marvelous housekeeper: Every time I leave a man I keep his house." When asked how many husbands she had had, she used to say: "You mean other than my own?" Gabor dated German composer Willy Schmidt-Gentner and Dominican diplomat Porfirio Rubirosa . She also claimed to have had a sexual encounter with her stepson, Nicky . In 1970, Gabor purchased a nearly 9,000-square-foot Hollywood Regency -style home in Bel Air . It was originally built for Howard Hughes in 1955 and featured a copper French style roof . Gabor's only child, daughter Constance Francesca Hilton , was born on March 10, 1947. According to Gabor's 1991 autobiography, One Lifetime Is Not Enough , her pregnancy resulted from rape by then-husband Conrad Hilton . She was the only Gabor sister who had a child. In 2005, a lawsuit was filed accusing Constance of larceny and fraud. She allegedly forged her mother's signature to get a US$2 million loan by using her mother's Bel Air house as collateral. However, the Los Angeles County Superior Court , Santa Monica, threw out the case due to Gabor's failure to appear in court, or to sign an affidavit that she indeed was a co-plaintiff on the original lawsuit filed by her husband, Frédéric von Anhalt. Francesca Hilton died in 2015 at the age of 67 from a stroke. Gabor's husband never told her about her daughter's death, out of concern for her physical and emotional state. Gabor and her last husband, Frédéric Prinz von Anhalt , adopted at least ten adult men who paid them a fee of up to $2 million to legally become descendants of Princess Marie-Auguste of Anhalt . Prinz von Anhalt had himself paid Marie-Auguste to adopt him when he was 36 years old. While Gabor's parents were Jewish, she was a practicing Catholic. On June 14, 1989, in Beverly Hills, California , Gabor was accused of slapping the face of Beverly Hills police officer Paul Kramer when he stopped her for a traffic violation at 8551 Olympic Boulevard . At trial three months later, a jury convicted her of slapping Kramer. They also found her guilty of driving without a license and possessing an open container of alcohol—a flask of Jack Daniel's —in her $215,000 Rolls-Royce , but acquitted her of the charge of disobeying Kramer when she drove away from the traffic stop. On October 25, 1989, Beverly Hills Municipal Judge Charles G. Rubin sentenced Gabor to serve three days in jail, to pay fines and restitution totaling $12,937, to perform 120 hours of community service, and to undergo a psychiatric evaluation. On June 14, 1990, Gabor dropped her conviction appeal and agreed to serve her sentence. However, she refused to take part in community service and served three days in jail from July 27 to July 30, 1990. Gabor had a long-running feud with German-born actress Elke Sommer , that began in 1984 when both appeared on Circus of the Stars , and escalated into a multimillion-dollar libel suit by 1993. The suit resulted in an order for Gabor and her husband to pay Sommer $3.3 million in general and punitive damages. On January 25, 2009, the Associated Press reported that her attorney stated that forensic accountants determined that Gabor may have lost as much as $10 million invested in Bernie Madoff's company, possibly through a third-party money manager. On November 27, 2002, Gabor was a front seat passenger in an automobile crash on Sunset Boulevard , Los Angeles, from which she remained partially paralyzed and reliant on a wheelchair for mobility. She survived strokes in 2005 and 2007 and underwent surgeries. In 2010, she fractured her hip and underwent a successful hip replacement. In August 2010, Gabor was admitted to Ronald Reagan UCLA Medical Center in serious condition and received last rites from a Catholic priest, but survived. In 2011, her right leg was amputated above the knee to save her life from an infection. She was hospitalized again in 2011 for a number of emergencies, and fell into a coma. On February 8, 2016, two days after her 99th birthday, Gabor was rushed to hospital after suffering from breathing difficulties. She was diagnosed with a feeding tube -related lung infection and was scheduled to undergo surgery to have her feeding tube removed. In April 2016, it was reported that Prinz von Anhalt was arranging to move with Gabor to Hungary in time for her 100th birthday in 2017, in accordance with her wishes that she return to the country and spend the rest of her life there. On June 14, 1989, in Beverly Hills, California , Gabor was accused of slapping the face of Beverly Hills police officer Paul Kramer when he stopped her for a traffic violation at 8551 Olympic Boulevard . At trial three months later, a jury convicted her of slapping Kramer. They also found her guilty of driving without a license and possessing an open container of alcohol—a flask of Jack Daniel's —in her $215,000 Rolls-Royce , but acquitted her of the charge of disobeying Kramer when she drove away from the traffic stop. On October 25, 1989, Beverly Hills Municipal Judge Charles G. Rubin sentenced Gabor to serve three days in jail, to pay fines and restitution totaling $12,937, to perform 120 hours of community service, and to undergo a psychiatric evaluation. On June 14, 1990, Gabor dropped her conviction appeal and agreed to serve her sentence. However, she refused to take part in community service and served three days in jail from July 27 to July 30, 1990. Gabor had a long-running feud with German-born actress Elke Sommer , that began in 1984 when both appeared on Circus of the Stars , and escalated into a multimillion-dollar libel suit by 1993. The suit resulted in an order for Gabor and her husband to pay Sommer $3.3 million in general and punitive damages. On January 25, 2009, the Associated Press reported that her attorney stated that forensic accountants determined that Gabor may have lost as much as $10 million invested in Bernie Madoff's company, possibly through a third-party money manager. On November 27, 2002, Gabor was a front seat passenger in an automobile crash on Sunset Boulevard , Los Angeles, from which she remained partially paralyzed and reliant on a wheelchair for mobility. She survived strokes in 2005 and 2007 and underwent surgeries. In 2010, she fractured her hip and underwent a successful hip replacement. In August 2010, Gabor was admitted to Ronald Reagan UCLA Medical Center in serious condition and received last rites from a Catholic priest, but survived. In 2011, her right leg was amputated above the knee to save her life from an infection. She was hospitalized again in 2011 for a number of emergencies, and fell into a coma. On February 8, 2016, two days after her 99th birthday, Gabor was rushed to hospital after suffering from breathing difficulties. She was diagnosed with a feeding tube -related lung infection and was scheduled to undergo surgery to have her feeding tube removed. In April 2016, it was reported that Prinz von Anhalt was arranging to move with Gabor to Hungary in time for her 100th birthday in 2017, in accordance with her wishes that she return to the country and spend the rest of her life there. While in a coma, Gabor died from cardiac arrest at Ronald Reagan UCLA Medical Center on December 18, 2016, at the age of 99. On her death certificate, coronary artery disease and cerebrovascular disease are listed as contributing causes. She had been on life support for the previous five years. Her funeral was held on December 30 in a Catholic ceremony at the Church of the Good Shepherd in Beverly Hills, where around 100 mourners attended. Her ashes, placed in a gold rectangular box, were interred at the Westwood Village Memorial Park Cemetery ; in July 2021, Prinz von Anhalt had them reinterred in the artists' section of Kerepesi Cemetery in Budapest in order to fulfil her wish to return to Hungary. He said that the remains were transported in their own first-class airline seat.

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Sári Barabás

Sári Barabás (14 March 1914 – 16 April 2012) was a Hungarian operatic soprano , particularly associated with coloratura roles. Sári Barabás was born in Budapest . She planned to be a dancer, but after an injury she turned to singing. She studied in Budapest with Frau Speckler, and made her debut at the Budapest Opera in 1939, as Gilda in Rigoletto . World War II interrupted her career. After the war, she appeared at the Zurich Opera and the Vienna Volksoper , and then joined the Munich State Opera in 1949, where she remained until 1971, she was also a guest at the Vienna State Opera , in The Barber of Seville , The Magic Flute and Capriccio , where she established a reputation as a soprano of agility and glamorous personality. [ citation needed ] She made guest appearances as Gilda , at the Royal Opera House in London in 1951, and at the Glyndebourne Festival , where she sang Konstanze in Die Entführung aus dem Serail , Adele in Le comte Ory , and Zerbinetta in Ariadne auf Naxos to great acclaim. She made her American debut at the San Francisco Opera in 1950, as the Queen of the Night in The Magic Flute . She also sang operetta , and enjoyed considerable success in London in 1970, in a revival of the musical The Great Waltz at the Theatre Royal Drury Lane, which coincided with her appearance on Desert Island Discs . Billy Mayerl had in 1958 requested to take Barabás with him to the desert island as his luxury item. Having appeared in the title role of the 1951 German film Die Dubarry , for the 1955 Powell and Pressburger musical Oh... Rosalinda!! , she sang the title role for the actress Ludmilla Tchérina (Nixa NLP 18001). She made her final stage appearance at the Gärtnerplatz in 2007, in the speaking role of Princess Anhilte in Die Csárdásfürstin . From 1956 Barabás was married to tenor Franz Klarwein (1914–1991). She died on 16 April 2012, aged 98, after suffering a stroke.

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Sari Schorr

Sari Beth Schorr is an American blues rock singer and songwriter. She has released three albums, with the most recent being a live recording issued in 2020. Schorr has worked with Mike Vernon , Walter Trout , Innes Sibun , Joe Louis Walker , Popa Chubby , Warren Haynes , Keb Mo' , Taj Mahal , Eric Burdon , Robin Trower and Carly Simon .She was born in New York , New York , United States, to a father who was a pilot in the United States Air Force , and a mother who worked as a fashion model. Through her parents love of music, as a youngster Schorr heard recordings by Ella Fitzgerald and Billie Holiday . This in turn sparked her interest to explore other female singers, such as Bessie Smith , Ma Rainey , Mamie Smith and Etta James . Schorr had her own classic singing training, both in high school and college. She was advised to pursue a career in opera, in view of her five-octave range and strength of her singing. To begin her career, Schorr worked her way around the blues clubs and nightspots of South Bronx and the Lower East Side of Manhattan , New York . She went on to progress by touring for several years, both in the US and across Europe, by working as a backing singer with Joe Louis Walker and Popa Chubby . Schorr admitted she felt comfortable in that role stating, "Part of my problem is that I have always enjoyed slipping into someone else's band and becoming a part of their family... It was very easy for me to be in a secondary role supporting someone else's musical vision". In 2013, Schorr sang back up on Popa Chubby's album, Universal Breakdown Blues . In January 2015, the veteran English record producer Mike Vernon , received a Keeping The Music Alive Award at the International Blues Challenge in Memphis, Tennessee . Later at the event Schorr performed a couple of numbers, and Vernon was so impressed with her that he offered to come out of retirement and produce her debut album. Through Vernon's connections, Schorr signed a recording contract with the British independent record label , Manhaton Records . Schorr later commented, "... the moment that I met Mike in Memphis it literally changed everything for me. I suddenly found myself in the company of someone who has such great vision and someone who knows just how to bring out the very best of all the artists that he works with without imprinting his own particular brand... Working with Mike gave me a lot more confidence". In September 2016, Schorr's debut album, A Force of Nature , produced by Vernon was released. Schorr wrote or co-wrote most of the songs on the album, although at Vernon's suggestion Schorr recorded her interpretation of the Supremes , " Stop! In the Name of Love ". Walter Trout , who had known Schorr for a number of years, agreed to contribute his guitar work on one of the tracks, which turned out to be "Work No More", which Trout himself had written. Also included on the album was Schorr's reworking of " Black Betty ". It was this song that Schorr performed at the Lead Belly Tribute Festival at Carnegie Hall in New York. Also in 2015, Schorr was inducted into the New York Blues Hall of Fame. She also made some appearances on television including on Late Night with Conan O'Brien . To tour in promotion of her debut album, Schorr put together her backing band known as The Engine Room. This included the British guitarist Innes Sibun , Kevin Jeffries on bass, Anders Olinder on keyboards and Kevin O'Rourke playing percussion. They toured across the United States and then in Europe. Dates there included an appearance on 29 August 2017 on the International Stage at the Great British R & B Festival in Colne , Lancashire , England. In 2018, Schorr released her sophomore album, Never Say Never . The tracks were recorded live to capture the energy of her live performances. Never Say Never was produced by Henning Gehrke and mixed by Tom Tapley. Most of the tracks were written by Schorr, although the title track was penned by Ian McLagan . In 2020, Schorr released her first live album, Live in Europe , again via Manhaton Records. The 12-track collection was recorded during her then recent touring obligations, and incorporated original songs from her two studio albums along with reworked versions of " Black Betty " and " I Just Want to Make Love to You ", both audience favorites. She has collaborated with others for humanitarian causes, including on " Toast to Freedom " for Amnesty International , where she worked alongside Warren Haynes , Keb' Mo' , Taj Mahal , Eric Burdon and Carly Simon . She also founded 'Matters' – a non-profit organisation. Schorr is a long distance cyclist, marathon runner and animal rights activist. She currently lives in Brooklyn , New York, with her husband and rescued pit bull triplets. Schorr performed at The Half Moon, Putney , London , on April 13, 2022. She undertook further UK gigs in 2022, at Lytham St. Annes , Troon , and in Holmfirth plus, in April 2023, in Wolverhampton . She is the featured vocalist on Robin Trower 's album, Joyful Sky , which was released on Provogue Records in October 2023.

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Šariš

Šariš is the traditional name of a region situated in northeastern Slovakia . It encompasses the territory of the former ( comitatus ) Sáros county .Sáros county was created in the 13th century from the comitatus Novi Castri (named after Novum Castrum , today Abaújvár ), which also included the territories of the later counties of Abaúj and Heves . The county's territory was situated along Torysa and upper Topľa rivers. Its area was 3,652 km 2 (1,410 sq mi) around 1910. The original seat of the county was Šariš Castle and since the 17th century, Prešov .Šariš region is one of the 21 Slovakia's official tourist regions , however, it isn't an administrative region unlike its predecessor. Today, the region is mostly in the Prešov Region , fully including Prešov , Sabinov , and Bardejov districts, and partly including Stará Ľubovňa , Kežmarok , Vranov nad Topľou , Svidník and Stropkov districts. A small part of the region is located in the Košice Region , with Košice-okolie , and very small parts of Košice I and Gelnica districts. Major towns in the region include Prešov , Bardejov and Svidník .49°00′06″N 21°14′24″E / 49.0017°N 21.2400°E / 49.0017; 21.2400 This Slovak geography article is a stub . You can help Wikipedia by expanding it .

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Tant sari

Lores Genres Institutions Awards Folk genres Devotional Classical genres Modern genres People Instruments Dance Theater Organizations People Tant sari is a traditional Bengali sari , originating from the Bengal region in the eastern part and usually used by Bengali women. Tant sari are woven from cotton threads and distinguished by its lightness and transparency. It is considered to be the most comfortable sari for the hot and humid climate in the Indian subcontinent. Under the royal guidance the tant (specially jamdani ) and muslin became famous in and around Dacca (now Dhaka , Bangladesh) and Murshidabad (now West Bengal, India ) in the Mughal era . British government tried to destroy this art to protect the textile industry of Manchester , but the tant culture managed to survive. With the division of Bengal province during the partition of 1947, some of the weavers migrated to West Bengal and continued their craftsmanship there. Thus the tant weavers are now seen in both parts of Bengal . Weaving of tant sari is famous and an age old crafting of Bengal . The craftsmen deftly weave the cotton to thread which is woven to tant sari. Two shuttles are used for this purpose. Traditionally, handlooms were used by the weavers, which have today been largely replaced by power looms to weave these saris.The typical Tant sari is characterised by a thick border and a decorative pallav, woven using a variety of floral, paisley and other artistic motifs. Some of the popular traditional motifs are: bhomra (bumble bee), tabij (amulet), rajmahal (royal palace), ardha-chandra (half moon), chandmala (garland of moons), ansh (fish scale), hathi (elephant), nilambari (blue sky), ratan chokh (gem-eyed), benki (spiral), tara (star), kalka (paisley) and phool (flower). Printed, hand-painted and embroidered patterns are also used to get a larger variety of designs. Different motifs including floral element, solar element and recently even modern art are depicted in this sari. Tant Sari comes with colourful design and borders are made thicker because it is subjected to tear easily. The traditional art of weaving jamdani , considered the best variety of tant clothing, has been enlisted by UNESCO as an Intangible Cultural Heritage of Humanity . Along with ordinary Bengali women of Bangladesh and West Bengal, many prominent Bengali female personalities also prefer to wear tant sari as their regular outfit. Bangladesh prime minister Sheikh Hasina , speaker of Bangladesh parliament Shirin Sharmin Chaudhury , West Bengal chief minister Mamata Banerjee are notable among them.It is recommended that before the first wash, tant saris should be soaked briefly in warm water mixed with rock salt, to prevent the sari from bleeding colour during subsequent washes. Washing with a mild detergent, followed by starching and then hanging them to dry in a shaded area will ensure the longevity of these cotton saris.

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Gollabhama sari

Gollabhama sari also Siddipet Gollabhama are saris made in Siddipet , Telangana , India . These cotton saris are popular for their inlay figure work and motifs . The sari received Intellectual Property Rights Protection or Geographical Indication (GI) status.

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Sambalpuri sari

A Sambalpuri sari is a traditional handwoven bandha ( ikat ) sari (locally called "sambalpuri bandha" sadhi or saree) wherein the warp and the weft are tie-dyed before weaving. It is produced in the Sambalpur , Balangir , Bargarh , Boudh and Sonepur districts of Odisha , India. The sari is a traditional female garment in the Indian subcontinent consisting of a strip of unstitched cloth ranging from four to nine meters in length that is draped over the body in various styles. Sambalpuri saris are known for their incorporation of traditional motifs like shankha (Conch), chakra (wheel), phula (flower), all of which have deep symbolism with the native Odia culture. The colours red, black and white represents Lord Kaalia (Jagannatha)'s face colour. The salient feature of these saris is the traditional craftsmanship of the 'Bandhakala'- the Tie-dye art reflected in their intricate weaves, also known as Sambalpuri " Ikkat ". In this technique, the threads are first tie-dyed and later woven into a fabric, with the entire process taking many weeks. These saris first became popular outside the state when the late Prime Minister Indira Gandhi started wearing them. In the 1980s and 1990s they became popular across India . To provide protection to the weavers practicing this art, the handloom silk saris manufactured in Sambalpur and Berhampur (Berhampur Patta) in Odisha were included in the Government of India 's Geographical Indications (GI) registry. The Sambalpuri sari is made from fabric woven on a hand-loom . Varieties of the Sambalpuri sari include Sonepuri, Pasapali, Bomkai, Barpali, and Bapta saris, which are in high demand. Most of them have been named after their places of origin and are popularly known as Pata . Paintings on Tussar saris depicting Mathura Vijay, Raslila and Ayodhya Vijay owe their origin to 'Raghurajpur patta paintings'.Baandha fabric is created using a tie-dye technique. The yarns are tied according to the desired patterns to prevent absorption of dyes, and then dyed. The yarns or set of yarns so produced is called 'Baandha'. The unique feature of this form of designing is that the designs are reflected almost identically on both sides of the fabric. Once the fabric is dyed it can never be bleached into another colour. This versatile technique enables a craftsman to weave colourful designs, patterns and images into a fabric capable of inspiring a thought or conveying a message. Traditionally, craftsmen created Baandhas with images of flora or fauna or with geometrical patterns. More recently, [ when? ] new types of Baandha depicting portrait, landscape and flower pods are being designed. It is believed that this art migrated to Western Odisha along with the Bhulia community who fled Northern India in the year 1192 AD after the fall of the Chouhan empire at the hands of the Mughals . Since then and up to the year 1925 it flourished in Western Odisha in a limited number of designs and in vegetable colours and consisted mostly of saris used by the womenfolk of the Odisha .Today the Baandha fabric is popularly known by its geographical and cultural name Sambalpuri owing to the pioneering efforts of Sri Radhashyam Meher, who brought about a radical improvement in the skills of the craftsmen and the quality of the products. Other master craftsmen who contributed to the development of Sambalpuri textiles were Padmashree Kailash Chandra Meher , Padmashree Kunja Bihari Meher , Padmashree Chatrubhuja Meher and Padmashree Krutharth Acharya , Handloom Technologist Mr. Ramkrishna Meher. Sambalpuri textiles today include furnishing materials, dress materials and saris in silk , cotton and mercerised cotton in a variety of colours and many different designs. Baandha craftsmen are also masters of the 'extra warp' and 'extra weft' style of designing which can be seen in almost all forms of Baandha textiles.

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Ilkal sari

Ilkal sari is a traditional form of sari which is a common feminine wear in India . Ilkal sari takes its name from the town of Ilkal in the Bagalkot district of Karnataka state, India . Ilkal saris are woven using cotton warp on the body and art silk warp for border and art silk warp for pallu portion of the sari. In some cases instead of art silk, pure silk is also used.Ilkal was an ancient weaving centre where the weaving seems to have started in the 8th century AD. The growth of these saris is attributed to the patronage provided by the local chieftains in and around the town of Bellary . The availability of local raw materials helped in the growth of this sari. About 20000 people in the town of Ilkal are engaged in sari-weaving. The uniqueness of sari is joining of the body warp with pallu warp with a series of loops locally called as TOPE TENI technique. The weaver will gait only 6 yards, 8 yards, 9 yards warp due to above TOPE TENI technique. KONDI Technique is used for weft through inserting 3 shuttles (ಲಾಳಿ). Pallau portion-Design: "TOPE TENI SERAGU" Normally in tope teni seragu 3 solid portions would be in red colour, and in between 2 portions in white colour. Tope Teni seragu has been regarded as a state symbol and was greatly respected during festival occasions. Traditional Borders: (i) Chikki, (ii) Gomi, (iii) Jari and (iv) Gadidadi, and modern Gayathri are unique ones in Ilkal saris - width ranging from 2.5" to 4" Border Colour Uniqueness: Red usually or Maroon dominates.The peculiar characteristic of the sari is joining the body warp with the pallu warp which is locally called as TOPE TENI. This technique is used exclusively at Ilkal. If anyone requires Ilkal sari one must prepare a warp for every sari. Warp threads for body are prepared separately. Similarly pallu warp is prepared separately either with art silk or pure silk depending upon the quality required. Thirdly border portion of warp is prepared, like the pallu warp, either art silk or pure silk and the colour used for pallu and on border will be one and the same. In general, the length of the pallu will range 16" to 27". The pallu threads and body threads are joined in loop technique, a unique method locally called TOPE TENI.The distinctive feature of Ilkal saris is the use of a form of embroidery called Kasuti . The designs used in Kasuti reflect traditional patterns like palanquins, elephants and lotuses which are embroidered onto Ilkal saris. These saris are usually 9 yards in length and the pallu of the Ilkal sari (the part worn over the shoulder) carries designs of temple towers. This pallu is usually made of red silk with white patterns. The end region of the pallu is made up of patterns of different shapes like hanige (comb), koti kammli (fort ramparts), toputenne (jowar) and rampa (mountain range). The border of the sari is very broad (4 to 6 inches) and red or maroon in colour and is made of different designs with ochre patterns. The sari is either made of cotton, or a mixture of cotton and silk or in pure silk. The colors traditionally used are pomegranate red, brilliant peacock green and parrot green. The saris that are made for bridal wear are made of a particular colour called Giri Kumukum which is associated with the sindhoor worn by the wives of the priests in this region. Types of Borders The design woven in the length wise borders are mainly three types: Gomi (more popularly known as Ilkal dadi) Paraspet (Sub-divided into chikki paras and dodd paras) Gaadi Jari Main Body design Stripes Rectangles Squares Other Differences With above broad parameters the Ilkal saris differ in matters of size, nature and quality of yarn used for different portion of sari as also colour combination and combinations of designs on the borders and main body of the sari. The beauty of Tope-teni seragu is further enhanced at times by weaving in its middle portion, yet another design known as 'Kyadgi'.Weaving of Ilkal saris is mostly an indoor activity. It is essentially a household enterprise involving active participation of female members. To weave one sari with the help of the handloom, it takes about 7 days. We can weave it with the help of the powerloom also.Ilkal traditional saris are produced mainly on pit looms with the combination of three types of different yarns namely Silk x Silk, Silk x Cotton, Art silk x Cotton. Along with the above said yarn combination totally four different traditional designs are produced - they are Chikki Paras, Gomi, Jari and recently modified traditional design Gayathri. These saris are produced in different lengths 6.00 yards, 8.00 yards, and 9.00 yards with solid as well as contrast borders. The main distinction in these saris is its attached temple type Pallav (locally called as TOPE TENI) by inter locking body warp and pallav warp using loop system and inserting weft by three shuttles using two different colours yarn by Kondi technique. A weaver requires apart from himself two others for preparatory work.

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Morad Sari

Morad Sari (born June 20, 1973) is a French-Algerian kickboxer who is most well known for being the first non thai kickboxer to become a Lumpinee Boxing Stadium champion. 2003 "Le Grand Tournoi" Tournament Winner2003 "Le Grand Tournoi" Tournament Winner

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Sari-su

Sari-su , Sary-su . Sara-su , Sarısu , Sarisu , Sarysu , or Ṣáríṣú , the name means yellow water in Turkic languages, may refer to:

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Sarı Süleyman Pasha

Sarı Süleyman Pasha ( Serbo-Croatian : Sari Sulejman-paša ; died 14 October 1687) was the grand vizier of the Ottoman Empire from 18 November 1685 to 18 September 1687. He was executed after the defeat of the Ottoman forces in the Second Battle of Mohács . In Turkish , his epithet sarı means "blond (haired)", literally "yellow".He was of Bosnian descent. Sarı Süleyman Pasha was born in Taşlıca ( Pljevlja , now Montenegro ), in the Bosnia Eyalet . He was the kdhya of Grand Vizier Ahmed Köprülü (s. 1661–1676), and later the Sultan's master of the horse . After Sarı Süleyman Pasha was appointed grand vizier, he immediately began to write desperate letters to the Great Khan of the Crimean Khanate and the pashas of Timișoara , Székesfehérvár and Osijek in order to reorganize and reinforce the battered Ottoman Army in Hungary , struggling during the Battle of Buda (1686) . Although Sarı Süleyman Pasha made several attempts to break the blockade around Buda , the city was ultimately captured by Charles V, Duke of Lorraine . Soon afterwards the Ottomans had even lost Székesfehérvár . Süleyman Pasha thereafter commanded his forces to hold what remained of the Ottoman north against their opponents and even sent Mehmet Agha to negotiate peace with Donat John Heissler at Guttentag . After the defeat at Mohács , the Ottoman army started a rebellion against the grand vizier. Suleyman Pasha, fearful that the rebellion would result in his death, escaped from the commanding position, first to Belgrade and then, rather foolishly, to Constantinople , where he took refuge at the house of an old friend, a Jew named Salomon. At the beginning of September 1687, news about his defeat and escape came to Constantinople. After Mehmed IV received this news, he proclaimed Abaza Siyavuş Pasha as the new commander of the armed forces, and, eventually, as the new grand vizier. Soon after this, Süleyman Pasha was apprehended and executed. Two months later, the sultan himself was also removed from power as the result of the defeat in the Battle of Mohács, and was replaced by sultan Süleyman II .

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Sarı Süleyman

Sarı Süleyman ("Süleyman the Blond") may refer to:

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Sari temple

7°45′41.49″S 110°28′27″E / 7.7615250°S 110.47417°E / -7.7615250; 110.47417 The Sari Temple ( Indonesian : Candi Sari ; Javanese : ꦕꦤ꧀ꦝꦶ​ꦱꦫꦶ , romanized: Candhi Sari , also known as Candi Bendan ) is an 8th-century Buddhist temple : 90 located at Dusun Bendan, Tirtomartani village, Kalasan, Sleman Regency , Special Region of Yogyakarta , Indonesia . It is located about 130 meters (430 ft) northeast of the Kalasan temple. The temple was a two-story building with wooden beams, floors, and stairs completed with windows and doors; all from organic materials which now are decayed and gone. It is suggested that the original function of this building was a vihara ( Buddhist monastery ), a dwelling place for monks . The temple's name Sari or Saré translates as "to sleep" in Javanese , which also confirms the habitation nature of the building.Historians suggested that the temple was built around the same time as the Kalasan temple. The Kalasan inscription dated 778 AD, in Pranagari script written in Sanskrit , mentions that the temple was erected by the will of Guru Sang Raja Sailendravamçatilaka (the Jewel of the Shailendra dynasty ) who succeeded in persuading Maharaja Tejapurnapana Panangkaran (in other parts of the inscription also called as Kariyana Panangkaran) to construct a holy building for the boddhisattva Tara and also build a vihara ( monastery ) for Buddhist monks from Sailendra family's realm. Panangkaran awarded the Kalara village to the Sangha (the Buddhist monastic community). Based on this inscription, Candi Sari was probably the monastery for monks who served the nearby Kalasan temple. The ruins were discovered in the early 1920s, and in 1929, an effort to reconstruct the temple began and was finished in 1930. However, it was incomplete because many parts are missing including the outer base that surrounds the temple, and the extended front room and front stairs that once projected from the east wall of the temple. The temple consists of three parts; the base, the body, and the roof. The temple has a rectangular plan, measuring 17.3 m north-south, 10 m west-east, and soaring 17 m in height. Only some parts of the base remain, the outer base stone blocks are missing. The entrance door is located on the eastern side with a gate adorned with a Kala and elephant carving. Windows surround the walls and consist of lower and upper rows. There is also a horizontal middle "belt" line around the wall, suggesting that it was a two-story-tall building. The interior consists of three rooms; the north room, central room, and south room, each measuring 3 m x 5.8 m. These three rooms are connected with doorways on the eastern side of the room along the north-south axis. On the wall of each room are found rows of extruding stone blocks that used to support wooden beams and a wooden ceiling separating the upper and lower floors. In some places, there are diagonal stones which is probably the place where there used to be a wooden stairway. The upper level was probably used by monks for meditation or worship. Some suggest the upper rooms were used as the place for monks to stay, rest, or sleep, while the lower rooms were the place for worship. In the lower rooms, there are some elevated parts where statues were once placed, but now the statues are gone. On the side walls are found niches, probably to place oil lamps. In the inner part of each window, there are holes to install wooden window bars. These rooms were topped with three horse-shoe arched niches adorned with Kala-makaras and crowned with three rows of stupas. Between these arched niches are found rain-water drainage and "jaladwara" water spouts taking the form of a giant sitting on a snake. The outer wall is richly decorated with Buddhist deities. External decorations include Tara with flowers and Bodhisattvas with musical instruments. These figures are arranged in two upper and two lower rows and placed on each side of the windows. They form a total of 36 statues: 8 on the east, north, and south sides respectively, and 12 on the west side. These Buddhist figures are usually found in the graceful position of Tribhanga , holding red or blue lotuses and displaying peaceful and serene facial expressions. Images of Kinnara-Kinnari also adorn the walls. However, unlike the common depiction of Kinnara as a heavenly creature with an upper human-shaped part and a lower bird-shaped part, the unusual image of Kinnara found on the northern wall shows a winged deity (somewhat similar to how commonly angels are portrayed). On the outer wall of the temple are found traces of plaster called vajralepa (lit: diamond plaster). The same substance is also found in the nearby Kalasan temple. The white-yellowish plaster was applied to protect the temple wall, but now the plaster has worn off.

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Sari Yarqan

Sari Yarqan ( Persian : ساري يارقان , also Romanized as Sārī Yārqān ; also known as Sari Yarghān , Sārī Yārīqān , Sārī Yārreqān , Saryargan , and Ser-i-Argan ) is a village in Goyjah Bel Rural District , in the Central District of Ahar County , East Azerbaijan Province , Iran . At the 2006 census, its population was 155, in 33 families.

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Sari-Solenzara

Sari-Solenzara ( French pronunciation: [ saʁi sɔlɛntsaʁ(a) ] ; Corsican : Sari è Sulinzara ; formerly in French : Sari-de-Porto-Vecchio , Italian : Sari di Porto Vecchio , Corsican : Sari di Portivechju ) is a commune and municipality in the French department of Corse-du-Sud , on the island of Corsica . It is delineated by several natural borders: the Tyrrhenian Sea to its east, the River Solenzara to its north, and to its west the Aiguilles de Bavella , a beautiful mountain at the heart of the island. A rural district, it essentially consists of two settlements: the larger seaside village of Solenzara, and the smaller hilltop village of Sari. Smaller outlying hamlets include Togna, Canella, Tarcu and Favona. Highly mountainous and forested, Sari-Solenzara falls partially within the Alta Rocca district of the Corsican Regional Nature Reserve .Sausage : lonzu, coppa, wild boar sausage, figatelli Chestnut paste Ewe and goat cheeses

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Wedding sari

A wedding sari is a traditional South Asian wedding dress , especially popular in South Indian states. The sari often consists of a combination of red and green, with golden brocade. Wedding saris are predominantly red, a colour associated with married women, although colours and colour combinations vary by region, caste, and religion; non- Brahmin women in Tamil Nadu wear a red-and-white checked sari as traditional wedding attire. The Padmasali wedding sari is a white sari, dyed with turmeric . Sari fabric is also traditionally silk. Over time, colour options and fabric choices for Indian brides have expanded. Today fabrics like crêpe , Georgette , tissue, and satin are used, and colours have been expanded to include gold, pink, orange, maroon, brown, and yellow as well. Indian brides in Western countries often wear a sari at the wedding ceremony and change into other traditional Indian wear afterwards such as lehenga , or cholis etc. Types of wedding saris include Kanchipuram silk sari , Banarasi wedding sari , Sambalpuri sari , Assam silk, Gota sari, Resham sari, Zardosi sari, paithani sari, Bandhani sari, Neriyathum sari, as well as Jamdani , Dhakai , Katan and Rajshahi usually in red.

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Sari-d'Orcino

Sari-d'Orcino ( Italian : Sari d'Orcino , [ saʁi dɔrtʃino ] ; Corsican : Sari d'Orcinu , Sari d'Urcinu , or Sari di Cinarca ) is a commune in the Corse-du-Sud department of France on the island of Corsica .

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Taming Sari

Taming Sari (which means "flower shield", "beautiful shield" or "the main shield" in Malay ) is a famous kris in Malay folklore . It is believed to have been wielded by the legendary Malaccan warrior Hang Tuah , and is fabled to grant physical invulnerability to its wielder.The Kris Taming Sari was said to have been made of 21 different types of metal. The whole of the sampir (upper wooden part) and batang (lower part of the wooden sheath), was covered in gold leaf . It is classified as a keris gabus (sharp ) or keris terapang (having a cross-piece or sheath covered with gold). The Malay Annals ( Malay : Sejarah Melayu ) tells that the kris was made by a Javanese blacksmith ( pandai besi ) and wielded by the champion of Majapahit , a pendekar named Taming Sari from which the weapon derives its name. It was said to be so skillfully crafted that anyone wielding it was unbeatable. In some versions of the legend, the weapon was imbued with an enchantment that would make its user physically invulnerable. The Malaccan admiral Hang Tuah eventually won it in a duel to the death after which Singhavikramavardhana, the king of Majapahit presented the weapon to the victor. Later when Hang Tuah failed to bring back the princess from Mount Ledang , he gave the kris to Tun Mamat to be returned to Sultan Mahmud Shah . Hang Tuah then disappeared and was never seen or heard of again. Another version of the legend has it that Hang Tuah threw the dagger into the river, saying that he would return when the kris re-appeared. The Kris Taming Sari is said to have mystical powers such as hovering in the air during times of crisis or leaping out of its sheathe to fight on behalf of its wielder.When Malacca was captured by the Portuguese in 1511, Sultan Mahmud retreated to Kampar in Sumatra , bringing all of Malacca 's state regalia. He passed the weapon along with the other royal regalia to his son Muzaffar Shah who later became the ruler of Perak . It is still kept in the palace of his descendant Sultan Nazrin Muizzuddin Shah , and is today still part of the state's royal regalia. Before Taming Sari became part of the Perak royalty's regalia, it is believed to have been a hereditary article of the family of the laksamana (admiral) who for generations, through succession, ruled as the territorial chief of Hilir Perak . It is believed that the last territorial chief who had the famed kris in his possession was Laksamana Mohd Amin Alang Duakap. In 1876, he was arrested alongside many other aristocrats of his time for the alleged involvement in the murder of the first British Resident , James W.W. Birch . Together with Datuk Shahbandar Uda Kediti (the territorial chief of Kerian), Sultan Abdullah (the reigning Perak monarch of the time) and Menteri Paduka Ngah Ibrahim (the administrator of tin-rich Larut ), Laksamana Mohd Amin was banished to the Seychelles .

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