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Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Hantavirus_hemorrhagic_fever_with_renal_syndrome/html
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".
646
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/West_Nile_fever/html
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.
4,492
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Hantavirus_pulmonary_syndrome/html
Hantavirus pulmonary syndrome
Hantavirus pulmonary syndrome ( HPS ) is one of two potentially fatal syndromes of zoonotic origin caused by species of hantavirus . These include Black Creek Canal virus (BCCV), New York orthohantavirus (NYV), Monongahela virus (MGLV), Sin Nombre orthohantavirus (SNV), and certain other members of hantavirus genera that are native to the United States and Canada. Specific rodents are the principal hosts of the hantaviruses including the hispid cotton rat ( Sigmodon hispidus ) in southern Florida , which is the principal host of Black Creek Canal virus. The deer mouse ( Peromyscus maniculatus ) in Canada and the Western United States is the principal host of Sin Nombre virus . The white-footed mouse ( Peromyscus leucopus ) in the eastern United States is the principal host of New York virus. In South America , the long-tailed mouse ( Oligoryzomys longicaudatus ) and other species of the genus Oligoryzomys have been documented as the reservoir for Andes virus . Initially, HPS has an incubation phase of 2–4 weeks, in which patients remain asymptomatic. Subsequently, patients can experience 3–5 days of flu-like prodromal phase symptoms, including fever , cough, muscle pain , headache, lethargy, shortness of breath , nausea, vomiting and diarrhea. In the following 5–7 day cardiopulmonary phase, the patient's condition rapidly deteriorates into acute respiratory failure , characterized by the sudden onset of shortness of breath with rapidly evolving pulmonary edema , as well as cardiac failure , with hypotension, tachycardia and shock. In this phase, patients may develop acute respiratory distress syndrome . It is often fatal despite mechanical ventilation and intervention with diuretics . [ citation needed ] After the cardiopulmonary phase, patients can enter a diuretic phase of 2–3 days characterized by symptom improvement and diuresis . Subsequent convalescence can last months to years. As of 2017, patient mortality in the US from HPS is 36%. The virus can be transmitted to humans by a direct bite or inhalation of aerosolized virus, shed from stool, urine, or saliva from a natural reservoir rodent. In general, droplet and/or fomite transfer has not been shown in the hantaviruses in either the pulmonary or hemorrhagic forms. The preferred method for diagnosis of Hantavirus Pulmonary Syndrome is serological testing which identifies both acute (IgM) and remote infections (IgG); however, PCR may also be used to identify early infections. Rodent control in and around the home or dwellings remains the primary prevention strategy, as well as eliminating contact with rodents in the workplace and at campsites. Closed storage sheds and cabins are often ideal sites for rodent infestations. Airing out of such spaces prior to use is recommended. People are advised to avoid direct contact with rodent droppings and wear a mask while cleaning such areas to avoid inhalation of aerosolized rodent secretions. There is no cure or vaccine for HPS. Treatment involves supportive therapy, including mechanical ventilation with supplemental oxygen during the critical respiratory-failure stage of the illness. Although ribavirin can be used to treat hantavirus infections, it is not recommended as a treatment for HPS due to unclear clinical efficacy and likelihood of medication side effects. Early recognition of HPS and admission to an intensive care setting offers the best prognosis . Hantavirus pulmonary syndrome was first recognized during the 1993 outbreak in the Four Corners region of the southwestern United States . It was identified by Dr. Bruce Tempest. It was originally called Four Corners disease , but the name was changed to Sin Nombre virus after complaints by Native Americans that the name "Four Corners" stigmatized the region. It has since been identified throughout the United States. [ citation needed ]
604
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Biological_hazard/html
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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Ross_River_fever/html
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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Oropouche_orthobunyavirus/html
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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Nipah_virus/html
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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Redeemer's_University_Nigeria/html
Redeemer's University Nigeria
Redeemer's University is a private university in Ede , Osun State , Nigeria. Established in 2005, it is owned by the Redeemed Christian Church of God and situated off the Ibadan-Osogbo Road.The university was founded by the Redeemed Christian Church of God in 2005. Headed by the General Overseer, Pastor Enoch Adeboye , a PhD holder in applied mathematics. The Federal Government of Nigeria granted an operating license to the Redeemer's University on 7 January 2005. In order to realize its dream, the Redeemed Christian Church of God , the Proprietors of the university, initially acquired a large expanse of land in Ede, Osun state, having obtained the Certificate of Statutory Right of Occupancy in 1997. The site of the university covers an area of about 812 hectares (2,010 acres) . The university took off at the temporary site in the Redemption Camp on 11 October 2005 with 4 78 students admitted into three colleges. On 1 February 2006, 473 students matriculated into the colleges to pursue bachelor's degrees in various programmes, and the university has produced 13 sets of graduates. Below is the list of vice-chancellors, from inception:Below is the list of vice-chancellors, from inception:Redeemer's University provides on-campus accommodations for its students. It offers rooms designed to accommodate three students. Undergraduate students at the University reside in the halls of residence, located on campus. The hall of residence is divided into two: Queen Esther Hall for female students and Prophet Moses Hall for male students. Undergraduate students at the University reside in the halls of residence, located on campus. The hall of residence is divided into two: Queen Esther Hall for female students and Prophet Moses Hall for male students. In 2013, the university won a World Bank Grant to fund the establishment of the African Centre of Excellence for Genomics of Infectious Diseases (ACEGID).In 2013, the university won a World Bank Grant to fund the establishment of the African Centre of Excellence for Genomics of Infectious Diseases (ACEGID). To win the grant, Redeemer's University entered a competition with 15 prestigious universities selected from West and Central Africa and after a rigorous exercise and based on the quality of work exhibited in her proposal, the university was awarded the grant which gave birth to the centre. It is a World Bank funded collaborative research center. The partners are West African academic and medical institutions (Redeemer's University, University of Ibadan , Irrua Specialist Teaching Hospital in Nigeria, University of Sierra Leone , Kenema Government Hospital in Sierra Leone and Universite Cheik Anta-Diop de Dakar). ACEGID has a mandate to build capacity in the field of genomics in young African scientists and identify and characterize pathogens of unknown origin using microbial metagenomics . Ultimately, the project aims to translate the research outcome into products that can be deployed to the field to contribute to the control, management and elimination of infectious diseases in the African continent. The university runs both undergraduate and postgraduate programmes. Undergraduate programmes started at inception in 2005 with three colleges . They were the College of Natural Sciences, College of Management and Social Sciences and College of Humanities. In the 2012–2013 academic year, the university admitted its first set of M.A., M.Sc., and PhD. students. So far, the university has produced 12 sets of graduates as of November 2020. In the 2019/2020 Academic Session, the university changed from the Collegiate system to the Faculty system. Also in that academic year, the university added two new Faculties, namely the Faculty of Engineering and the Faculty of Environmental Sciences. Earlier in 2017/2018, the university commenced the Faculty of Law and the Faculty of Basic Medical Sciences. Redeemer's University has received notable recognition and awards for its contributions to academia , research, and community engagement.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Fever_hospital/html
Fever hospital
A fever hospital or isolation hospital is a hospital for infectious diseases such as Scarlet fever , Tuberculosis , Lassa fever and Smallpox . Their purpose is to treat affected people while isolating them from the general population. Early examples included the Liverpool Fever Hospital (1801) and the London Fever Hospital (1802). : 13 Other examples occurred elsewhere in the British Isles and India. The hospitals became common in England when laws were passed at the end of the 19th century, requiring notification of infectious diseases so that public health officers could ensure that the patients were isolated. During the 20th century, immunisation and antibiotics reduced the impact of these diseases. After the introduction of the National Health Service in 1948, the hospitals were wound down so that, by 1968, there were few left. : 27 As a result of the COVID-19 pandemic a number of temporary isolation wards within existing hospitals were established as well as several temporary hospitals, such as the nightingale hospitals in England which were little used in many countries with the notable exception of China. It has been suggested that creating modern isolation hospitals might be an effective way of managing highly infectious diseases as was shown in China during the COVID-19 pandemic. however the lack of staff to operate these facilities, the large costs for no ongoing direct patient benefit and the inability to use other hospital facilities to provide care for patients have been cited as the key reasons why fever hospitals are not appropriate in modern healthcare. The first hospital specifically for smallpox was the London Smallpox Hospital , founded in 1741. The first specialist hospital for other infectious diseases was the Liverpool Fever Hospital which was founded in 1801. Fever hospitals or "houses of recovery" were then established in other major cities – Chester, Hull, London, Manchester , Newcastle upon Tyne and Norwich. These were mainly for the treatment of typhus which was common. By 1879, isolation hospitals of some sort were established in 296 local authorities, out of a total of 1,593 – about 18.5%. As the germ theory of disease and nature of infection became established, more fever hospitals were established so that, by 1914, they were the most common sort of hospital. : 20 The numbers and sizes of the different sort of institutions at that time were : 20 After the London Fever Hospital was established in 1802, six more hospitals were established in London by the Metropolitan Asylums Board . These were designed with two separate buildings – one for smallpox patients and one for sufferers from other infectious diseases: cholera , diphtheria , dysentery , measles , scarlet fever , typhoid fever , typhus and whooping cough . : 23 In London, there were protests and legal action against fever hospitals by residents who were concerned about the risk of infection. Precautions were taken, such as disinfection of ambulances, but it was found that the incidence of smallpox increased near smallpox hospitals. Siting of the hospitals next to rivers, so that transport of patients could be limited to ambulance steamers was found to reduce this. Ships, moored on the Thames at Long Reach , were also used as isolation hospitals. The UK Infectious Disease (Notification) Act 1889 ( 52 & 53 Vict. c. 72) required that local authorities be notified of the occurrence of such infectious diseases. The medical officer of health was then empowered to isolate the patients to prevent spreading. Well-to-do patients could be isolated at home but poorer people lacked the facilities and space for this. The requirement for isolation thus drove the need for provision of hospitals for this purpose. These measures were compulsory in the London area and were made compulsory in the rest of the country by a similar act of 1899. Cross-infection was a significant issue because patients with different diseases might be put in the same ward and share facilities such as towels. Isolation hospitals were then criticised as places "where a person goes in with one infectious disease and catches all the rest." : 4 Patients returning from such hospitals might then spread the acquired infections to members of their families. These were called return cases and they could result in complaints and lawsuits. A major difficulty was a lack of understanding of scarlet fever, which was the most common disease at that time. The nature of the disease and how it was transmitted was uncertain. To prevent return cases, hospitals tried extending the period of isolation and giving patients disinfectant washes with formalin or Lysol when discharging them. The UK Infectious Disease (Notification) Act 1889 ( 52 & 53 Vict. c. 72) required that local authorities be notified of the occurrence of such infectious diseases. The medical officer of health was then empowered to isolate the patients to prevent spreading. Well-to-do patients could be isolated at home but poorer people lacked the facilities and space for this. The requirement for isolation thus drove the need for provision of hospitals for this purpose. These measures were compulsory in the London area and were made compulsory in the rest of the country by a similar act of 1899. Cross-infection was a significant issue because patients with different diseases might be put in the same ward and share facilities such as towels. Isolation hospitals were then criticised as places "where a person goes in with one infectious disease and catches all the rest." : 4 Patients returning from such hospitals might then spread the acquired infections to members of their families. These were called return cases and they could result in complaints and lawsuits. A major difficulty was a lack of understanding of scarlet fever, which was the most common disease at that time. The nature of the disease and how it was transmitted was uncertain. To prevent return cases, hospitals tried extending the period of isolation and giving patients disinfectant washes with formalin or Lysol when discharging them.
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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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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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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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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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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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Omsk hemorrhagic fever
Omsk hemorrhagic fever is a viral hemorrhagic fever caused by a Flavivirus . It was found in Siberia and was named for an outbreak in the city of Omsk . First records of the new virus appeared around 1940–1943.There are a number of symptoms of the virus. In the first 1–8 days the first phase begins. The symptoms in this phase are: In 1–2 weeks, some people may recover, although others might not. They might experience a focal hemorrhage in mucosa of gingival, uterus , and lungs , a papulovesicular rash on the soft palate, cervical lymphadenopathy (it occurs in the neck which that enlarges the lymph glandular tissue), and occasional neurological involvement. If the patient still has OHF after 3 weeks, then a second wave of symptoms will occur. It also includes signs of encephalitis. In most cases if the sickness does not fade away after this period, the patient will die. Patients that recover from OHF may experience hearing loss, hair loss, and behavioral or psychological difficulties associated with neurological conditions.Omsk haemorrhagic fever virus , Orthoflavivirus omskense Omsk hemorrhagic fever is caused by Omsk hemorrhagic fever virus (OHFV), a member of the Flavivirus family. The current species name is Orthoflavivirus omskense according to International Committee on Taxonomy of Viruses taxonomy standards. The virus was discovered by Mikhail Chumakov and his colleagues between 1945 and 1947 in Omsk , Russia . The infection is found in Western Siberia , in places including Omsk Oblast , Novosibirsk Oblast , Kurgan Oblast , Tyumen Oblast . The virus survives in water and is transferred to humans via contaminated water or an infected tick. The main hosts of OHFV are rodents like the non-native muskrat . OHFV originates in ticks, who then transmit it to rodents by biting them. Humans become infected through tick bites or contact with a muskrat. Humans can also become infected through contact with blood , feces or urine of a dead or sick muskrat (or any type of rat). The virus can also spread through milk from infected goats or sheep. There is no evidence that the virus is contagious among humans. The virus appears to have evolved within the last 1000 years. The viral genomes can be divided into 2 clades—A and B. Clade A has five genotypes and clade B has one. These clades separated about 700 years ago. This separation appears to have occurred in the Kurgan province. Clade A subsequently underwent division into clade C, D and E 230 years ago. Clade C and E appear to have originated in the Novosibirsk and Omsk Provinces respectively. The muskrat Ondatra zibethicus which is highly susceptible to this virus was introduced into this area in the 1930s.The main hosts of OHFV are rodents like the non-native muskrat . OHFV originates in ticks, who then transmit it to rodents by biting them. Humans become infected through tick bites or contact with a muskrat. Humans can also become infected through contact with blood , feces or urine of a dead or sick muskrat (or any type of rat). The virus can also spread through milk from infected goats or sheep. There is no evidence that the virus is contagious among humans.The virus appears to have evolved within the last 1000 years. The viral genomes can be divided into 2 clades—A and B. Clade A has five genotypes and clade B has one. These clades separated about 700 years ago. This separation appears to have occurred in the Kurgan province. Clade A subsequently underwent division into clade C, D and E 230 years ago. Clade C and E appear to have originated in the Novosibirsk and Omsk Provinces respectively. The muskrat Ondatra zibethicus which is highly susceptible to this virus was introduced into this area in the 1930s.Omsk Hemorrhagic Fever could be diagnosed by isolating virus from blood, or by serologic testing using immunosorbent serological assay. OHF rating of fatality is 0.5–3%. Treatment is supportive; there is no specific treatment for OHF. This helps maintain hydration and provides precautions for patients with bleeding disorders.Preventing Omsk Hemorrhagic Fever consists primarily in avoiding being exposed to tick . Persons engaged in camping, farming, forestry, hunting (especially the Siberian muskrat ) are at greater risk and should wear protective clothing or use insect repellent for protection. The same is generally recommended for persons at sheltered locations.
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Fati Niger
Binta Labaran (professionally known as Fati Niger ) is a Nigerien singer and actress who has earned the title "Gimbiyar Mawakan Hausa" (translated to "Princess of Hausa music " ). She was born and bought up in Maradi, Niger where she had her Quranic education before moving to Nigeria to pursue her singing career. Fati Niger has produced 4 albums with over 500 songs to her credit. She is from the Hausa ethnic group. Fati Niger was born and bought up in Maradi, Niger . Growing up, she has always had a passion for singing especially traditional Hausa songs which are mostly sung during a full moon night among the youngsters in Hausa Villages. After visiting her sister in 2004 in Nigeria, she discovered a thriving music industry in the city of Kano . There, she sought her sister's advice and consent before recording her first song at the studio of Ali Baba in the city of Kano . Fati has produced 4 albums and over 500 songs. She has also appeared in various Hausa Kannywood movies. Fati Nijar, she is famous for many movie songs, political and party songs. Her song 'Girma-Girma',(in English; God is greater -God is greater) raised her status where she became famous and known around the world. Fati Nijar, she is famous for many movie songs, political and party songs. Her song 'Girma-Girma',(in English; God is greater -God is greater) raised her status where she became famous and known around the world.
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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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College of Medicine, University of Lagos
College of Medicine, University of Lagos (CMUL) also known as Medilag is the medical school affiliated with the University of Lagos . It is located in Idi-Araba, Lagos beside its sister institution, the Lagos University Teaching Hospital . The college has a total staff of 1,850 in 32 departments. The college of medicine was established on 13 April 1962 by an act of the Federal Parliament within the University of Lagos to train professionals in medicine, dentistry and other health-allied fields. The first batch of 28 medical students were admitted into the college in October 1962 and they received their first lectures on October 3, 1962. The college has 3 faculties including: Faculty of Basic Medical Sciences Faculty of Clinical Sciences Faculty of Dental Sciences The degrees awarded include: Bachelor of Medicine, Bachelor of Surgery (MB;BS) Bachelor of Dental Surgery (BDS) Bachelor of Pharmacy (BPharm) Bachelor of Science, Physiotherapy (BSc. Physio) Bachelor of Nursing Science (BN.Sc) Bachelor of Science, Physiology (BSc. Physiology) Bachelor of Science, Pharmacology (BSc. Pharmacology) Bachelor of Science, Medical Radiography (BSc. Radiography) Bachelor of Medical Laboratory Science (BMLS) The college also offers postgraduate training in Anatomy, Physiology, Biochemistry, Microbiology and Public Health.The college is involved in research including research on HIV/AIDS , malaria, MDR Tuberculosis, Lassa fever and so on. It has a Central Research Laboratory (CRC) that serves as a research hub. It also has a research ethics committee which approves all research. It has ongoing collaborations with WHO/TDR , CDC , Hospital for Tropical Diseases [HTD], Australia Army Malaria Institute, Foundation for Innovative New Diagnostics (FIND), Geneva, Family Health International (FHI), Harvard/APINS and Volkswagen Stifung Foundation, Germany on issues relating to malaria, HIV/AIDS, Lassa fever, Tuberculosis and so on. Prof. Tolu Olukayode Odugbemi Prof. Folashade Ogunsola Jemima Osunde Fola David Dr. Sylvan Ebigwei , medical doctor and dental surgeon
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Lisa Hensley (microbiologist)
Lisa Ellen Hensley is the associate director of science at the Office of the Chief Scientist, National Institute of Allergy and Infectious Disease Integrated Research Facility in Frederick, Maryland. She was previously a civilian microbiologist in the virology division of the United States Army Medical Research Institute of Infectious Diseases (USAMRIID). Hensley is one of the premier researchers of some of the world's most dangerous infections, including Ebola hemorrhagic fever , Lassa fever , the coronavirus diseases Severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), and smallpox . She has been involved in research uncovering critical mechanisms in the pathogenesis of hemorrhagic fever viruses, and has used those discoveries to develop candidate therapeutic drugs for their treatment. Hensley is a native of Winston-Salem, North Carolina . Before working with USAMRIID, she worked as a staff fellow at the National Institute of Diabetes and Digestive and Kidney Diseases , part of the National Institutes of Health (NIH). She also held graduate teaching and research posts at the University of North Carolina at Chapel Hill , where she achieved her PhD (advisor Ralph S. Baric ), and at Duke University Medical Center in Durham, North Carolina. Hensley joined USAMRIID in 1998 as a research associate in the Pathology Division. She has co-authored over 180 publications in peer-reviewed scientific journals on a variety of infectious disease topics. She now serves as the Chief of Viral Therapeutics, Virology Division at USAMRIID. A 2006 Lancet article co-authored by Hensley published results on progress for treatment of Marburg virus , a severe hemorrhagic virus with potential utility as a biological weapon. The study tested the efficacy of a new post-exposure vaccine for Marburg using a rhesus macaque model. It found that rhesus monkeys exposed to the vaccine survived a high-dose lethal challenge of Marburg for at least 80 days, while the control monkeys died after day 12. A co-authored 2005 paper in PLOS Medicine reviewed the development of a vaccine for Lassa fever , for which there are currently no vaccines licensed. Their trial vaccine elicited a protective immune response in nonhuman primates, and when infected with Lassa, they showed no evidence of clinical disease. Hensley is the subject of a chapter in journalist Richard Preston 's 2002 book Demon in the Freezer , which covers the history of smallpox eradication and the current debates over remaining smallpox stocks. In Chapter 5, "A Woman With a Peaceful Life", Preston recounts Hensley's beginnings as a researcher with USAMRIID and her eventual recruitment to the CDC to collaborate on smallpox research. Hensley was part of the team responsible for the first nonhuman smallpox infection (in monkeys), proving the potential for continued live-animal smallpox research. Some would argue [ who? ] that the experiment's success bolsters the argument of "retentionists", who oppose elimination of smallpox stores largely so that they can continue to be researched. In 2007, Hensley was recognized as one of the year's " Ten Outstanding Young Americans " (TOYA) by the United States Junior Chamber (Jaycees). The award honors Americans ages 18–40 who "exemplify the best attributes of the nation's young people". In 2008, she was selected as one of the year's Ten Outstanding Young Persons of the world (" TOYP ") by JCI ( Junior Chamber International ). Similar to the TOYA award, this program recognizes young people who excel in their chosen fields and exemplify the best attributes of the world's young people.Daddario-DiCaprio, Kathleen M. "Postexposure protection against Marburg haemorrhagic fever with recombinant vesicular stomatitis virus vectors in non-human primates: an efficacy assessment". The Lancet 367.9520 (2006): 1399-1404 Civilian Personnel Online. " Army Civilians Profile of the Month: Oct 2007 Profile of the Month—Dr. Lisa Hensley. " Accessed 13 Jan 2014. Preston, Richard. Demon in the Freezer. New York, NY: Random House, 2002.
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History of virology
The history of virology – the scientific study of viruses and the infections they cause – began in the closing years of the 19th century. Although Edward Jenner and Louis Pasteur developed the first vaccines to protect against viral infections, they did not know that viruses existed. The first evidence of the existence of viruses came from experiments with filters that had pores small enough to retain bacteria. In 1892, Dmitri Ivanovsky used one of these filters to show that sap from a diseased tobacco plant remained infectious to healthy tobacco plants despite having been filtered. Martinus Beijerinck called the filtered, infectious substance a "virus" and this discovery is considered to be the beginning of virology . The subsequent discovery and partial characterization of bacteriophages by Frederick Twort and Félix d'Herelle further catalyzed the field, and by the early 20th century many viruses had been discovered. In 1926, Thomas Milton Rivers defined viruses as obligate parasites. Viruses were demonstrated to be particles, rather than a fluid, by Wendell Meredith Stanley , and the invention of the electron microscope in 1931 allowed their complex structures to be visualised.Despite his other successes, Louis Pasteur (1822–1895) was unable to find a causative agent for rabies and speculated about a pathogen too small to be detected using a microscope. In 1884, the French microbiologist Charles Chamberland (1851–1931) invented a filter – known today as the Chamberland filter – that had pores smaller than bacteria. Thus, he could pass a solution containing bacteria through the filter and completely remove them from the solution. In 1876, Adolf Mayer , who directed the Agricultural Experimental Station in Wageningen , was the first to show that what he called "Tobacco Mosaic Disease" was infectious. He thought that it was caused by either a toxin or a very small bacterium. Later, in 1892, the Russian biologist Dmitry Ivanovsky (1864–1920) used a Chamberland filter to study what is now known as the tobacco mosaic virus . His experiments showed that crushed leaf extracts from infected tobacco plants remain infectious after filtration. Ivanovsky suggested the infection might be caused by a toxin produced by bacteria, but did not pursue the idea. In 1898, the Dutch microbiologist Martinus Beijerinck (1851–1931), a microbiology teacher at the Agricultural School in Wageningen repeated experiments by Adolf Mayer and became convinced that filtrate contained a new form of infectious agent. He observed that the agent multiplied only in cells that were dividing and he called it a contagium vivum fluidum (soluble living germ) and re-introduced the word virus . Beijerinck maintained that viruses were liquid in nature, a theory later discredited by the American biochemist and virologist Wendell Meredith Stanley (1904–1971), who proved that they were in fact, particles. In the same year, 1898, Friedrich Loeffler (1852–1915) and Paul Frosch (1860–1928) passed the first animal virus through a similar filter and discovered the cause of foot-and-mouth disease . The first human virus to be identified was the yellow fever virus . In 1881, Carlos Finlay (1833–1915), a Cuban physician, first conducted and published research that indicated that mosquitoes were carrying the cause of yellow fever, a theory proved in 1900 by commission headed by Walter Reed (1851–1902). During 1901 and 1902, William Crawford Gorgas (1854–1920) organised the destruction of the mosquitoes' breeding habitats in Cuba, which dramatically reduced the prevalence of the disease. Gorgas later organised the elimination of the mosquitoes from Panama, which allowed the Panama Canal to be opened in 1914. The virus was finally isolated by Max Theiler (1899–1972) in 1932 who went on to develop a successful vaccine. By 1928 enough was known about viruses to enable the publication of Filterable Viruses , a collection of essays covering all known viruses edited by Thomas Milton Rivers (1888–1962). Rivers, a survivor of typhoid fever contracted at the age of twelve, went on to have a distinguished career in virology. In 1926, he was invited to speak at a meeting organised by the Society of American Bacteriology where he said for the first time, "Viruses appear to be obligate parasites in the sense that their reproduction is dependent on living cells." The notion that viruses were particles was not considered unnatural and fitted in nicely with the germ theory . It is assumed that Dr. J. Buist of Edinburgh was the first person to see virus particles in 1886, when he reported seeing "micrococci" in vaccine lymph, though he had probably observed clumps of vaccinia . In the years that followed, as optical microscopes were improved "inclusion bodies" were seen in many virus-infected cells, but these aggregates of virus particles were still too small to reveal any detailed structure. It was not until the invention of the electron microscope in 1931 by the German engineers Ernst Ruska (1906–1988) and Max Knoll (1887–1969), that virus particles, especially bacteriophages , were shown to have complex structures. The sizes of viruses determined using this new microscope fitted in well with those estimated by filtration experiments. Viruses were expected to be small, but the range of sizes came as a surprise. Some were only a little smaller than the smallest known bacteria, and the smaller viruses were of similar sizes to complex organic molecules. In 1935, Wendell Stanley examined the tobacco mosaic virus and found it was mostly made of protein. In 1939, Stanley and Max Lauffer (1914) separated the virus into protein and nucleic acid , which was shown by Stanley's postdoctoral fellow Hubert S. Loring to be specifically RNA . The discovery of RNA in the particles was important because in 1928, Fred Griffith ( c. 1879 –1941) provided the first evidence that its "cousin", DNA , formed genes . In Pasteur's day, and for many years after his death, the word "virus" was used to describe any cause of infectious disease. Many bacteriologists soon discovered the cause of numerous infections. However, some infections remained, many of them horrendous, for which no bacterial cause could be found. These agents were invisible and could only be grown in living animals. The discovery of viruses paved the way to understanding these mysterious infections. And, although Koch's postulates could not be fulfilled for many of these infections, this did not stop the pioneer virologists from looking for viruses in infections for which no other cause could be found. Bacteriophages are the viruses that infect and replicate in bacteria. They were discovered in the early 20th century, by the English bacteriologist Frederick Twort (1877–1950). But before this time, in 1896, the bacteriologist Ernest Hanbury Hankin (1865–1939) reported that something in the waters of the River Ganges could kill Vibrio cholerae – the cause of cholera . The agent in the water could be passed through filters that remove bacteria but was destroyed by boiling. Twort discovered the action of bacteriophages on staphylococci bacteria. He noticed that when grown on nutrient agar some colonies of the bacteria became watery. He collected some of these watery colonies and passed them through a Chamberland filter to remove the bacteria and discovered that when the filtrate was added to fresh cultures of bacteria, they in turn became watery. He proposed that the agent might be "an amoeba, an ultramicroscopic virus, a living protoplasm, or an enzyme with the power of growth". Félix d'Herelle (1873–1949) was a mainly self-taught French-Canadian microbiologist. In 1917 he discovered that "an invisible antagonist", when added to bacteria on agar , would produce areas of dead bacteria. The antagonist, now known to be a bacteriophage, could pass through a Chamberland filter. He accurately diluted a suspension of these viruses and discovered that the highest dilutions (lowest virus concentrations), rather than killing all the bacteria, formed discrete areas of dead organisms. Counting these areas and multiplying by the dilution factor allowed him to calculate the number of viruses in the original suspension. He realised that he had discovered a new form of virus and later coined the term "bacteriophage". Between 1918 and 1921 d'Herelle discovered different types of bacteriophages that could infect several other species of bacteria including Vibrio cholerae . Bacteriophages were heralded as a potential treatment for diseases such as typhoid and cholera , but their promise was forgotten with the development of penicillin . Since the early 1970s, bacteria have continued to develop resistance to antibiotics such as penicillin , and this has led to a renewed interest in the use of bacteriophages to treat serious infections . D'Herelle travelled widely to promote the use of bacteriophages in the treatment of bacterial infections. In 1928, he became professor of biology at Yale and founded several research institutes. He was convinced that bacteriophages were viruses despite opposition from established bacteriologists such as the Nobel Prize winner Jules Bordet (1870–1961). Bordet argued that bacteriophages were not viruses but just enzymes released from "lysogenic" bacteria. He said "the invisible world of d'Herelle does not exist". But in the 1930s, the proof that bacteriophages were viruses was provided by Christopher Andrewes (1896–1988) and others. They showed that these viruses differed in size and in their chemical and serological properties. In 1940, the first electron micrograph of a bacteriophage was published and this silenced sceptics who had argued that bacteriophages were relatively simple enzymes and not viruses. Numerous other types of bacteriophages were quickly discovered and were shown to infect bacteria wherever they are found. Early research was interrupted by World War II . d'Herelle, despite his Canadian citizenship, was interned by the Vichy Government until the end of the war. Knowledge of bacteriophages increased in the 1940s following the formation of the Phage Group by scientists throughout the US. Among the members were Max Delbrück (1906–1981) who founded a course on bacteriophages at Cold Spring Harbor Laboratory . Other key members of the Phage Group included Salvador Luria (1912–1991) and Alfred Hershey (1908–1997). During the 1950s, Hershey and Chase made important discoveries on the replication of DNA during their studies on a bacteriophage called T2 . Together with Delbruck they were jointly awarded the 1969 Nobel Prize in Physiology or Medicine "for their discoveries concerning the replication mechanism and the genetic structure of viruses". Since then, the study of bacteriophages has provided insights into the switching on and off of genes, and a useful mechanism for introducing foreign genes into bacteria and many other fundamental mechanisms of molecular biology . Bacteriophages are the viruses that infect and replicate in bacteria. They were discovered in the early 20th century, by the English bacteriologist Frederick Twort (1877–1950). But before this time, in 1896, the bacteriologist Ernest Hanbury Hankin (1865–1939) reported that something in the waters of the River Ganges could kill Vibrio cholerae – the cause of cholera . The agent in the water could be passed through filters that remove bacteria but was destroyed by boiling. Twort discovered the action of bacteriophages on staphylococci bacteria. He noticed that when grown on nutrient agar some colonies of the bacteria became watery. He collected some of these watery colonies and passed them through a Chamberland filter to remove the bacteria and discovered that when the filtrate was added to fresh cultures of bacteria, they in turn became watery. He proposed that the agent might be "an amoeba, an ultramicroscopic virus, a living protoplasm, or an enzyme with the power of growth". Félix d'Herelle (1873–1949) was a mainly self-taught French-Canadian microbiologist. In 1917 he discovered that "an invisible antagonist", when added to bacteria on agar , would produce areas of dead bacteria. The antagonist, now known to be a bacteriophage, could pass through a Chamberland filter. He accurately diluted a suspension of these viruses and discovered that the highest dilutions (lowest virus concentrations), rather than killing all the bacteria, formed discrete areas of dead organisms. Counting these areas and multiplying by the dilution factor allowed him to calculate the number of viruses in the original suspension. He realised that he had discovered a new form of virus and later coined the term "bacteriophage". Between 1918 and 1921 d'Herelle discovered different types of bacteriophages that could infect several other species of bacteria including Vibrio cholerae . Bacteriophages were heralded as a potential treatment for diseases such as typhoid and cholera , but their promise was forgotten with the development of penicillin . Since the early 1970s, bacteria have continued to develop resistance to antibiotics such as penicillin , and this has led to a renewed interest in the use of bacteriophages to treat serious infections . D'Herelle travelled widely to promote the use of bacteriophages in the treatment of bacterial infections. In 1928, he became professor of biology at Yale and founded several research institutes. He was convinced that bacteriophages were viruses despite opposition from established bacteriologists such as the Nobel Prize winner Jules Bordet (1870–1961). Bordet argued that bacteriophages were not viruses but just enzymes released from "lysogenic" bacteria. He said "the invisible world of d'Herelle does not exist". But in the 1930s, the proof that bacteriophages were viruses was provided by Christopher Andrewes (1896–1988) and others. They showed that these viruses differed in size and in their chemical and serological properties. In 1940, the first electron micrograph of a bacteriophage was published and this silenced sceptics who had argued that bacteriophages were relatively simple enzymes and not viruses. Numerous other types of bacteriophages were quickly discovered and were shown to infect bacteria wherever they are found. Early research was interrupted by World War II . d'Herelle, despite his Canadian citizenship, was interned by the Vichy Government until the end of the war. Knowledge of bacteriophages increased in the 1940s following the formation of the Phage Group by scientists throughout the US. Among the members were Max Delbrück (1906–1981) who founded a course on bacteriophages at Cold Spring Harbor Laboratory . Other key members of the Phage Group included Salvador Luria (1912–1991) and Alfred Hershey (1908–1997). During the 1950s, Hershey and Chase made important discoveries on the replication of DNA during their studies on a bacteriophage called T2 . Together with Delbruck they were jointly awarded the 1969 Nobel Prize in Physiology or Medicine "for their discoveries concerning the replication mechanism and the genetic structure of viruses". Since then, the study of bacteriophages has provided insights into the switching on and off of genes, and a useful mechanism for introducing foreign genes into bacteria and many other fundamental mechanisms of molecular biology . In 1882, Adolf Mayer (1843–1942) described a condition of tobacco plants, which he called "mosaic disease" ("mozaïkziekte"). The diseased plants had variegated leaves that were mottled . He excluded the possibility of a fungal infection and could not detect any bacterium and speculated that a "soluble, enzyme-like infectious principle was involved". He did not pursue his idea any further, and it was the filtration experiments of Ivanovsky and Beijerinck that suggested the cause was a previously unrecognised infectious agent. After tobacco mosaic was recognized as a virus disease, virus infections of many other plants were discovered. The importance of tobacco mosaic virus in the history of viruses cannot be overstated. It was the first virus to be discovered, and the first to be crystallised and its structure shown in detail. The first X-ray diffraction pictures of the crystallised virus were obtained by Bernal and Fankuchen in 1941. On the basis of her pictures, Rosalind Franklin discovered the full structure of the virus in 1955. In the same year, Heinz Fraenkel-Conrat and Robley Williams showed that purified tobacco mosaic virus RNA and its coat protein can assemble by themselves to form functional viruses, suggesting that this simple mechanism was probably the means through which viruses were created within their host cells. By 1935, many plant diseases were thought to be caused by viruses. In 1922, John Kunkel Small (1869–1938) discovered that insects could act as vectors and transmit virus to plants. In the following decade many diseases of plants were shown to be caused by viruses that were carried by insects and in 1939, Francis Holmes , a pioneer in plant virology, described 129 viruses that caused disease of plants. Modern, intensive agriculture provides a rich environment for many plant viruses. In 1948, in Kansas, US, 7% of the wheat crop was destroyed by wheat streak mosaic virus . The virus was spread by mites called Aceria tulipae . In 1970, the Russian plant virologist Joseph Atabekov discovered that many plant viruses only infect a single species of host plant. The International Committee on Taxonomy of Viruses now recognises over 900 plant viruses. By the end of the 19th century, viruses were defined in terms of their infectivity , their ability to be filtered, and their requirement for living hosts. Up until this time, viruses had only been grown in plants and animals, but in 1906, Ross Granville Harrison (1870–1959) invented a method for growing tissue in lymph , and, in 1913, E Steinhardt, C Israeli, and RA Lambert used this method to grow vaccinia virus in fragments of guinea pig corneal tissue. In 1928, HB and MC Maitland grew vaccinia virus in suspensions of minced hens' kidneys. Their method was not widely adopted until the 1950s, when poliovirus was grown on a large scale for vaccine production. In 1941–42, George Hirst (1909–94) developed assays based on haemagglutination to quantify a wide range of viruses as well as virus-specific antibodies in serum. Although the influenza virus that caused the 1918–1919 influenza pandemic was not discovered until the 1930s, the descriptions of the disease and subsequent research has proved it was to blame. The pandemic killed 40–50 million people in less than a year, but the proof that it was caused by a virus was not obtained until 1933. Haemophilus influenzae is an opportunistic bacterium which commonly follows influenza infections; this led the eminent German bacteriologist Richard Pfeiffer (1858–1945) to incorrectly conclude that this bacterium was the cause of influenza. A major breakthrough came in 1931, when the American pathologist Ernest William Goodpasture grew influenza and several other viruses in fertilised chickens' eggs. Hirst identified an enzymic activity associated with the virus particle, later characterised as the neuraminidase , the first demonstration that viruses could contain enzymes. Frank Macfarlane Burnet showed in the early 1950s that the virus recombines at high frequencies, and Hirst later deduced that it has a segmented genome. In 1949, John F. Enders (1897–1985) Thomas Weller (1915–2008), and Frederick Robbins (1916–2003) grew polio virus for the first time in cultured human embryo cells, the first virus to be grown without using solid animal tissue or eggs. Infections by poliovirus most often cause the mildest of symptoms. This was not known until the virus was isolated in cultured cells and many people were shown to have had mild infections that did not lead to poliomyelitis. But, unlike other viral infections, the incidence of polio – the rarer severe form of the infection – increased in the 20th century and reached a peak around 1952. The invention of a cell culture system for growing the virus enabled Jonas Salk (1914–1995) to make an effective polio vaccine . Denis Parsons Burkitt (1911–1993) was born in Enniskillen, County Fermanagh, Ireland. He was the first to describe a type of cancer that now bears his name Burkitt's lymphoma . This type of cancer was endemic in equatorial Africa and was the commonest malignancy of children in the early 1960s. In an attempt to find a cause for the cancer, Burkitt sent cells from the tumour to Anthony Epstein (b. 1921) a British virologist, who along with Yvonne Barr and Bert Achong (1928–1996), and after many failures, discovered viruses that resembled herpes virus in the fluid that surrounded the cells. The virus was later shown to be a previously unrecognised herpes virus, which is now called Epstein–Barr virus . Surprisingly, Epstein–Barr virus is a very common but relatively mild infection of Europeans. Why it can cause such a devastating illness in Africans is not fully understood, but reduced immunity to virus caused by malaria might be to blame. Epstein–Barr virus is important in the history of viruses for being the first virus shown to cause cancer in humans. The second half of the 20th century was the golden age of virus discovery and most of the 2,000 recognised species of animal, plant, and bacterial viruses were discovered during these years. In 1946, bovine virus diarrhea was discovered, which is still possibly the most common pathogen of cattle throughout the world and in 1957, equine arterivirus was discovered. In the 1950s, improvements in virus isolation and detection methods resulted in the discovery of several important human viruses including varicella zoster virus , the paramyxoviruses – which include measles virus and respiratory syncytial virus – and the rhinoviruses that cause the common cold . In the 1960s more viruses were discovered. In 1963, the hepatitis B virus was discovered by Baruch Blumberg (b. 1925). Reverse transcriptase , the key enzyme that retroviruses use to translate their RNA into DNA, was first described in 1970, independently by Howard Temin and David Baltimore (b. 1938). This was important to the development of antiviral drugs – a key turning-point in the history of viral infections. In 1983, Luc Montagnier (b. 1932) and his team at the Pasteur Institute in France first isolated the retrovirus now called HIV. In 1989 Michael Houghton 's team at Chiron Corporation discovered hepatitis C . New viruses and strains of viruses were discovered in every decade of the second half of the 20th century. These discoveries have continued in the 21st century as new viral diseases such as SARS and nipah virus have emerged. Despite scientists' achievements over the past one hundred years, viruses continue to pose new threats and challenges. Although the influenza virus that caused the 1918–1919 influenza pandemic was not discovered until the 1930s, the descriptions of the disease and subsequent research has proved it was to blame. The pandemic killed 40–50 million people in less than a year, but the proof that it was caused by a virus was not obtained until 1933. Haemophilus influenzae is an opportunistic bacterium which commonly follows influenza infections; this led the eminent German bacteriologist Richard Pfeiffer (1858–1945) to incorrectly conclude that this bacterium was the cause of influenza. A major breakthrough came in 1931, when the American pathologist Ernest William Goodpasture grew influenza and several other viruses in fertilised chickens' eggs. Hirst identified an enzymic activity associated with the virus particle, later characterised as the neuraminidase , the first demonstration that viruses could contain enzymes. Frank Macfarlane Burnet showed in the early 1950s that the virus recombines at high frequencies, and Hirst later deduced that it has a segmented genome. In 1949, John F. Enders (1897–1985) Thomas Weller (1915–2008), and Frederick Robbins (1916–2003) grew polio virus for the first time in cultured human embryo cells, the first virus to be grown without using solid animal tissue or eggs. Infections by poliovirus most often cause the mildest of symptoms. This was not known until the virus was isolated in cultured cells and many people were shown to have had mild infections that did not lead to poliomyelitis. But, unlike other viral infections, the incidence of polio – the rarer severe form of the infection – increased in the 20th century and reached a peak around 1952. The invention of a cell culture system for growing the virus enabled Jonas Salk (1914–1995) to make an effective polio vaccine . Denis Parsons Burkitt (1911–1993) was born in Enniskillen, County Fermanagh, Ireland. He was the first to describe a type of cancer that now bears his name Burkitt's lymphoma . This type of cancer was endemic in equatorial Africa and was the commonest malignancy of children in the early 1960s. In an attempt to find a cause for the cancer, Burkitt sent cells from the tumour to Anthony Epstein (b. 1921) a British virologist, who along with Yvonne Barr and Bert Achong (1928–1996), and after many failures, discovered viruses that resembled herpes virus in the fluid that surrounded the cells. The virus was later shown to be a previously unrecognised herpes virus, which is now called Epstein–Barr virus . Surprisingly, Epstein–Barr virus is a very common but relatively mild infection of Europeans. Why it can cause such a devastating illness in Africans is not fully understood, but reduced immunity to virus caused by malaria might be to blame. Epstein–Barr virus is important in the history of viruses for being the first virus shown to cause cancer in humans. The second half of the 20th century was the golden age of virus discovery and most of the 2,000 recognised species of animal, plant, and bacterial viruses were discovered during these years. In 1946, bovine virus diarrhea was discovered, which is still possibly the most common pathogen of cattle throughout the world and in 1957, equine arterivirus was discovered. In the 1950s, improvements in virus isolation and detection methods resulted in the discovery of several important human viruses including varicella zoster virus , the paramyxoviruses – which include measles virus and respiratory syncytial virus – and the rhinoviruses that cause the common cold . In the 1960s more viruses were discovered. In 1963, the hepatitis B virus was discovered by Baruch Blumberg (b. 1925). Reverse transcriptase , the key enzyme that retroviruses use to translate their RNA into DNA, was first described in 1970, independently by Howard Temin and David Baltimore (b. 1938). This was important to the development of antiviral drugs – a key turning-point in the history of viral infections. In 1983, Luc Montagnier (b. 1932) and his team at the Pasteur Institute in France first isolated the retrovirus now called HIV. In 1989 Michael Houghton 's team at Chiron Corporation discovered hepatitis C . New viruses and strains of viruses were discovered in every decade of the second half of the 20th century. These discoveries have continued in the 21st century as new viral diseases such as SARS and nipah virus have emerged. Despite scientists' achievements over the past one hundred years, viruses continue to pose new threats and challenges.
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Minna
Minna is a city in Middle Belt Nigeria . It is the capital city of Niger State , one of Nigeria's 36 federal states . It consists of two major ethnic groups: the Gbagyi and the Nupe .Archaeological evidence suggests settlement in the area dates back to about 47,000–37,000 years ago. Muslim culture filtered into Minna by way of the ancient Saharan trade routes much later, and the city contains many mosques including Minna Central Mosque and Muslim organizations like the Islamic Education Trust , Minna, Muslim Students' Society of Nigeria - Minna Area Council (MSSN-MNAC), Da'watu-Ilallahi-Wa-Rasulihi Association (DAWRA), etc. Sharia law is practiced. Christianity is the second major population in Niger State , and institutions include a Faith Church , a Grace Baptist Church , Nupe Kalvari Churches , Anglican Churches , ECWA Churches , Baptist Churches , Victory Christian Church , the Apostolic Church and many others. Minna is the home state of Nigeria's former military President Gen. Ibrahim B. Babangida , and of former Head of State Gen. Abdulsalami Abubakar . Dr. Mu'azu Babangida Aliyu was the former governor of Niger State , serving the maximum term of eight years (2007–2015). Abubakar Sani Bello is also former governor of Niger state served from 2015 - 2023. Mohammed Umar Bago is the present governor of Niger state.Based on research carried out, it was reported that minna is being affected by land pollution caused by non-proper disposal of solid waste products. This has cause several disease such as Malaria fever, Yellow fever, Lassa fever, etc. Minna has a typical Middle Belt tropical savanna climate ( Köppen Aw ) with two seasons: an arid, dusty, harmattan -dominate dry season from November to April and a humid, oppressive wet season dominated by monsoonal air masses from May to October. Temperatures are hot to sweltering year round, except at the height of the wet season when air temperatures are merely very warm but the high humidity makes it equally or more uncomfortable than the hotter dry season. Due to the monsoon, summer (June, July, August) is cooler than spring, fall and winter.Cotton , guinea corn (sorghum), Maize and ginger are the main agricultural products of the city. Yam is also extensively cultivated throughout the city. The economy also supports cattle trading, brewing, shea nut processing and gold mining. There are also FMCGs such as PZ Cussons that deal in toilet soaps, baby products, medicaments and so on. Traditional industries and crafts in Minna include leather work and metalworking .Minna is connected to neighbouring cities by road. Abuja , the capital of the country, is only 150 km away. Minna is also connected by railroad to both Kano in the north and Ibadan and Lagos in the south. The city is served by Minna Airport .Minna has many educational institutions, including: Fati Lami Abubakar Institute for Legal and Administrative Studies , The Federal University of Technology Minna , Niger state school of health , Niger state school of nursing and Midwifery , Niger state university of Education among others. With many high schools as Father O'Connell Science College, Minna , Waziri Primary School, Chiroma Primary School, D.S.S Limawa, Kowa Schools, El-Bethel Academy, Jocis Schools, Hilltop Model School, Mypa schools, Himma international school, Police secondary school, El-Amin International School , FOMWAN Schools, New Horizon College , Divine Excellence International Schools and Brighter International Schools, among many others. The above-mentioned schools are the pioneering high schools in Minna. Minna has many primary health clinics with the General Hospital, Minna serving as the general health care.
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Virus classification
Virus classification is the process of naming viruses and placing them into a taxonomic system similar to the classification systems used for cellular organisms . Viruses are classified by phenotypic characteristics, such as morphology , nucleic acid type, mode of replication, host organisms , and the type of disease they cause. The formal taxonomic classification of viruses is the responsibility of the International Committee on Taxonomy of Viruses (ICTV) system, although the Baltimore classification system can be used to place viruses into one of seven groups based on their manner of mRNA synthesis. Specific naming conventions and further classification guidelines are set out by the ICTV. In 2021, the ICTV changed the International Code of Virus Classification and Nomenclature (ICVCN) to mandate a binomial format (genus|| ||species) for naming new viral species similar to that used for cellular organisms; the names of species coined prior to 2021 are gradually being converted to the new format, a process which has been stated to be planned to be completed by end 2023. As at 2022, the ICTV taxonomy listed 11,273 named virus species (including some classed as satellite viruses and others as viroids) in 2,818 genera, 264 families, 72 orders, 40 classes, 17 phyla, 9 kingdoms and 6 realms. However, the number of named viruses considerably exceeds the number of named virus species since, by contrast to the classification systems used elsewhere in biology, a virus "species" is a collective name for a group of (presumably related) viruses sharing certain common features (see below). Also, the use of the term "kingdom" in virology does not equate to its usage in other biological groups, where it reflects high level groupings that separate completely different kinds of organisms (see Kingdom (biology) ).The currently accepted and formal definition of a 'virus' was accepted by the ICTV Executive Committee in November 2020 and ratified in March 2021, and is as follows: Viruses sensu stricto are defined operationally by the ICTV as a type of MGE that encodes at least one protein that is a major component of the virion encasing the nucleic acid of the respective MGE and therefore the gene encoding the major virion protein itself or MGEs that are clearly demonstrable to be members of a line of evolutionary descent of such major virion protein-encoding entities. Any monophyletic group of MGEs that originates from a virion protein-encoding ancestor should be classified as a group of viruses. Species form the basis for any biological classification system. Before 1982, it was thought that viruses could not be made to fit Ernst Mayr 's reproductive concept of species, and so were not amenable to such treatment. In 1982, the ICTV started to define a species as "a cluster of strains" with unique identifying qualities. In 1991, the more specific principle that a virus species is a polythetic class of viruses that constitutes a replicating lineage and occupies a particular ecological niche was adopted. As at 2021 (the latest edition of the ICVCN), the ICTV definition of species states: "A species is the lowest taxonomic level in the hierarchy approved by the ICTV. A species is a monophyletic group of MGEs ( mobile genetic elements ) whose properties can be distinguished from those of other species by multiple criteria", with the comment "The criteria by which different species within a genus are distinguished shall be established by the appropriate Study Group. These criteria may include, but are not limited to, natural and experimental host range, cell and tissue tropism, pathogenicity, vector specificity, antigenicity, and the degree of relatedness of their genomes or genes. The criteria used should be published in the relevant section of the ICTV Report and reviewed periodically by the appropriate Study Group." Many individually named viruses (sometimes referred to as "virus strains") exist at below the rank of virus species . The ICVCN gives the examples of blackeye cowpea mosaic virus and peanut stripe virus, which are both classified in the species Bean common mosaic virus , the latter a member of the genus Potyvirus that will in due course receive a binomial name as Potyvirus [species...] . As another example, the virus SARS-CoV-1 , that causes severe acute respiratory syndrome ( SARS ) is different from the virus SARS-CoV-2 , the cause of the COVID-19 pandemic, but both are classified within the same virus species, a member of the genus Betacoronavirus that is currently known as Severe acute respiratory syndrome-related coronavirus which, per the 2021 mandate from the ICTV, will also receive a binomial name in due course. As set out in the ICVCN, section 3.4, the names [and definitions] of taxa below the rank of species are not governed by the ICTV; "Naming of such entities is not the responsibility of the ICTV but of international specialty groups. It is the responsibility of ICTV Study Groups to consider how these entities may best be classified into species." Using the example given above, the virus causing the COVID-19 pandemic was given the designation "SARS-CoV-2" by the Coronaviridae Study Group (CSG) of the International Committee on Taxonomy of Viruses in 2020; in the same publication, this Study Group recommended a naming convention for particular isolates of this virus "resembl[ing] the formats used for isolates of avian coronaviruses, filoviruses and influenza virus" in the format virus/host/location/isolate/date, with a cited example as "SARS-CoV-2/human/Wuhan/X1/2019". The currently accepted and formal definition of a 'virus' was accepted by the ICTV Executive Committee in November 2020 and ratified in March 2021, and is as follows: Viruses sensu stricto are defined operationally by the ICTV as a type of MGE that encodes at least one protein that is a major component of the virion encasing the nucleic acid of the respective MGE and therefore the gene encoding the major virion protein itself or MGEs that are clearly demonstrable to be members of a line of evolutionary descent of such major virion protein-encoding entities. Any monophyletic group of MGEs that originates from a virion protein-encoding ancestor should be classified as a group of viruses.Species form the basis for any biological classification system. Before 1982, it was thought that viruses could not be made to fit Ernst Mayr 's reproductive concept of species, and so were not amenable to such treatment. In 1982, the ICTV started to define a species as "a cluster of strains" with unique identifying qualities. In 1991, the more specific principle that a virus species is a polythetic class of viruses that constitutes a replicating lineage and occupies a particular ecological niche was adopted. As at 2021 (the latest edition of the ICVCN), the ICTV definition of species states: "A species is the lowest taxonomic level in the hierarchy approved by the ICTV. A species is a monophyletic group of MGEs ( mobile genetic elements ) whose properties can be distinguished from those of other species by multiple criteria", with the comment "The criteria by which different species within a genus are distinguished shall be established by the appropriate Study Group. These criteria may include, but are not limited to, natural and experimental host range, cell and tissue tropism, pathogenicity, vector specificity, antigenicity, and the degree of relatedness of their genomes or genes. The criteria used should be published in the relevant section of the ICTV Report and reviewed periodically by the appropriate Study Group." Many individually named viruses (sometimes referred to as "virus strains") exist at below the rank of virus species . The ICVCN gives the examples of blackeye cowpea mosaic virus and peanut stripe virus, which are both classified in the species Bean common mosaic virus , the latter a member of the genus Potyvirus that will in due course receive a binomial name as Potyvirus [species...] . As another example, the virus SARS-CoV-1 , that causes severe acute respiratory syndrome ( SARS ) is different from the virus SARS-CoV-2 , the cause of the COVID-19 pandemic, but both are classified within the same virus species, a member of the genus Betacoronavirus that is currently known as Severe acute respiratory syndrome-related coronavirus which, per the 2021 mandate from the ICTV, will also receive a binomial name in due course. As set out in the ICVCN, section 3.4, the names [and definitions] of taxa below the rank of species are not governed by the ICTV; "Naming of such entities is not the responsibility of the ICTV but of international specialty groups. It is the responsibility of ICTV Study Groups to consider how these entities may best be classified into species." Using the example given above, the virus causing the COVID-19 pandemic was given the designation "SARS-CoV-2" by the Coronaviridae Study Group (CSG) of the International Committee on Taxonomy of Viruses in 2020; in the same publication, this Study Group recommended a naming convention for particular isolates of this virus "resembl[ing] the formats used for isolates of avian coronaviruses, filoviruses and influenza virus" in the format virus/host/location/isolate/date, with a cited example as "SARS-CoV-2/human/Wuhan/X1/2019". The International Committee on Taxonomy of Viruses began to devise and implement rules for the naming and classification of viruses early in the 1970s, an effort that continues to the present. The ICTV is the only body charged by the International Union of Microbiological Societies with the task of developing, refining, and maintaining a universal virus taxonomy, following the methods set out in the International Code of Virus Classification and Nomenclature. The system shares many features with the classification system of cellular organisms , such as taxon structure. However, some differences exist, such as the universal use of italics for all taxonomic names, unlike in the International Code of Nomenclature for algae, fungi, and plants and International Code of Zoological Nomenclature . Viral classification starts at the level of realm and continues as follows, with the taxonomic suffixes in parentheses: In parallel to the system of binomial nomenclature adopted in cellular species, the ICTV has recently (2021) mandated that new virus species be named in a binomial format (genus|| species), and that pre-existing virus species names be progressively replaced with new names in the binomial format. A mid-2023 review of the status of this changeover stated: "...a large number of proposals [concerning virus nomenclature, submitted to the ICTV Executive Committee (EC) for its consideration] renamed existing species for compliance with the recently mandated binomial nomenclature format. As a result, 8,982 out of the current 11,273 species (80%) now have binomial names. The process will be concluded in 2023, with the remaining 2,291 species being renamed." As of 2021, all levels of taxa except subrealm, subkingdom, and subclass are used. Six realms, one incertae sedis class, 22 incertae sedis families, and two incertae sedis genera are recognized: Realms : Incertae sedis classes : Incertae sedis families : Incertae sedis genera : It has been suggested that similarity in virion assembly and structure observed for certain viral groups infecting hosts from different domains of life (e.g., bacterial tectiviruses and eukaryotic adenoviruses or prokaryotic Caudovirales and eukaryotic herpesviruses) reflects an evolutionary relationship between these viruses. Therefore, structural relationship between viruses has been suggested to be used as a basis for defining higher-level taxa – structure-based viral lineages – that could complement the ICTV classification scheme of 2010. The ICTV has gradually added many higher-level taxa using relationships in protein folds. All four realms defined in the 2019 release are defined by the presence of a protein of a certain structural family. It has been suggested that similarity in virion assembly and structure observed for certain viral groups infecting hosts from different domains of life (e.g., bacterial tectiviruses and eukaryotic adenoviruses or prokaryotic Caudovirales and eukaryotic herpesviruses) reflects an evolutionary relationship between these viruses. Therefore, structural relationship between viruses has been suggested to be used as a basis for defining higher-level taxa – structure-based viral lineages – that could complement the ICTV classification scheme of 2010. The ICTV has gradually added many higher-level taxa using relationships in protein folds. All four realms defined in the 2019 release are defined by the presence of a protein of a certain structural family. Baltimore classification (first defined in 1971) is a classification system that places viruses into one of seven groups depending on a combination of their nucleic acid ( DNA or RNA ), strandedness (single-stranded or double-stranded), sense , and method of replication . Named after David Baltimore , a Nobel Prize -winning biologist, these groups are designated by Roman numerals . Other classifications are determined by the disease caused by the virus or its morphology, neither of which are satisfactory due to different viruses either causing the same disease or looking very similar. In addition, viral structures are often difficult to determine under the microscope. Classifying viruses according to their genome means that those in a given category will all behave in a similar fashion, offering some indication of how to proceed with further research. Viruses can be placed in one of the seven following groups: Viruses with a DNA genome , except for the DNA reverse transcribing viruses , are members of three of the four recognized viral realms : Duplodnaviria , Monodnaviria , and Varidnaviria . But the incertae sedis order Ligamenvirales , and many other incertae sedis families and genera, are also used to classify DNA viruses. The domains Duplodnaviria and Varidnaviria consist of double-stranded DNA viruses; other double-stranded DNA viruses are incertae sedis . The domain Monodnaviria consists of single-stranded DNA viruses that generally encode a HUH endonuclease ; other single-stranded DNA viruses are incertae sedis . All viruses that have an RNA genome , and that encode an RNA-dependent RNA polymerase (RdRp), are members of the kingdom Orthornavirae , within the realm Riboviria . All viruses that encode a reverse transcriptase (also known as RT or RNA-dependent DNA polymerase) are members of the class Revtraviricetes , within the phylum Arterviricota , kingdom Pararnavirae , and realm Riboviria . The class Blubervirales contains the single family Hepadnaviridae of DNA RT (reverse transcribing) viruses; all other RT viruses are members of the class Ortervirales . Viruses with a DNA genome , except for the DNA reverse transcribing viruses , are members of three of the four recognized viral realms : Duplodnaviria , Monodnaviria , and Varidnaviria . But the incertae sedis order Ligamenvirales , and many other incertae sedis families and genera, are also used to classify DNA viruses. The domains Duplodnaviria and Varidnaviria consist of double-stranded DNA viruses; other double-stranded DNA viruses are incertae sedis . The domain Monodnaviria consists of single-stranded DNA viruses that generally encode a HUH endonuclease ; other single-stranded DNA viruses are incertae sedis . All viruses that have an RNA genome , and that encode an RNA-dependent RNA polymerase (RdRp), are members of the kingdom Orthornavirae , within the realm Riboviria . All viruses that encode a reverse transcriptase (also known as RT or RNA-dependent DNA polymerase) are members of the class Revtraviricetes , within the phylum Arterviricota , kingdom Pararnavirae , and realm Riboviria . The class Blubervirales contains the single family Hepadnaviridae of DNA RT (reverse transcribing) viruses; all other RT viruses are members of the class Ortervirales . Holmes (1948) used a Linnaean taxonomy with binomial nomenclature to classify viruses into 3 groups under one order, Virales . They are placed as follows: The system was not accepted by others due to its neglect of morphological similarities. Holmes (1948) used a Linnaean taxonomy with binomial nomenclature to classify viruses into 3 groups under one order, Virales . They are placed as follows: The system was not accepted by others due to its neglect of morphological similarities. Infectious agents are smaller than viruses and have only some of their properties. Since 2015, the ICTV has allowed them to be classified in a similar way as viruses are. Satellites depend on co-infection of a host cell with a helper virus for productive multiplication. Their nucleic acids have substantially distinct nucleotide sequences from either their helper virus or host. When a satellite subviral agent encodes the coat protein in which it is encapsulated, it is then called a satellite virus. Satellite-like nucleic acids resemble satellite nucleic acids, in that they replicate with the aid of helper viruses. However they differ in that they can encode functions that can contribute to the success of their helper viruses; while they are sometimes considered to be genomic elements of their helper viruses, they are not always found within their helper viruses. Single-stranded satellite DNAs Family Alphasatellitidae (encoding a replication initiator protein) Family Tolecusatellitidae (encoding a pathogenicity determinant βC1) Double-stranded satellite RNAs Single-stranded satellite RNAs Subgroup 1: Large satellite RNAs Subgroup 2: Small linear satellite RNAs Subgroup 3: Circular satellite RNAs ( virusoids ) Genus Deltavirus Polerovirus -associated RNAs Satellite-like RNA Satellite-like DNA Defective interfering particles are defective viruses that have lost their ability to replicate except in the presence of a helper virus, which is normally the parental virus. They can also interfere with the helper virus. Defective interfering particles (RNA) Defective interfering particles (DNA) Viriforms are a polyphyletic category of endogenous viral elements . Sometime in their evolution, they became "domesticated" by their host as a key part of the host's lifecycle. The prototypical example is members of the (also polyphyletic) Polydnaviriformidae , which are used by wasps to send pieces of immunity-blunting DNA into the prey by packing them into virion-like particles . Other members are so-called gene transfer agents (GTAs) found among prokaryotes. GTA particles resemble tailed phages, but are smaller and carry mostly random pieces of host DNA. GTAs are produced by the host in times of stress; releasing GTAs kills the host cell, but allows pieces of its genetic material to live on in other bacteria, usually of the same species. The three known clades of GTAs, Rhodogtaviriformidae , Bartogtaviriformidae , and Brachygtaviriformidae , all arised independently from different parts of the Caudoviricetes family tree. Satellites depend on co-infection of a host cell with a helper virus for productive multiplication. Their nucleic acids have substantially distinct nucleotide sequences from either their helper virus or host. When a satellite subviral agent encodes the coat protein in which it is encapsulated, it is then called a satellite virus. Satellite-like nucleic acids resemble satellite nucleic acids, in that they replicate with the aid of helper viruses. However they differ in that they can encode functions that can contribute to the success of their helper viruses; while they are sometimes considered to be genomic elements of their helper viruses, they are not always found within their helper viruses. Single-stranded satellite DNAs Family Alphasatellitidae (encoding a replication initiator protein) Family Tolecusatellitidae (encoding a pathogenicity determinant βC1) Double-stranded satellite RNAs Single-stranded satellite RNAs Subgroup 1: Large satellite RNAs Subgroup 2: Small linear satellite RNAs Subgroup 3: Circular satellite RNAs ( virusoids ) Genus Deltavirus Polerovirus -associated RNAs Satellite-like RNA Satellite-like DNA Defective interfering particles are defective viruses that have lost their ability to replicate except in the presence of a helper virus, which is normally the parental virus. They can also interfere with the helper virus. Defective interfering particles (RNA) Defective interfering particles (DNA)Satellites depend on co-infection of a host cell with a helper virus for productive multiplication. Their nucleic acids have substantially distinct nucleotide sequences from either their helper virus or host. When a satellite subviral agent encodes the coat protein in which it is encapsulated, it is then called a satellite virus. Satellite-like nucleic acids resemble satellite nucleic acids, in that they replicate with the aid of helper viruses. However they differ in that they can encode functions that can contribute to the success of their helper viruses; while they are sometimes considered to be genomic elements of their helper viruses, they are not always found within their helper viruses. Single-stranded satellite DNAs Family Alphasatellitidae (encoding a replication initiator protein) Family Tolecusatellitidae (encoding a pathogenicity determinant βC1) Double-stranded satellite RNAs Single-stranded satellite RNAs Subgroup 1: Large satellite RNAs Subgroup 2: Small linear satellite RNAs Subgroup 3: Circular satellite RNAs ( virusoids ) Genus Deltavirus Polerovirus -associated RNAs Satellite-like RNA Satellite-like DNADefective interfering particles are defective viruses that have lost their ability to replicate except in the presence of a helper virus, which is normally the parental virus. They can also interfere with the helper virus. Defective interfering particles (RNA) Defective interfering particles (DNA)Viriforms are a polyphyletic category of endogenous viral elements . Sometime in their evolution, they became "domesticated" by their host as a key part of the host's lifecycle. The prototypical example is members of the (also polyphyletic) Polydnaviriformidae , which are used by wasps to send pieces of immunity-blunting DNA into the prey by packing them into virion-like particles . Other members are so-called gene transfer agents (GTAs) found among prokaryotes. GTA particles resemble tailed phages, but are smaller and carry mostly random pieces of host DNA. GTAs are produced by the host in times of stress; releasing GTAs kills the host cell, but allows pieces of its genetic material to live on in other bacteria, usually of the same species. The three known clades of GTAs, Rhodogtaviriformidae , Bartogtaviriformidae , and Brachygtaviriformidae , all arised independently from different parts of the Caudoviricetes family tree.
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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 ]
2,330
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Bolivian_hemorrhagic_fever/html
Bolivian hemorrhagic fever
Machupo virus Bolivian hemorrhagic fever ( BHF ), also known as black typhus or Ordog Fever , is a hemorrhagic fever and zoonotic infectious disease originating in Bolivia after infection by Machupo mammarenavirus . BHF was first identified in 1963 as an ambisense RNA virus of the Arenaviridae family, by a research group led by Karl Johnson . The mortality rate is estimated at 5 to 30 percent. Due to its pathogenicity , Machupo virus requires Biosafety Level Four conditions, the highest level. During the period between February and March 2007, some 20 suspected BHF cases (3 fatal) were reported to the Servicio Departamental de Salud (SEDES) in Beni Department , Bolivia. In February 2008, at least 200 suspected new cases (12 fatal) were reported to SEDES. In November 2011, a second case was confirmed near the departmental capital of Trinidad , and a serosurvey was conducted to determine the extent of Machupo virus infections in the department. A SEDES expert involved in the survey expressed his concerns about the expansion of the virus to other provinces outside the endemic regions of Mamoré and Iténez provinces . The disease was first encountered in 1962, in the Bolivian village of San Joaquín, hence the name "Bolivian" Hemorrhagic Fever. When initial investigations failed to find an arthropod carrier, other sources were sought before finally determining that the disease was carried by infected mice. Although mosquitoes were not the cause as originally suspected, the extermination of mosquitoes using DDT to prevent malaria proved to be indirectly responsible for the outbreak in that the accumulation of DDT in various animals along the food chain led to a shortage of cats in the village; subsequently, a mouse plague erupted in the village, leading to an epidemic. The vector is the large vesper mouse ( Calomys callosus ), a rodent indigenous to northern Bolivia. Infected animals are asymptomatic and shed the virus in excreta, thereby infecting humans. Evidence of person-to-person transmission of BHF exists but is believed to be rare. The infection has a slow onset with fever , malaise , headache and myalgia , very similar to Malaria symptoms. Petechiae (blood spots) on the upper body and bleeding from the nose and gums are observed when the disease progresses to the hemorrhagic phase, usually within seven days of onset. Severe hemorrhagic or neurologic symptoms are observed in about one third of patients. Neurologic symptoms involve tremors, delirium, and convulsions. The mortality rate is about 25%. Measures to reduce contact between the vesper mouse and humans may have contributed to limiting the number of outbreaks, with no cases identified between 1973 and 1994. Although there are no cures or vaccine for the disease, a vaccine developed for the genetically related Junín virus which causes Argentine hemorrhagic fever has shown evidence of cross-reactivity to Machupo virus, and may therefore be an effective prophylactic measure for people at high risk of infection. Post infection (and providing that the person survives the infection), those that have contracted BHF are usually immune to further infection of the disease. The disease was first encountered in 1962, in the Bolivian village of San Joaquín, hence the name "Bolivian" Hemorrhagic Fever. When initial investigations failed to find an arthropod carrier, other sources were sought before finally determining that the disease was carried by infected mice. Although mosquitoes were not the cause as originally suspected, the extermination of mosquitoes using DDT to prevent malaria proved to be indirectly responsible for the outbreak in that the accumulation of DDT in various animals along the food chain led to a shortage of cats in the village; subsequently, a mouse plague erupted in the village, leading to an epidemic. The vector is the large vesper mouse ( Calomys callosus ), a rodent indigenous to northern Bolivia. Infected animals are asymptomatic and shed the virus in excreta, thereby infecting humans. Evidence of person-to-person transmission of BHF exists but is believed to be rare. The infection has a slow onset with fever , malaise , headache and myalgia , very similar to Malaria symptoms. Petechiae (blood spots) on the upper body and bleeding from the nose and gums are observed when the disease progresses to the hemorrhagic phase, usually within seven days of onset. Severe hemorrhagic or neurologic symptoms are observed in about one third of patients. Neurologic symptoms involve tremors, delirium, and convulsions. The mortality rate is about 25%. Measures to reduce contact between the vesper mouse and humans may have contributed to limiting the number of outbreaks, with no cases identified between 1973 and 1994. Although there are no cures or vaccine for the disease, a vaccine developed for the genetically related Junín virus which causes Argentine hemorrhagic fever has shown evidence of cross-reactivity to Machupo virus, and may therefore be an effective prophylactic measure for people at high risk of infection. Post infection (and providing that the person survives the infection), those that have contracted BHF are usually immune to further infection of the disease. Bolivian hemorrhagic fever was one of three hemorrhagic fevers and 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. Albert Nickel, a 53-year old animal caretaker at Fort Detrick , died in 1964 from the disease after being bitten by an infected mouse. Nickel Place, on Fort Detrick, is named in his honor. It was also under research by the Soviet Union, under the Biopreparat bureau. Investigational vaccines exist for Argentine hemorrhagic fever and RVF; however, neither is approved by FDA or commonly available in the United States. The structure of the attachment glycoprotein has been determined by X-ray crystallography and this glycoprotein is likely to be an essential component of any successful vaccine.
960
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Australian_bat_lyssavirus/html
Australian bat lyssavirus
Australian bat lyssavirus ( ABLV ), originally named Pteropid lyssavirus ( PLV ), is a enzootic virus closely related to the rabies virus . It was first identified in a 5-month-old juvenile black flying fox ( Pteropus alecto ) collected near Ballina in northern New South Wales , Australia , in January 1995 during a national surveillance program for the recently identified Hendra virus . ABLV is the seventh member of the genus Lyssavirus (which includes Rabies virus ) and the only Lyssavirus member present in Australia. ABLV has been categorized to the Phylogroup I of the Lyssaviruses. The Australian bat lyssavirus (ABVL) shares many structural characteristics with the other Lyssaviruses, despite being genetically and serologically distinct from the others. Visually, ABLV is a bullet shaped virus. Molecularly, ABVL is an enveloped, negative-sense, single-stranded RNA virus. The (-)ssRNA genome is relatively small, containing 12kilobases of genetic material and encoding five viral proteins. The five viral proteins, their symbol, and their functional roles are: Helps virus evade host immune system - suppressing host immunity Interacts with P and L ABLV has a similar entry mechanism to other rabies viruses, utilizing receptor-mediated endocytosis by the host cells. The glycoprotein (G) is a trimeric spike protein that extends through the virus's envelope and can interact with surface receptors of host cells. While the specific receptors remain mostly unknown at this time, it is thought that ABLV enters the nervous system of host through the neuromuscular junction of the peripheral nervous system. Additionally, it is believed that the spike protein either binds to a highly specific host receptor or uses a co-receptor in lipid rafts. Some of the proposed receptors include nicotinic acetylcholine receptor (nAchR), p75 neurotrophin receptor (p75NTR), and neuronal cell adhesion molecule (NCAM). After attaching to the host cell surface, ABLV uses a clathrin-dynamin-dependent pathway to invaginate the host membrane and pinch off a vesicle. Actin polymerization at the site of invagination is also required for successful viral entry. The virus is endocytosed fully, unenveloped. The vesicle fuses with a lysosome, causing the pH within the infected vesicle to drop. The lowering of pH in the early-endosome causes a conformational change in the spike protein G. This allows the viral envelope to fuse with the endosome, releasing the nucleocapsid into the cytoplasm of the host cell. The Australian bat lyssavirus (ABVL) shares many structural characteristics with the other Lyssaviruses, despite being genetically and serologically distinct from the others. Visually, ABLV is a bullet shaped virus. Molecularly, ABVL is an enveloped, negative-sense, single-stranded RNA virus. The (-)ssRNA genome is relatively small, containing 12kilobases of genetic material and encoding five viral proteins. The five viral proteins, their symbol, and their functional roles are: Helps virus evade host immune system - suppressing host immunity Interacts with P and L ABLV has a similar entry mechanism to other rabies viruses, utilizing receptor-mediated endocytosis by the host cells. The glycoprotein (G) is a trimeric spike protein that extends through the virus's envelope and can interact with surface receptors of host cells. While the specific receptors remain mostly unknown at this time, it is thought that ABLV enters the nervous system of host through the neuromuscular junction of the peripheral nervous system. Additionally, it is believed that the spike protein either binds to a highly specific host receptor or uses a co-receptor in lipid rafts. Some of the proposed receptors include nicotinic acetylcholine receptor (nAchR), p75 neurotrophin receptor (p75NTR), and neuronal cell adhesion molecule (NCAM). After attaching to the host cell surface, ABLV uses a clathrin-dynamin-dependent pathway to invaginate the host membrane and pinch off a vesicle. Actin polymerization at the site of invagination is also required for successful viral entry. The virus is endocytosed fully, unenveloped. The vesicle fuses with a lysosome, causing the pH within the infected vesicle to drop. The lowering of pH in the early-endosome causes a conformational change in the spike protein G. This allows the viral envelope to fuse with the endosome, releasing the nucleocapsid into the cytoplasm of the host cell. Bats, both flying foxes and insectivorous bats , are the only known host reservoir for ABLV. The known species of bat reservoirs are the Black Flying Fox ( Pteropus alecto ), the Grey-headed Flying Fox ( P. poliocephalus ), the Spectacled Flying Fox ( P. conscpicullatus ), the Little Red Flying Fox ( P. scapulatus ), and the Yellow-bellied Sheathtail Bat ( Saccolaimus flaviventris ). These species are distributed throughout the Australian continent, and ABLV has only been serologically and phylogenetically in Australia. : 251 It is estimated that less than 1% of healthy bats are ABLV carriers. As for sick or injured bats, it is estimated that 5-10% have been infected, detected with fluorescent antibody testing. As for other species that are susceptible to ABLV infection, human and horse cases have been reported since 1996 and 2013, respectively. No other terrestrial animals have been reported to be infected with ABLV, despite known exposure to infected bats. However, recent studies have found that the ABLV receptor for host cell entry is conserved amongst a variety of mammals, including but not limited to small rodents, monkeys, and rabbits. As of now, ABLV has only been isolated and reported in Australia. The distribution of ABLV across the Australian continent is based on the ecological distribution of the bat reservoirs. From the four flying fox species identified as host reservoirs, ABLV is present in areas of Western Australia, North Territory, Queensland, New South Wales, and Victoria. From the Yellow-bellied Sheathtail Bat, ABLV is present throughout mainland Australia. Bats, both flying foxes and insectivorous bats , are the only known host reservoir for ABLV. The known species of bat reservoirs are the Black Flying Fox ( Pteropus alecto ), the Grey-headed Flying Fox ( P. poliocephalus ), the Spectacled Flying Fox ( P. conscpicullatus ), the Little Red Flying Fox ( P. scapulatus ), and the Yellow-bellied Sheathtail Bat ( Saccolaimus flaviventris ). These species are distributed throughout the Australian continent, and ABLV has only been serologically and phylogenetically in Australia. : 251 It is estimated that less than 1% of healthy bats are ABLV carriers. As for sick or injured bats, it is estimated that 5-10% have been infected, detected with fluorescent antibody testing. As for other species that are susceptible to ABLV infection, human and horse cases have been reported since 1996 and 2013, respectively. No other terrestrial animals have been reported to be infected with ABLV, despite known exposure to infected bats. However, recent studies have found that the ABLV receptor for host cell entry is conserved amongst a variety of mammals, including but not limited to small rodents, monkeys, and rabbits. As of now, ABLV has only been isolated and reported in Australia. The distribution of ABLV across the Australian continent is based on the ecological distribution of the bat reservoirs. From the four flying fox species identified as host reservoirs, ABLV is present in areas of Western Australia, North Territory, Queensland, New South Wales, and Victoria. From the Yellow-bellied Sheathtail Bat, ABLV is present throughout mainland Australia. The first case occurred in November 1996, when an animal caregiver in Rockhampton sustained several scratches from fruit bats she was working with. She reported to the hospital four to five weeks later for shoulder pain, dizziness, vomiting, headache, fever, and chills. While hospitalized, her condition rapidly deteriorated, with slurred speech, diplopia (double-vision), dysphagia (difficulty swallowing), and progressive weakness in her limbs. From cerebrospinal fluid samples, no organisms were found with microscopy or culturing, despite elevated white blood cell levels. She was treated with several broad spectrum antibiotics with no improvement. An electroencephalogram was performed and found diffuse encephalitis. She eventually fell into a depressed conscious state, with a single incidence of extreme agitation. By her 11th day of hospitalization, she was fully ventilation dependent, nonresponsive, and hyperthermic. She died 20 days after her initial admittance. ABLV was identified from brain tissue by polymerase chain reaction and immunohistochemistry . The second case began in August 1996, 37 year old Monique Todhunter from Mackay was bitten on the finger by a flying fox at a birthday party, while attempting to remove it from a child on whom it had landed. Six months later, following heightened public attention from the first ABLV death, she consulted a general practitioner regarding testing for the virus. Post-exposure prophylaxis was advised, but for an unknown reason she declined the treatment. After a 27-month incubation, a rabies-like illness developed in November of 1998. She came in with symptoms of fever, vomiting, pain in her shoulder, dysphagia, and muscle spasms. Her condition worsened after hospital admission, as her dysphagia increased, her muscle spasms became more pronounced and frequent, and she became increasingly agitated. She became ventilation dependent and unable to communicate due to full paralysis. On the day the woman was hospitalized, cerebrospinal fluid, serum, and saliva were submitted for testing. On the fourth day of her hospital admission, these tests were returned with results of probable ABLV infection. ABLV infection was confirmed by PCR on the 8th day of hospitalization. She died 19 days after the onset of illness. Postmortem tests were all strongly positive for ABLV. A notable feature of this case is that the patient underwent a 27 month incubation period; in comparison, the majority of rabies cases have an incubation period of 20-90 days, with 95% of cases exhibiting symptoms within a year of exposure to the virus. The third, and most recent, case occurred in December of 2012, when an eight-year-old boy was scratched by a bat in north Queensland. He became ill eight weeks later, showing symptoms including fever, anorexia, and abdominal pain. His condition worsened through his hospitalization, with abnormal and aggressive bouts between normal behavior and intense muscle spasms. He repeatedly needed to be extubated and sedated due to his spasms. The hospital performed several tests through his stay, including sending cerebrospinal fluid and blood samples off for testing, taking computed tomography images of his chest and abdomen, and performing neuroimaging (MRIs, electroencephalography's). Initially, tests for the ABLV antigens were negative, but repeated testing 12 days into his hospitalization provided positive results. The child died 28 days after the onset of symptoms on February 22, 2013. ABLV (and the other Lyssaviruses) present similarly to the traditional encephalitic rabies virus (RABV) in humans. The symptoms first are flu-like with fevers, headaches, and fatigue. The symptoms progress with paralysis, delirium, convulsions, and death. There are no known human survivors of ABLV infection after symptoms have manifested. The pathogenesis of ABLV is still widely unknown and still being studied. The virus initially infects the host through the peripheral nervous system following a bite or scratch from an infected animal. For the three reported ABLV cases in humans, the incubation period ranged from a few weeks to almost two years. Due to its difficulty in diagnosing, low number of reported cases, and relative novelty as an endemic virus, there are no successful treatment plans once the symptoms have begun. As previously stated, all intervention methods used on the three human cases of ABLV were not curative and all three cases resulted in fatality. However, it is highly recommended by physicians to receive the RABV post-exposure prophylaxis (PEP) protocol immediately after potential lyssavirus exposure (i.e.. exposure/interaction with bats). Additionally, the incident should be reported to the relevant public health unit. Currently, the PEP protocol involves thoroughly cleaning the wound and surrounding tissue, administration of the rabies vaccine, and administration of rabies immunoglobulin (RIG). Currently, there are two effective variations of RIGs used in PEP protocol, human RIG (HRIG) and equine RIG (ERIG). Drawbacks for HRIG are that there are limited supplies and the cost of production is high. HRIG is overall inaccessible for the general population. Drawbacks for ERIG are potential immunogenicity, which is when the immune system recognizes the RIG as foreign and causes an immune reaction. In a 2021 study performed by Weir, Coggins, et.al., a new treatment method was proposed that used human monoclonal antibodies over RIGs. They identified two (A6 and F11) that recognized the G protein of lyssaviruses in phylogroup I (including ABLV) and completely neutralized the virus. They also proposed it as a potential diagnostic tool, in which there are only limited methods with PCR and are late into the symptomatic phase to positively identify ABLV. Rabies vaccine and immunoglobulin are effective in prophylactic and therapeutic protection from ABLV infection. Since the emergence of the virus, rabies vaccine is administered to individuals with a heightened risk of exposure, and vaccine and immunoglobulin are provided for post-exposure treatment. The public health units in Australia advise that the population avoid and limit their interactions and physical contact with bats as much as possible. ABLV is one of four zoonotic viruses discovered in pteropid bats since 1994, the others being Hendra virus , Nipah virus , and Menangle virus . Of these, ABLV is the only virus known to be transmissible to humans directly from bats without an intermediate host. Thus education and awareness in the general population is a must. If a bat is found and/or appears injured, one should avoid contact with it and instead call local pest and animal control to appropriately remove the bat. The first case occurred in November 1996, when an animal caregiver in Rockhampton sustained several scratches from fruit bats she was working with. She reported to the hospital four to five weeks later for shoulder pain, dizziness, vomiting, headache, fever, and chills. While hospitalized, her condition rapidly deteriorated, with slurred speech, diplopia (double-vision), dysphagia (difficulty swallowing), and progressive weakness in her limbs. From cerebrospinal fluid samples, no organisms were found with microscopy or culturing, despite elevated white blood cell levels. She was treated with several broad spectrum antibiotics with no improvement. An electroencephalogram was performed and found diffuse encephalitis. She eventually fell into a depressed conscious state, with a single incidence of extreme agitation. By her 11th day of hospitalization, she was fully ventilation dependent, nonresponsive, and hyperthermic. She died 20 days after her initial admittance. ABLV was identified from brain tissue by polymerase chain reaction and immunohistochemistry . The second case began in August 1996, 37 year old Monique Todhunter from Mackay was bitten on the finger by a flying fox at a birthday party, while attempting to remove it from a child on whom it had landed. Six months later, following heightened public attention from the first ABLV death, she consulted a general practitioner regarding testing for the virus. Post-exposure prophylaxis was advised, but for an unknown reason she declined the treatment. After a 27-month incubation, a rabies-like illness developed in November of 1998. She came in with symptoms of fever, vomiting, pain in her shoulder, dysphagia, and muscle spasms. Her condition worsened after hospital admission, as her dysphagia increased, her muscle spasms became more pronounced and frequent, and she became increasingly agitated. She became ventilation dependent and unable to communicate due to full paralysis. On the day the woman was hospitalized, cerebrospinal fluid, serum, and saliva were submitted for testing. On the fourth day of her hospital admission, these tests were returned with results of probable ABLV infection. ABLV infection was confirmed by PCR on the 8th day of hospitalization. She died 19 days after the onset of illness. Postmortem tests were all strongly positive for ABLV. A notable feature of this case is that the patient underwent a 27 month incubation period; in comparison, the majority of rabies cases have an incubation period of 20-90 days, with 95% of cases exhibiting symptoms within a year of exposure to the virus. The third, and most recent, case occurred in December of 2012, when an eight-year-old boy was scratched by a bat in north Queensland. He became ill eight weeks later, showing symptoms including fever, anorexia, and abdominal pain. His condition worsened through his hospitalization, with abnormal and aggressive bouts between normal behavior and intense muscle spasms. He repeatedly needed to be extubated and sedated due to his spasms. The hospital performed several tests through his stay, including sending cerebrospinal fluid and blood samples off for testing, taking computed tomography images of his chest and abdomen, and performing neuroimaging (MRIs, electroencephalography's). Initially, tests for the ABLV antigens were negative, but repeated testing 12 days into his hospitalization provided positive results. The child died 28 days after the onset of symptoms on February 22, 2013. ABLV (and the other Lyssaviruses) present similarly to the traditional encephalitic rabies virus (RABV) in humans. The symptoms first are flu-like with fevers, headaches, and fatigue. The symptoms progress with paralysis, delirium, convulsions, and death. There are no known human survivors of ABLV infection after symptoms have manifested. The pathogenesis of ABLV is still widely unknown and still being studied. The virus initially infects the host through the peripheral nervous system following a bite or scratch from an infected animal. For the three reported ABLV cases in humans, the incubation period ranged from a few weeks to almost two years. Due to its difficulty in diagnosing, low number of reported cases, and relative novelty as an endemic virus, there are no successful treatment plans once the symptoms have begun. As previously stated, all intervention methods used on the three human cases of ABLV were not curative and all three cases resulted in fatality. However, it is highly recommended by physicians to receive the RABV post-exposure prophylaxis (PEP) protocol immediately after potential lyssavirus exposure (i.e.. exposure/interaction with bats). Additionally, the incident should be reported to the relevant public health unit. Currently, the PEP protocol involves thoroughly cleaning the wound and surrounding tissue, administration of the rabies vaccine, and administration of rabies immunoglobulin (RIG). Currently, there are two effective variations of RIGs used in PEP protocol, human RIG (HRIG) and equine RIG (ERIG). Drawbacks for HRIG are that there are limited supplies and the cost of production is high. HRIG is overall inaccessible for the general population. Drawbacks for ERIG are potential immunogenicity, which is when the immune system recognizes the RIG as foreign and causes an immune reaction. In a 2021 study performed by Weir, Coggins, et.al., a new treatment method was proposed that used human monoclonal antibodies over RIGs. They identified two (A6 and F11) that recognized the G protein of lyssaviruses in phylogroup I (including ABLV) and completely neutralized the virus. They also proposed it as a potential diagnostic tool, in which there are only limited methods with PCR and are late into the symptomatic phase to positively identify ABLV. Rabies vaccine and immunoglobulin are effective in prophylactic and therapeutic protection from ABLV infection. Since the emergence of the virus, rabies vaccine is administered to individuals with a heightened risk of exposure, and vaccine and immunoglobulin are provided for post-exposure treatment. The public health units in Australia advise that the population avoid and limit their interactions and physical contact with bats as much as possible. ABLV is one of four zoonotic viruses discovered in pteropid bats since 1994, the others being Hendra virus , Nipah virus , and Menangle virus . Of these, ABLV is the only virus known to be transmissible to humans directly from bats without an intermediate host. Thus education and awareness in the general population is a must. If a bat is found and/or appears injured, one should avoid contact with it and instead call local pest and animal control to appropriately remove the bat. ABLV has also been reported to have the ability to transfer to horses. Currently, this is the only other known susceptible species. ABLV was confirmed in two horses on Queensland's Darling Downs in May 2013. Both horses were euthanized when their condition deteriorated despite treatment and the attending veterinarian performed a post mortem examination obtaining samples that allowed for the laboratory diagnosis. The property was then quarantined. Three dogs and the four horses in closest contact received post exposure prophylaxis, as did all nine in-contact people. The virus was isolated and identified as the insectivorous bat strain. These cases have prompted reconsideration of the potential spillover of ABLV into domestic animal species. Veterinarians are urged to consider ABLV as a differential diagnosis in cases of progressive generalized neurological disease.
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Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Nigeria_Centre_for_Disease_Control/html
Nigeria Centre for Disease Control
The Nigeria Centre for Disease Control ( NCDC ) is the national public health institute for Nigeria. It is a federal government agency under the Federal Ministry of Health (Nigeria) , with its headquarters in Abuja , Federal Capital Territory. The agency's goal is to protect Nigerians from the impact of communicable diseases through the coordination of public health preparedness, surveillance , laboratory, and response functions for all infectious diseases. The NCDC targets its activities towards the prevention and control of diseases of public health importance. This includes the preparedness, detection and response to public health emergencies, research, training and knowledge management, health promotion and other activities to protect the health of Nigerians. The NCDC serves as Nigeria's International Health Regulations National Focal Point and is a member of the International Association of National Public Health Institutes . The NCDC was established in 2011, following a mandate from the Permanent Secretary of the Federal Ministry of Health (Nigeria) , to integrate specific units of the Ministry to serve as the foundation of the agency - the Epidemiology Division, the Avian Influenza Project, and the Nigeria Field Epidemiology and Laboratory Training Program (NFELTP). Prior to this, the request for the establishment of NCDC was endorsed in 2007 at the 51st National Council on Health. The Council recognized the need for a technical agency to respond to the challenges of public health emergencies in Nigeria and to enhance the country's preparedness to epidemics through the prevention, detection, and control of communicable diseases. The NCDC is modelled after the United States Centers for Disease Control and Prevention . Examples of epidemics that occurred before the inception of NCDC include the yellow fever epidemic in 1986 and 1987, the meningococcal meningitis epidemic in 1996, and cholera outbreaks in 2001 and 2004. On 15 March 2017, the Bill supporting the formal establishment of the NCDC was approved by the Federal Executive Council. This was presented to the 8th National Assembly (Nigeria) as an Executive Bill. Following deliberations by the National Assembly and approval, President Muhammadu Buhari signed the Bill for an Act to establish the NCDC as a federal government agency on November 13, 2018. The Nigeria Centre for Disease Control and Prevention Establishment Act 2018 gives NCDC the mandate to promote, coordinate, and facilitate the prevention, detection, and control of communicable diseases in Nigeria and other events of public health importance. To provide a framework for the strategic implementation of activities, the NCDC Strategy and Implementation Plan 2017 - 2021 was launched on 21 November 2017. The NCDC Vision and Mission Statement were created to guide the key activities outlined in the 2017-2021 strategic plan. The Mission Statement was further broken down into 5 strategic goals with defined outcomes, 22 objectives, and 89 corresponding activities to support the multiple initiatives of the 2017-2021 horizon. A three-day review process took place for internal and external stakeholders to identify the successes and challenges that require addressing and to identify and prioritise activities to execute in the subsequent years [ citation needed ] .The NCDC was established in 2011, following a mandate from the Permanent Secretary of the Federal Ministry of Health (Nigeria) , to integrate specific units of the Ministry to serve as the foundation of the agency - the Epidemiology Division, the Avian Influenza Project, and the Nigeria Field Epidemiology and Laboratory Training Program (NFELTP). Prior to this, the request for the establishment of NCDC was endorsed in 2007 at the 51st National Council on Health. The Council recognized the need for a technical agency to respond to the challenges of public health emergencies in Nigeria and to enhance the country's preparedness to epidemics through the prevention, detection, and control of communicable diseases. The NCDC is modelled after the United States Centers for Disease Control and Prevention . Examples of epidemics that occurred before the inception of NCDC include the yellow fever epidemic in 1986 and 1987, the meningococcal meningitis epidemic in 1996, and cholera outbreaks in 2001 and 2004. On 15 March 2017, the Bill supporting the formal establishment of the NCDC was approved by the Federal Executive Council. This was presented to the 8th National Assembly (Nigeria) as an Executive Bill. Following deliberations by the National Assembly and approval, President Muhammadu Buhari signed the Bill for an Act to establish the NCDC as a federal government agency on November 13, 2018. The Nigeria Centre for Disease Control and Prevention Establishment Act 2018 gives NCDC the mandate to promote, coordinate, and facilitate the prevention, detection, and control of communicable diseases in Nigeria and other events of public health importance. To provide a framework for the strategic implementation of activities, the NCDC Strategy and Implementation Plan 2017 - 2021 was launched on 21 November 2017. The NCDC Vision and Mission Statement were created to guide the key activities outlined in the 2017-2021 strategic plan. The Mission Statement was further broken down into 5 strategic goals with defined outcomes, 22 objectives, and 89 corresponding activities to support the multiple initiatives of the 2017-2021 horizon. A three-day review process took place for internal and external stakeholders to identify the successes and challenges that require addressing and to identify and prioritise activities to execute in the subsequent years [ citation needed ] .There are three campuses within the NCDC in Nigeria, located in Abuja, Federal Capital Territory , and Yaba , Lagos State. The NCDC led by a director-general is composed of six directorates: Surveillance and Epidemiology, Public Health Laboratory Services (PHL), Health Emergency Preparedness and Response (HEPR), Prevention Programs and Knowledge Management (PPKM), Administration and Human Resources, and Finance and Accounts. Each directorate is headed by a director, alongside deputy directors. All directors report directly to the director-general. The Directorate of Surveillance and Epidemiology collects, collates, and analyses data on Nigeria's priority diseases to detect outbreaks and inform policy. It ensures the implementation of the Integrated Disease Surveillance and Response (IDSR) strategy which include indicator-based and event-based surveillance system, that detects and verifies rumours related to diseases and outbreaks. The Directorate also hosts the IHR desk on behalf of the agency. The Directorate of Public Health Laboratory Services maintains and manages the NCDC's national and reference laboratories and network of public health laboratories. It provides diagnostic services for Nigeria's diseases of public health importance like viral hemorrhagic fevers , meningitis , cholera , measles , yellow fever , rubella , COVID-19 , and others. The Directorate also coordinates and manages the National Public Health Laboratory Information Management System (LIMS) for Nigeria. The NRL currently conducts sample testing for Yellow fever , Influenza , Cholera , CSM, Lassa fever , Monkeypox , Measles , Rubella , HIV , SARS-CoV-2 and other pathogens. The Directorate of Health Emergency Preparedness and Response is responsible for the mitigation of emergencies and the management of their impact. It builds capacity by advocating and sensitizing emergency preparedness and response. The Directorate also provides primary and secondary outbreak response activities through Rapid Response Teams. Its Public Health Emergency Operations Centre (PHEOC) was established during the 2016/2017 meningitis outbreak in Nigeria. It supports the coordination of outbreak response activities in the country. The Directorate of Prevention Programs and Knowledge Management develops health promotion and disease prevention plans that address endemic infectious diseases and non-communicable diseases. The Directorate mainly conducts research to support evidence-based policies and practices. The Directorate also manages the Nigeria Field Epidemiology Training Program. The Directorate of Administration and Human Resources oversees the management of human and material resources of the NCDC. It is organized into two sub-divisions: Human Resources and General Services. Human Resources is responsible for employee-related activities such as recruitment/appointment, promotion, training, and staff welfare. General Services is accountable for the management and maintenance of all the NCDC's assets. The Directorate of Finance and Accounts is responsible for all financial and accounting activities of the NCDC. It operates under the Nigerian accounting standards, as approved by the Accountant General of the Federation, which are in line with the Nigeria Public Service Reforms and the International Public Sector Accounting Standards.There are three campuses within the NCDC in Nigeria, located in Abuja, Federal Capital Territory , and Yaba , Lagos State. The NCDC led by a director-general is composed of six directorates: Surveillance and Epidemiology, Public Health Laboratory Services (PHL), Health Emergency Preparedness and Response (HEPR), Prevention Programs and Knowledge Management (PPKM), Administration and Human Resources, and Finance and Accounts. Each directorate is headed by a director, alongside deputy directors. All directors report directly to the director-general. The Directorate of Surveillance and Epidemiology collects, collates, and analyses data on Nigeria's priority diseases to detect outbreaks and inform policy. It ensures the implementation of the Integrated Disease Surveillance and Response (IDSR) strategy which include indicator-based and event-based surveillance system, that detects and verifies rumours related to diseases and outbreaks. The Directorate also hosts the IHR desk on behalf of the agency. The Directorate of Public Health Laboratory Services maintains and manages the NCDC's national and reference laboratories and network of public health laboratories. It provides diagnostic services for Nigeria's diseases of public health importance like viral hemorrhagic fevers , meningitis , cholera , measles , yellow fever , rubella , COVID-19 , and others. The Directorate also coordinates and manages the National Public Health Laboratory Information Management System (LIMS) for Nigeria. The NRL currently conducts sample testing for Yellow fever , Influenza , Cholera , CSM, Lassa fever , Monkeypox , Measles , Rubella , HIV , SARS-CoV-2 and other pathogens. The Directorate of Health Emergency Preparedness and Response is responsible for the mitigation of emergencies and the management of their impact. It builds capacity by advocating and sensitizing emergency preparedness and response. The Directorate also provides primary and secondary outbreak response activities through Rapid Response Teams. Its Public Health Emergency Operations Centre (PHEOC) was established during the 2016/2017 meningitis outbreak in Nigeria. It supports the coordination of outbreak response activities in the country. The Directorate of Prevention Programs and Knowledge Management develops health promotion and disease prevention plans that address endemic infectious diseases and non-communicable diseases. The Directorate mainly conducts research to support evidence-based policies and practices. The Directorate also manages the Nigeria Field Epidemiology Training Program. The Directorate of Administration and Human Resources oversees the management of human and material resources of the NCDC. It is organized into two sub-divisions: Human Resources and General Services. Human Resources is responsible for employee-related activities such as recruitment/appointment, promotion, training, and staff welfare. General Services is accountable for the management and maintenance of all the NCDC's assets. The Directorate of Finance and Accounts is responsible for all financial and accounting activities of the NCDC. It operates under the Nigerian accounting standards, as approved by the Accountant General of the Federation, which are in line with the Nigeria Public Service Reforms and the International Public Sector Accounting Standards.As of 2021, the NCDC has over 500 staff members who work across its three campuses. Several of its employees have at least one degree in the bachelor's , master's , or doctoral level. The various job roles at NCDC are in line with Nigeria's public service rules and include Surveillance and Epidemiology Officer,Medical laboratory Scientist, Data Officer/Manager, Research Coordinator, Program Officer/Manager, Health Communicator, Response Officer, Scientific Officer, and Project Coordinator. In addition to full-time employment, the NCDC also offers positions for short-term consultancies, internships, and fellowships for applicants worldwide throughout various times of each year. The Nigeria Field Epidemiology Training Program (NFETP) is a two-year field-based training and service program in applied epidemiology and public health that helps participants to build their capacity in strengthening disease surveillance and response systems. It trains medical epidemiology residents, public health laboratory residents, and veterinary epidemiology residents for leadership positions nationally and globally. There are over 300 graduates of the program working in public health across Nigeria. It is managed by NCDC in partnership with the African Field Epidemiology Network and with support from the United States Centers for Disease Control and Prevention . Since 2016, the NCDC and NFETP have held a yearly annual scientific conference in Abuja. It has provided a platform for experts in the epidemiology field to convey new knowledge to advance public health science. In 2021, the conference was renamed the 'Nigerian Conference of Applied and Field Epidemiology' (NICAFE). Graduates and residents of the NFETP are involved at the strategic, technical, and operational levels in the response to epidemic-prone and pandemic-prone diseases. They operate under various roles to serve different capacities within contact tracing, risk communications , infection prevention and control, surveillance, and coordination. The Nigeria Field Epidemiology Training Program (NFETP) is a two-year field-based training and service program in applied epidemiology and public health that helps participants to build their capacity in strengthening disease surveillance and response systems. It trains medical epidemiology residents, public health laboratory residents, and veterinary epidemiology residents for leadership positions nationally and globally. There are over 300 graduates of the program working in public health across Nigeria. It is managed by NCDC in partnership with the African Field Epidemiology Network and with support from the United States Centers for Disease Control and Prevention . Since 2016, the NCDC and NFETP have held a yearly annual scientific conference in Abuja. It has provided a platform for experts in the epidemiology field to convey new knowledge to advance public health science. In 2021, the conference was renamed the 'Nigerian Conference of Applied and Field Epidemiology' (NICAFE). Graduates and residents of the NFETP are involved at the strategic, technical, and operational levels in the response to epidemic-prone and pandemic-prone diseases. They operate under various roles to serve different capacities within contact tracing, risk communications , infection prevention and control, surveillance, and coordination. The Director-General of the NCDC is a senior-level position that is appointed by the President of the Federal Republic of Nigeria . It must be occupied by a health professional who has at least 15 years of postgraduate qualification experience in the relevant fields of medicine or public health . The Director-General is appointed under the following conditions: Serve as the Chief Executive Officer of the Centre and be responsible for the administration of the Centre. Receive supervision of the Governing Board of the Centre and the honourable Minister of Health. Shall hold office for a term of 4 years and be eligible for re-appointment for another term of 4 years and no more on such terms and conditions as may be determined by the President of Nigeria on the recommendation by the honourable Minister of Health. Since August 15 of 2016, Dr. Chikwe Ihekweazu has served as the Director-General of the NCDC. In July 2019, the Presidency through the Federal Ministry of Information announced that Dr. Ihekweazu was re-appointed into office by President Muhammadu Buhari for a second term. On 18 October 2021, Dr. Ifedayo Adetifa assumed duties as the 2nd Director-General of the NCDC upon Dr. Ihekweazu's recruitment to WHO. Under the Office of the Director-General, there are six Heads of Departments who represent each Directorate of the NCDC.The Director-General of the NCDC is a senior-level position that is appointed by the President of the Federal Republic of Nigeria . It must be occupied by a health professional who has at least 15 years of postgraduate qualification experience in the relevant fields of medicine or public health . The Director-General is appointed under the following conditions: Serve as the Chief Executive Officer of the Centre and be responsible for the administration of the Centre. Receive supervision of the Governing Board of the Centre and the honourable Minister of Health. Shall hold office for a term of 4 years and be eligible for re-appointment for another term of 4 years and no more on such terms and conditions as may be determined by the President of Nigeria on the recommendation by the honourable Minister of Health. Since August 15 of 2016, Dr. Chikwe Ihekweazu has served as the Director-General of the NCDC. In July 2019, the Presidency through the Federal Ministry of Information announced that Dr. Ihekweazu was re-appointed into office by President Muhammadu Buhari for a second term. On 18 October 2021, Dr. Ifedayo Adetifa assumed duties as the 2nd Director-General of the NCDC upon Dr. Ihekweazu's recruitment to WHO.Under the Office of the Director-General, there are six Heads of Departments who represent each Directorate of the NCDC.The Department of Surveillance and Epidemiology produces and publishes a 'Weekly Epidemiological Report' on the NCDC website weekly. The report provides a summary of key infectious diseases in Nigeria, showcasing data of case activities (e.g. the number of suspected cases, the number of confirmed cases, the number of deaths, the number of States and LGAs affected and the case fatality rate) within the previous week and year-to-date. Diseases of importance include Yellow fever, Measles, Cholera, Lassa fever, Cerebrospinal Meningitis (CSM), Acute Flaccid Paralysis, and the National Influenza Sentinel Surveillance (NISS). The WER includes an editorial that highlights key activities and events that occurred at the NCDC within the previous week of the posting date. Located on the NCDC website, the National Disease Outbreak Dashboard is an interactive dashboard that provides users with case-based data on Nigeria's prioritized infectious diseases from 2006 to date. Diseases include Cholera , CSM, Lassa fever , Measles , Monkeypox , and yellow fever . A detailed map of Nigeria displays every State and LGA in the country, alongside an interactive line chart. Data displayed on the dashboard include the number of confirmed cases by year, the names and number of affected States, the names and number of affected LGAs, and the percentage of case victims based on gender. The NCDC collects, analyses, and publishes national COVID-19 updates for Nigeria daily. The COVID-19 dashboard features cumulative and State-specified figures of samples tested, active cases, confirmed cases, discharged cases, and deaths. A comprehensive situation report about Nigeria's COVID-19 response is also uploaded on the website weekly. The website also has a laboratory directory composed of government-owned and private laboratories in Nigeria that are accredited to conduct COVID-19 testing, and other policies/guidelines for the response. The website also has a laboratory directory composed of government-owned and private laboratories in Nigeria that are accredited to conduct COVID-19 testing and other policies/guidelines for the response. In 2017, NCDC established a national Public Health Emergency Operations Centre (PHEOC) as the Incident Coordination Centre. It currently serves as Nigeria's public health intelligence and response coordination hub by supporting disease detection and the coordination of information resources during public health events. Since 2018, NCDC has been supporting all 36 States and the Federal Capital territory to establish State-level PHEOCs to effectively promote communication and resource management on a State-wide level during public health emergencies. Towards the end of 2020, 34 states in Nigeria have established a PHEOC, supported by NCDC. The NCDC supports the State PHEOCs through training, mentorship, and regular simulations. The Infection Prevention and Control (IPC) Unit housed under the PPKM Directorate is responsible for disseminating information on the standard precautions of preventing and controlling infections. The Unit mainly based its activities to the safety of health care practitioners and the general population by strengthening IPC capacity in Nigeria. In 2019, NCDC launched the 'Turn Nigeria Orange' project, a comprehensive five-year program that aims to support Nigerian healthcare facilities and initiate IPC programs. The program has supported the establishment of the Orange Network, a network of dedicated tertiary health facilities in Nigeria that aim to transform into centre of excellence in infection prevention and control. On November 26, 2016, the honourable Minister of Health approved the establishment of a National Antimicrobial Resistance (AMR) coordinating body at the NCDC. This action was in response to WHO Member States' commitment to developing multi-sectoral national action plans based on the WHO Global Action Plan on AMR. It also positioned the NCDC to serve as the lead representative for coordinating AMR control in Nigeria. Members of the AMR coordinating body inaugurated on the 16th and 17th January, 2017 to review Nigeria's requirement for its National Action Plan for AMR. Launched in May 2017, the National Action Plan for AMR outlines the implementation of strategic and operational activities to ensure measurable containment of AMR in Nigeria. The Plan's objectives was formed through a SWOT analysis of the AMR condition in Nigeria. Recommendations on AMR containment were based on the five strategic objectives outlined in the Global Action Plan on AMR. Since its inception, the plan has guided the NCDC's advisory and campaign efforts of promoting the responsible use of antibiotics to Nigerian citizens. The NCDC adopted the Surveillance and Outbreak Response Management and Analysis System (SORMAS) in October 2017. SORMAS is a digital system for comprehensive disease surveillance. The multifunctional tool has assisted the NCDC in performing outbreak management response tasks by contact tracing, laboratory data management, and rumor management. During the 2017-2019 monkeypox outbreak in Nigeria, the NCDC utilized SORMAS to conduct contact tracing for case notification and analyze data for the production of weekly epidemiological reports on the epidemic for the general public. By September 2020, SORMAS was fully deployed and adopted by all States and the Federal Capital Territory in prioritized health facilities for reporting use. The SORMAS team at the NCDC conducts training in the States to teach surveillance officers the use of the system for enhanced surveillance and outbreak response on epidemic-prone diseases.The Department of Surveillance and Epidemiology produces and publishes a 'Weekly Epidemiological Report' on the NCDC website weekly. The report provides a summary of key infectious diseases in Nigeria, showcasing data of case activities (e.g. the number of suspected cases, the number of confirmed cases, the number of deaths, the number of States and LGAs affected and the case fatality rate) within the previous week and year-to-date. Diseases of importance include Yellow fever, Measles, Cholera, Lassa fever, Cerebrospinal Meningitis (CSM), Acute Flaccid Paralysis, and the National Influenza Sentinel Surveillance (NISS). The WER includes an editorial that highlights key activities and events that occurred at the NCDC within the previous week of the posting date.Located on the NCDC website, the National Disease Outbreak Dashboard is an interactive dashboard that provides users with case-based data on Nigeria's prioritized infectious diseases from 2006 to date. Diseases include Cholera , CSM, Lassa fever , Measles , Monkeypox , and yellow fever . A detailed map of Nigeria displays every State and LGA in the country, alongside an interactive line chart. Data displayed on the dashboard include the number of confirmed cases by year, the names and number of affected States, the names and number of affected LGAs, and the percentage of case victims based on gender.The NCDC collects, analyses, and publishes national COVID-19 updates for Nigeria daily. The COVID-19 dashboard features cumulative and State-specified figures of samples tested, active cases, confirmed cases, discharged cases, and deaths. A comprehensive situation report about Nigeria's COVID-19 response is also uploaded on the website weekly. The website also has a laboratory directory composed of government-owned and private laboratories in Nigeria that are accredited to conduct COVID-19 testing, and other policies/guidelines for the response. The website also has a laboratory directory composed of government-owned and private laboratories in Nigeria that are accredited to conduct COVID-19 testing and other policies/guidelines for the response.In 2017, NCDC established a national Public Health Emergency Operations Centre (PHEOC) as the Incident Coordination Centre. It currently serves as Nigeria's public health intelligence and response coordination hub by supporting disease detection and the coordination of information resources during public health events. Since 2018, NCDC has been supporting all 36 States and the Federal Capital territory to establish State-level PHEOCs to effectively promote communication and resource management on a State-wide level during public health emergencies. Towards the end of 2020, 34 states in Nigeria have established a PHEOC, supported by NCDC. The NCDC supports the State PHEOCs through training, mentorship, and regular simulations.The Infection Prevention and Control (IPC) Unit housed under the PPKM Directorate is responsible for disseminating information on the standard precautions of preventing and controlling infections. The Unit mainly based its activities to the safety of health care practitioners and the general population by strengthening IPC capacity in Nigeria. In 2019, NCDC launched the 'Turn Nigeria Orange' project, a comprehensive five-year program that aims to support Nigerian healthcare facilities and initiate IPC programs. The program has supported the establishment of the Orange Network, a network of dedicated tertiary health facilities in Nigeria that aim to transform into centre of excellence in infection prevention and control. On November 26, 2016, the honourable Minister of Health approved the establishment of a National Antimicrobial Resistance (AMR) coordinating body at the NCDC. This action was in response to WHO Member States' commitment to developing multi-sectoral national action plans based on the WHO Global Action Plan on AMR. It also positioned the NCDC to serve as the lead representative for coordinating AMR control in Nigeria. Members of the AMR coordinating body inaugurated on the 16th and 17th January, 2017 to review Nigeria's requirement for its National Action Plan for AMR. Launched in May 2017, the National Action Plan for AMR outlines the implementation of strategic and operational activities to ensure measurable containment of AMR in Nigeria. The Plan's objectives was formed through a SWOT analysis of the AMR condition in Nigeria. Recommendations on AMR containment were based on the five strategic objectives outlined in the Global Action Plan on AMR. Since its inception, the plan has guided the NCDC's advisory and campaign efforts of promoting the responsible use of antibiotics to Nigerian citizens.The NCDC adopted the Surveillance and Outbreak Response Management and Analysis System (SORMAS) in October 2017. SORMAS is a digital system for comprehensive disease surveillance. The multifunctional tool has assisted the NCDC in performing outbreak management response tasks by contact tracing, laboratory data management, and rumor management. During the 2017-2019 monkeypox outbreak in Nigeria, the NCDC utilized SORMAS to conduct contact tracing for case notification and analyze data for the production of weekly epidemiological reports on the epidemic for the general public. By September 2020, SORMAS was fully deployed and adopted by all States and the Federal Capital Territory in prioritized health facilities for reporting use. The SORMAS team at the NCDC conducts training in the States to teach surveillance officers the use of the system for enhanced surveillance and outbreak response on epidemic-prone diseases.The first confirmed case of COVID-19 in Nigeria was discovered at the Mainland Infectious Disease Hospital, Yaba , on 27 February 2020. Before the arrival of the index case, the NCDC had developed various measures to prevent the entry of COVID-19 into the country and to detect its presence on arrival. Some of the measures included increasing surveillance at ports of entry through body temperature measurements, collecting the contact details of travelers arriving from COVID-19 hotspots, and using SORMAS and the Mobile Strengthening and Outbreak Response Management System (MSERS) for case-cased reporting and aggregate reporting of suspected cases respectively. The NCDC established a multi-sectoral National Coronavirus Preparedness Group (NCPG) on 26 January 2020 to execute regular epidemic intelligence gathering, intensive risk communications, and strengthening of laboratory capacity for testing in preparation for the disease. It then transitioned into a PHEOC on February 28, 2021, when the first case in Nigeria was detected. The PHEOC promptly developed an incident action plan to coordinate NCDC's COVID-19 response activities across key response areas of coordination, epidemiology and surveillance, laboratory, IPC, case management, risk communication, logistics and several others. State PHEOCs also adopted the pillars to increase response efforts in controlling COVID-19 within their respective States. The first COVID-19 case in Nigeria prompted President Muhammadu Buhari to establish the Presidential Steering Committee (PSC) on COVID-19, formally known as the Presidential Task Force (PTF) on COVID-19, on March 9, 2020. The Director-General represents the NCDC as a member of the PSC by supporting the implementation of multi-sectoral activities. With oversight from the PSC, the NCDC leads the national public health response on COVID-19 in Nigeria. The NCDC's role in the PSC has contributed to the execution of several measures such as the compulsory use of face masks in public settings, temporary closure and safe re-opening of National Youth Service Corps orientation camps, temporary closure and safe re-opening of airports for domestic and international travel, temporary closure and safe re-opening of educational institutions, and restriction of large gatherings. During the onset of the COVID-19 pandemic in Nigeria, the NCDC supported the deployment of Rapid Response Teams in States and the Federal Capital Territory to support case tracking. 52 Rapid Response Teams were deployed to several States in 2020. The NCDC rapidly increased the testing capacity in Nigeria by scaling up diagnostic testing of COVID-19 nationwide for accessibility. By March 2020, only five laboratories in the NCDC molecular laboratory network could diagnose COVID-19 in Nigeria: the NRL, Virology Laboratory of Lagos University Teaching Hospital , Irru Specialist Teaching Hospital, Nigerian Institute of Medical Research , and African Centre of Excellence for Genomics of Infectious Diseases. Nearly a year later, NCDC supported the activation for every State in Nigeria to have at least one public health laboratory that conducts COVID-19 testing. The NCDC has also promoted the use of the GeneXpert System to further scale up diagnostic activities nationwide. Alongside several partners, the NCDC reported the first genome sequence of SARS-CoV-2 from Africa from the first confirmed case of COVID-19 in Nigeria. SORMAS has been leveraged at the NCDC to support COVID-19 contact tracing and disease surveillance at State and national levels. By October 2020, 80% of Nigeria's States reported 90% of their contacts traced, and 35% of States reported a contact-to-case ratio of more than 5. The NCDC also supported SORMAS training for epidemiologists in various treatment Centres and Laboratories across the nation. The NCDC and the Federal Ministry of Health, in collaboration with Tertiary Education Trust Fund and National Universities Commission , established the Nigeria COVID-19 Research Coalition, a national platform to coordinate the generation of evidence-based research to support Nigeria's response to the COVID-19 pandemic. The research coalition currently has a membership of over 40 institutions. Members of the NCDC have collaborated with partnering institutions to produce several research manuscripts about the COVID-19 response in Nigeria. In collaboration with Port Health Services of the Federal Ministry of Health (Nigeria) , the NCDC hosts and manages the Nigeria International Travel Portal. The platform regulates mandatory testing for international travelers departing from or arriving in Nigeria. It also aids Nigeria in contact tracing and surveillance at international borders to detect COVID-19 cases. As of June 2021, the NCDC has developed over 60 guidelines relating to COVID-19 for the population of Nigeria. The NCDC actively disseminates relevant information on the COVID-19 pandemic through its website, SMS messaging platform, and social media accounts. Daily statistics of COVID-19 in Nigeria are published by the NCDC on all of its online platforms and third-party applications.
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Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Colorado_tick_fever/html
Colorado tick fever
Colorado tick fever (CTF) is a viral infection ( Coltivirus ) transmitted from the bite of an infected Rocky Mountain wood tick ( Dermacentor andersoni ). It should not be confused with the bacterial tick-borne infection, Rocky Mountain spotted fever . Colorado tick fever is probably the same disease that American pioneers referred to as "mountain fever". Colorado tick fever virus (CTFV) infects haemopoietic cells, particularly erythrocytes , which explains how the virus is transmitted by ticks and also accounts for the incidence of transmission by blood transfusion. [ citation needed ]The first signs and symptoms of Colorado Tick Fever are shown between the 1 and 14th day after the bite from the tick. Once bit by the tick and the onset of symptoms is presented, one will more often then not experience a biphasic fever. A biphasic fever, is a fever that will attack, only to let you feel better, just to infect you once again. Although the virus may only last a couple of weeks, the Virus can be found in the red blood cells for up to 6 months after being cured . Initial symptoms include fever, chills, headaches, pain behind the eyes, light sensitivity, muscle pain, generalized malaise, abdominal pain, hepatosplenomegaly, nausea and vomiting, and a flat or pimply rash. During the second phase of the virus, a high fever can return with an increase in symptoms. CTF can be very severe in cases involving children and can even require hospitalization. Complications with this disease have included aseptic meningitis, encephalitis, and hemorrhagic fever, but these are rare. [ citation needed ] CTF is seasonal, mostly occurring in the Rocky Mountain region of the United States and usually in altitudes from 4,000 to 10,000 feet (1,600 to 3,000 meters). Patients with CTF are mostly campers and young males, who most likely have been bitten because of their activities.The virus particle, like other coltiviruses, is about 80 nm in diameter and is generally not enveloped. The double-stranded RNA viral genome is about 20,000 bp long and is divided into 12 segments, which are termed Seg-1 to Seg-12. Viral replication in infected cells is associated with characteristic cytoplasmic granular matrices. Evidence suggests the viral presence in mature erythrocytes is a result of replication of the virus in hematopoietic erythrocyte precursor cells and simultaneous maturation of the infected immature cells rather than of direct entry and replication of CTFV in mature erythrocytes. The Rocky Mountain wood tick is usually found attached to a host, but when it is without a host, it hides in cracks and crevices, as well as soil. If for some reason the tick is not able to find a host before the winter, it will stay under ground cover until spring, when it can resume its search. The behavior of the Rocky Mountain wood tick varies with its life stages: adults are active as early as March, peaking in April and May, while nymphs and larvae are active around April and June respectively. By late summer or early fall, all these stages typically disappear. Small mammals are common hosts for larvae and nymphs, while adults generally feed on larger mammals such as horses, cattle, and deer. Colorado tick fever (CTF) is transmitted through the bite of an infected Rocky Mountain wood tick . The ticks become carriers of the CTF virus by feeding on infected reservoir animals like small rodents. Transmission from a tick to person is the most common cause of infection. Person-to-person transmission is not typical but can occur rarely through blood transfusions. Post-infection, the CTF virus can linger in red blood cells for several months, hence, blood and bone marrow donations are discouraged for six months following infection. The virus particle, like other coltiviruses, is about 80 nm in diameter and is generally not enveloped. The double-stranded RNA viral genome is about 20,000 bp long and is divided into 12 segments, which are termed Seg-1 to Seg-12. Viral replication in infected cells is associated with characteristic cytoplasmic granular matrices. Evidence suggests the viral presence in mature erythrocytes is a result of replication of the virus in hematopoietic erythrocyte precursor cells and simultaneous maturation of the infected immature cells rather than of direct entry and replication of CTFV in mature erythrocytes. The Rocky Mountain wood tick is usually found attached to a host, but when it is without a host, it hides in cracks and crevices, as well as soil. If for some reason the tick is not able to find a host before the winter, it will stay under ground cover until spring, when it can resume its search. The behavior of the Rocky Mountain wood tick varies with its life stages: adults are active as early as March, peaking in April and May, while nymphs and larvae are active around April and June respectively. By late summer or early fall, all these stages typically disappear. Small mammals are common hosts for larvae and nymphs, while adults generally feed on larger mammals such as horses, cattle, and deer. Colorado tick fever (CTF) is transmitted through the bite of an infected Rocky Mountain wood tick . The ticks become carriers of the CTF virus by feeding on infected reservoir animals like small rodents. Transmission from a tick to person is the most common cause of infection. Person-to-person transmission is not typical but can occur rarely through blood transfusions. Post-infection, the CTF virus can linger in red blood cells for several months, hence, blood and bone marrow donations are discouraged for six months following infection. A combination of clinical signs, symptoms, and laboratory tests can confirm the likelihood of having CTF. Some tests include complement fixation to Colorado tick virus, immunofluorescence for Colorado tick fever, and some other common laboratory findings suggestive of CTF, including leucopenia, thrombocytopenia, and mildly elevated liver enzyme levels. Detection of viral antibodies on red blood cells is possible. To avoid tick bites and infection, experts advise: Avoid tick-infested areas, especially during the warmer months. Wear light-colored clothing so ticks can be easily seen. Wear a long sleeved shirt, hat, long pants, and tuck pant legs into socks. Walk in the center of trails to avoid overhanging grass and brush. Clothing and body parts should be checked every few hours for ticks when spending time outdoors in tick-infested areas. Ticks are most often found on the thigh, arms, underarms, and legs. Ticks can be very small (no bigger than a pinhead). Look carefully for new "freckles". The use of insect repellents containing DEET on skin or permethrin on clothing can be effective. Follow the directions on the container and wash off repellents when going indoors. Remove attached ticks immediately. Contracting the CTF virus is thought to provide long-lasting immunity against reinfection. However, it is always wise to be on the safe side and try to prevent tick bites. No specific treatment for CTF is yet available. The first action is to make sure the tick is fully removed from the skin, then acetaminophen and analgesics can be used to help relieve the fever and pain. Aspirin is not recommended for children, as it has been linked to Reye's syndrome in some viral illnesses. Salicylates should not be used because of thrombocytopenia , and the rare occurrence of bleeding disorders. People who suspect they have been bitten by a tick or are starting to show signs of CTF should contact their physicians immediately. Ticks should be removed promptly and carefully with tweezers and by applying gentle, steady traction. The tick's body should not be crushed when it is removed and the tweezers should be placed as close to the skin as possible to avoid leaving tick mouthparts in the skin. Mouthparts left in the skin can allow secondary infections. Ticks should not be removed with bare hands. Hands should be protected by gloves or tissues and thoroughly washed with soap and water after the removal process. A match or flame should not be used to remove a tick. This method, once thought safe, can cause the tick to regurgitate expelling any disease it may be carrying into the bite wound. Ticks should be removed promptly and carefully with tweezers and by applying gentle, steady traction. The tick's body should not be crushed when it is removed and the tweezers should be placed as close to the skin as possible to avoid leaving tick mouthparts in the skin. Mouthparts left in the skin can allow secondary infections. Ticks should not be removed with bare hands. Hands should be protected by gloves or tissues and thoroughly washed with soap and water after the removal process. A match or flame should not be used to remove a tick. This method, once thought safe, can cause the tick to regurgitate expelling any disease it may be carrying into the bite wound. The disease develops from March to September, with the highest infections occurring in June. The disease is found almost exclusively in the western United States and Canada, mostly in high mountain areas such as Colorado and Idaho. The CTFV was first isolated from human blood in 1944.
1,512
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Apilimod/html
Apilimod
N -[( E )-(3-methylphenyl)methylideneamino]-6-morpholin-4-yl-2-(2-pyridin-2-ylethoxy)pyrimidin-4-amine CC1=CC(=CC=C1)/C=N/NC2=CC(=NC(=N2)OCCC3=CC=CC=N3)N4CCOCC4 InChI=1S/C23H26N6O2/c1-18-5-4-6-19(15-18)17-25-28-21-16-22(29-10-13-30-14-11-29)27-23(26-21)31-12-8-20-7-2-3-9-24-20/h2-7,9,15-17H,8,10-14H2,1H3,(H,26,27,28)/b25-17+ Key:HSKAZIJJKRAJAV-KOEQRZSOSA-N Apilimod ( STA-5326 ) is a drug that was initially identified as an inhibitor of production of the interleukins IL-12 and IL-23 , and developed for the oral treatment of autoimmune conditions such as Crohn's disease and rheumatoid arthritis , though clinical trial results were disappointing and development for these applications was not continued. Subsequently, it was discovered that apilimod has an additional mode of action, as an inhibitor of the lipid kinase enzyme PIKfyve . PIKfyve makes two lipids, PtdIns5P and PtdIns(3,5)P2, whose syntheses are efficiently and similarly inhibited by apilimod (ID50 = 0.4 nM) in in vitro assays. Administration of apilimod (100 nM; 60 min) in human embryonic kidney cells powerfully reduces levels of both PtdIns5P and PtdIns(3,5)P2. Recently apilimod has been repurposed as a potential antiviral and anti-cancer drug, with possible applications in the treatment of non-Hodgkin lymphoma as well as viral diseases such as Ebola virus disease , Lassa fever and COVID-19 .
164
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Fever/html
Fever
Fever or pyrexia in humans is a body temperature above the normal range due to an increase in the body's temperature set point in the hypothalamus . There is no single agreed-upon upper limit for normal temperature: sources use values ranging between 37.2 and 38.3 °C (99.0 and 100.9 °F) in humans. The increase in set point triggers increased muscle contractions and causes a feeling of cold or chills . This results in greater heat production and efforts to conserve heat. When the set point temperature returns to normal, a person feels hot, becomes flushed , and may begin to sweat . Rarely a fever may trigger a febrile seizure , with this being more common in young children. Fevers do not typically go higher than 41 to 42 °C (106 to 108 °F) . A fever can be caused by many medical conditions ranging from non-serious to life-threatening . This includes viral , bacterial , and parasitic infections —such as influenza , the common cold , meningitis , urinary tract infections , appendicitis , Lassa , COVID-19 , and malaria . Non-infectious causes include vasculitis , deep vein thrombosis , connective tissue disease , side effects of medication or vaccination, and cancer . It differs from hyperthermia , in that hyperthermia is an increase in body temperature over the temperature set point, due to either too much heat production or not enough heat loss . Treatment to reduce fever is generally not required. Treatment of associated pain and inflammation, however, may be useful and help a person rest. Medications such as ibuprofen or paracetamol (acetaminophen) may help with this as well as lower temperature. Children younger than three months require medical attention, as might people with serious medical problems such as a compromised immune system or people with other symptoms. Hyperthermia requires treatment. Fever is one of the most common medical signs . It is part of about 30% of healthcare visits by children and occurs in up to 75% of adults who are seriously sick. While fever evolved as a defense mechanism, treating a fever does not appear to improve or worsen outcomes. Fever is often viewed with greater concern by parents and healthcare professionals than is usually deserved, a phenomenon known as "fever phobia." A fever is usually accompanied by sickness behavior , which consists of lethargy , depression , loss of appetite , sleepiness , hyperalgesia , dehydration, and the inability to concentrate. Sleeping with a fever can often cause intense or confusing nightmares, commonly called "fever dreams". Mild to severe delirium (which can also cause hallucinations ) may also present itself during high fevers. A range for normal temperatures has been found. Central temperatures, such as rectal temperatures, are more accurate than peripheral temperatures. Fever is generally agreed to be present if the elevated temperature is caused by a raised set point and: In adults, the normal range of oral temperatures in healthy individuals is 35.7–37.7 °C (96.3–99.9 °F) among men and 33.2–38.1 °C (91.8–100.6 °F) among women, while when taken rectally it is 36.7–37.5 °C (98.1–99.5 °F) among men and 36.8–37.1 °C (98.2–98.8 °F) among women, and for ear measurement it is 35.5–37.5 °C (95.9–99.5 °F) among men and 35.7–37.5 °C (96.3–99.5 °F) among women. Normal body temperatures vary depending on many factors, including age, sex, time of day, ambient temperature, activity level, and more. Normal daily temperature variation has been described as 0.5 °C (0.9 °F). : 4012 A raised temperature is not always a fever. For example, the temperature rises in healthy people when they exercise, but this is not considered a fever, as the set point is normal. On the other hand, a "normal" temperature may be a fever, if it is unusually high for that person; for example, medically frail elderly people have a decreased ability to generate body heat, so a "normal" temperature of 37.3 °C (99.1 °F) may represent a clinically significant fever. Hyperthermia is an elevation of body temperature over the temperature set point, due to either too much heat production or not enough heat loss . Hyperthermia is thus not considered fever. : 103 Hyperthermia should not be confused with hyperpyrexia (which is a very high fever). : 102 Clinically, it is important to distinguish between fever and hyperthermia as hyperthermia may quickly lead to death and does not respond to antipyretic medications. The distinction may however be difficult to make in an emergency setting, and is often established by identifying possible causes. : 103Hyperthermia is an elevation of body temperature over the temperature set point, due to either too much heat production or not enough heat loss . Hyperthermia is thus not considered fever. : 103 Hyperthermia should not be confused with hyperpyrexia (which is a very high fever). : 102 Clinically, it is important to distinguish between fever and hyperthermia as hyperthermia may quickly lead to death and does not respond to antipyretic medications. The distinction may however be difficult to make in an emergency setting, and is often established by identifying possible causes. : 103Various patterns of measured patient temperatures have been observed, some of which may be indicative of a particular medical diagnosis : Among the types of intermittent fever are ones specific to cases of malaria caused by different pathogens. These are: In addition, there is disagreement regarding whether a specific fever pattern is associated with Hodgkin's lymphoma —the Pel–Ebstein fever , with patients argued to present high temperature for one week, followed by low for the next week, and so on, where the generality of this pattern is debated. Persistent fever that cannot be explained after repeated routine clinical inquiries is called fever of unknown origin . A neutropenic fever , also called febrile neutropenia, is a fever in the absence of normal immune system function. Because of the lack of infection-fighting neutrophils , a bacterial infection can spread rapidly; this fever is, therefore, usually considered to require urgent medical attention. This kind of fever is more commonly seen in people receiving immune-suppressing chemotherapy than in apparently healthy people. Hyperpyrexia is an extreme elevation of body temperature which, depending upon the source, is classified as a core body temperature greater than or equal to 40 or 41 °C (104 or 106 °F) ; the range of hyperpyrexias includes cases considered severe (≥ 40 °C) and extreme (≥ 42 °C). It differs from hyperthermia in that one's thermoregulatory system's set point for body temperature is set above normal, then heat is generated to achieve it. In contrast, hyperthermia involves body temperature rising above its set point due to outside factors. The high temperatures of hyperpyrexia are considered medical emergencies , as they may indicate a serious underlying condition or lead to severe morbidity (including permanent brain damage ), or to death. A common cause of hyperpyrexia is an intracranial hemorrhage . Other causes in emergency room settings include sepsis , Kawasaki syndrome , neuroleptic malignant syndrome , drug overdose , serotonin syndrome , and thyroid storm . Hyperpyrexia is an extreme elevation of body temperature which, depending upon the source, is classified as a core body temperature greater than or equal to 40 or 41 °C (104 or 106 °F) ; the range of hyperpyrexias includes cases considered severe (≥ 40 °C) and extreme (≥ 42 °C). It differs from hyperthermia in that one's thermoregulatory system's set point for body temperature is set above normal, then heat is generated to achieve it. In contrast, hyperthermia involves body temperature rising above its set point due to outside factors. The high temperatures of hyperpyrexia are considered medical emergencies , as they may indicate a serious underlying condition or lead to severe morbidity (including permanent brain damage ), or to death. A common cause of hyperpyrexia is an intracranial hemorrhage . Other causes in emergency room settings include sepsis , Kawasaki syndrome , neuroleptic malignant syndrome , drug overdose , serotonin syndrome , and thyroid storm . Fever is a common symptom of many medical conditions: Adult and pediatric manifestations for the same disease may differ; for instance, in COVID-19 , one metastudy describes 92.8% of adults versus 43.9% of children presenting with fever. In addition, fever can result from a reaction to an incompatible blood product. Teething is not a cause of fever. Fever is thought to contribute to host defense, as the reproduction of pathogens with strict temperature requirements can be hindered, and the rates of some important immunological reactions are increased by temperature. Fever has been described in teaching texts as assisting the healing process in various ways, including: A fever response to an infectious disease is generally regarded as protective, whereas fever in non-infections may be maladaptive. Studies have not been consistent on whether treating fever generally worsens or improves mortality risk. Benefits or harms may depend on the type of infection, health status of the patient and other factors. Studies using warm-blooded vertebrates suggest that they recover more rapidly from infections or critical illness due to fever. In sepsis , fever is associated with reduced mortality. Fever is thought to contribute to host defense, as the reproduction of pathogens with strict temperature requirements can be hindered, and the rates of some important immunological reactions are increased by temperature. Fever has been described in teaching texts as assisting the healing process in various ways, including:A fever response to an infectious disease is generally regarded as protective, whereas fever in non-infections may be maladaptive. Studies have not been consistent on whether treating fever generally worsens or improves mortality risk. Benefits or harms may depend on the type of infection, health status of the patient and other factors. Studies using warm-blooded vertebrates suggest that they recover more rapidly from infections or critical illness due to fever. In sepsis , fever is associated with reduced mortality. Temperature is regulated in the hypothalamus . The trigger of a fever, called a pyrogen, results in the release of prostaglandin E2 (PGE2). PGE2 in turn acts on the hypothalamus, which creates a systemic response in the body, causing heat-generating effects to match a new higher temperature set point. There are four receptors in which PGE2 can bind (EP1-4), with a previous study showing the EP3 subtype is what mediates the fever response. Hence, the hypothalamus can be seen as working like a thermostat . When the set point is raised, the body increases its temperature through both active generation of heat and retention of heat. Peripheral vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. Norepinephrine increases thermogenesis in brown adipose tissue , and muscle contraction through shivering raises the metabolic rate . If these measures are insufficient to make the blood temperature in the brain match the new set point in the hypothalamus, the brain orchestrates heat effector mechanisms via the autonomic nervous system or primary motor center for shivering. These may be: [ citation needed ] When the hypothalamic set point moves back to baseline—either spontaneously or via medication—normal functions such as sweating, and the reverse of the foregoing processes (e.g., vasodilation, end of shivering, and nonshivering heat production) are used to cool the body to the new, lower setting. [ citation needed ] This contrasts with hyperthermia , in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an excessively hot environment ( heat stroke ) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications. [ verification needed ] In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis , also known as non-shivering thermogenesis). [ citation needed ] Increased heart rate and vasoconstriction contribute to increased blood pressure in fever. [ citation needed ] A pyrogen is a substance that induces fever. In the presence of an infectious agent, such as bacteria, viruses, viroids, etc ., the immune response of the body is to inhibit their growth and eliminate them. The most common pyrogens are endotoxins, which are lipopolysaccharides (LPS) produced by Gram-negative bacteria such as E. coli . But pyrogens include non-endotoxic substances (derived from microorganisms other than gram-negative-bacteria or from chemical substances) as well. The types of pyrogens include internal (endogenous) and external (exogenous) to the body. [ citation needed ] The "pyrogenicity" of given pyrogens varies: in extreme cases, bacterial pyrogens can act as superantigens and cause rapid and dangerous fevers. Endogenous pyrogens are cytokines released from monocytes (which are part of the immune system ). In general, they stimulate chemical responses, often in the presence of an antigen , leading to a fever. Whilst they can be a product of external factors like exogenous pyrogens, they can also be induced by internal factors like damage associated molecular patterns such as cases like rheumatoid arthritis or lupus. Major endogenous pyrogens are interleukin 1 (α and β) : 1237–1248 and interleukin 6 (IL-6). Minor endogenous pyrogens include interleukin-8 , tumor necrosis factor-β , macrophage inflammatory protein -α and macrophage inflammatory protein-β as well as interferon-α , interferon-β , and interferon-γ . : 1237–1248 Tumor necrosis factor-α (TNF) also acts as a pyrogen, mediated by interleukin 1 (IL-1) release. These cytokine factors are released into general circulation, where they migrate to the brain's circumventricular organs where they are more easily absorbed than in areas protected by the blood–brain barrier . [ citation needed ] The cytokines then bind to endothelial receptors on vessel walls to receptors on microglial cells , resulting in activation of the arachidonic acid pathway . [ citation needed ] Of these, IL-1β, TNF, and IL-6 are able to raise the temperature setpoint of an organism and cause fever. These proteins produce a cyclooxygenase which induces the hypothalamic production of PGE2 which then stimulates the release of neurotransmitters such as cyclic adenosine monophosphate and increases body temperature. Exogenous pyrogens are external to the body and are of microbial origin. In general, these pyrogens, including bacterial cell wall products, may act on Toll-like receptors in the hypothalamus and elevate the thermoregulatory setpoint. An example of a class of exogenous pyrogens are bacterial lipopolysaccharides (LPS) present in the cell wall of gram-negative bacteria . According to one mechanism of pyrogen action, an immune system protein, lipopolysaccharide-binding protein (LBP), binds to LPS, and the LBP–LPS complex then binds to a CD14 receptor on a macrophage . The LBP-LPS binding to CD14 results in cellular synthesis and release of various endogenous cytokines , e.g., interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNFα). A further downstream event is activation of the arachidonic acid pathway . PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase . These enzymes ultimately mediate the synthesis and release of PGE2. [ citation needed ] PGE2 is the ultimate mediator of the febrile response. The setpoint temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa), and the paraventricular nucleus (PVN) of the hypothalamus. Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs . [ citation needed ]Temperature is regulated in the hypothalamus . The trigger of a fever, called a pyrogen, results in the release of prostaglandin E2 (PGE2). PGE2 in turn acts on the hypothalamus, which creates a systemic response in the body, causing heat-generating effects to match a new higher temperature set point. There are four receptors in which PGE2 can bind (EP1-4), with a previous study showing the EP3 subtype is what mediates the fever response. Hence, the hypothalamus can be seen as working like a thermostat . When the set point is raised, the body increases its temperature through both active generation of heat and retention of heat. Peripheral vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. Norepinephrine increases thermogenesis in brown adipose tissue , and muscle contraction through shivering raises the metabolic rate . If these measures are insufficient to make the blood temperature in the brain match the new set point in the hypothalamus, the brain orchestrates heat effector mechanisms via the autonomic nervous system or primary motor center for shivering. These may be: [ citation needed ] When the hypothalamic set point moves back to baseline—either spontaneously or via medication—normal functions such as sweating, and the reverse of the foregoing processes (e.g., vasodilation, end of shivering, and nonshivering heat production) are used to cool the body to the new, lower setting. [ citation needed ] This contrasts with hyperthermia , in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat. Hyperthermia is usually the result of an excessively hot environment ( heat stroke ) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications. [ verification needed ] In infants, the autonomic nervous system may also activate brown adipose tissue to produce heat (non-exercise-associated thermogenesis , also known as non-shivering thermogenesis). [ citation needed ] Increased heart rate and vasoconstriction contribute to increased blood pressure in fever. [ citation needed ]A pyrogen is a substance that induces fever. In the presence of an infectious agent, such as bacteria, viruses, viroids, etc ., the immune response of the body is to inhibit their growth and eliminate them. The most common pyrogens are endotoxins, which are lipopolysaccharides (LPS) produced by Gram-negative bacteria such as E. coli . But pyrogens include non-endotoxic substances (derived from microorganisms other than gram-negative-bacteria or from chemical substances) as well. The types of pyrogens include internal (endogenous) and external (exogenous) to the body. [ citation needed ] The "pyrogenicity" of given pyrogens varies: in extreme cases, bacterial pyrogens can act as superantigens and cause rapid and dangerous fevers. Endogenous pyrogens are cytokines released from monocytes (which are part of the immune system ). In general, they stimulate chemical responses, often in the presence of an antigen , leading to a fever. Whilst they can be a product of external factors like exogenous pyrogens, they can also be induced by internal factors like damage associated molecular patterns such as cases like rheumatoid arthritis or lupus. Major endogenous pyrogens are interleukin 1 (α and β) : 1237–1248 and interleukin 6 (IL-6). Minor endogenous pyrogens include interleukin-8 , tumor necrosis factor-β , macrophage inflammatory protein -α and macrophage inflammatory protein-β as well as interferon-α , interferon-β , and interferon-γ . : 1237–1248 Tumor necrosis factor-α (TNF) also acts as a pyrogen, mediated by interleukin 1 (IL-1) release. These cytokine factors are released into general circulation, where they migrate to the brain's circumventricular organs where they are more easily absorbed than in areas protected by the blood–brain barrier . [ citation needed ] The cytokines then bind to endothelial receptors on vessel walls to receptors on microglial cells , resulting in activation of the arachidonic acid pathway . [ citation needed ] Of these, IL-1β, TNF, and IL-6 are able to raise the temperature setpoint of an organism and cause fever. These proteins produce a cyclooxygenase which induces the hypothalamic production of PGE2 which then stimulates the release of neurotransmitters such as cyclic adenosine monophosphate and increases body temperature. Exogenous pyrogens are external to the body and are of microbial origin. In general, these pyrogens, including bacterial cell wall products, may act on Toll-like receptors in the hypothalamus and elevate the thermoregulatory setpoint. An example of a class of exogenous pyrogens are bacterial lipopolysaccharides (LPS) present in the cell wall of gram-negative bacteria . According to one mechanism of pyrogen action, an immune system protein, lipopolysaccharide-binding protein (LBP), binds to LPS, and the LBP–LPS complex then binds to a CD14 receptor on a macrophage . The LBP-LPS binding to CD14 results in cellular synthesis and release of various endogenous cytokines , e.g., interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNFα). A further downstream event is activation of the arachidonic acid pathway . Endogenous pyrogens are cytokines released from monocytes (which are part of the immune system ). In general, they stimulate chemical responses, often in the presence of an antigen , leading to a fever. Whilst they can be a product of external factors like exogenous pyrogens, they can also be induced by internal factors like damage associated molecular patterns such as cases like rheumatoid arthritis or lupus. Major endogenous pyrogens are interleukin 1 (α and β) : 1237–1248 and interleukin 6 (IL-6). Minor endogenous pyrogens include interleukin-8 , tumor necrosis factor-β , macrophage inflammatory protein -α and macrophage inflammatory protein-β as well as interferon-α , interferon-β , and interferon-γ . : 1237–1248 Tumor necrosis factor-α (TNF) also acts as a pyrogen, mediated by interleukin 1 (IL-1) release. These cytokine factors are released into general circulation, where they migrate to the brain's circumventricular organs where they are more easily absorbed than in areas protected by the blood–brain barrier . [ citation needed ] The cytokines then bind to endothelial receptors on vessel walls to receptors on microglial cells , resulting in activation of the arachidonic acid pathway . [ citation needed ] Of these, IL-1β, TNF, and IL-6 are able to raise the temperature setpoint of an organism and cause fever. These proteins produce a cyclooxygenase which induces the hypothalamic production of PGE2 which then stimulates the release of neurotransmitters such as cyclic adenosine monophosphate and increases body temperature. Exogenous pyrogens are external to the body and are of microbial origin. In general, these pyrogens, including bacterial cell wall products, may act on Toll-like receptors in the hypothalamus and elevate the thermoregulatory setpoint. An example of a class of exogenous pyrogens are bacterial lipopolysaccharides (LPS) present in the cell wall of gram-negative bacteria . According to one mechanism of pyrogen action, an immune system protein, lipopolysaccharide-binding protein (LBP), binds to LPS, and the LBP–LPS complex then binds to a CD14 receptor on a macrophage . The LBP-LPS binding to CD14 results in cellular synthesis and release of various endogenous cytokines , e.g., interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNFα). A further downstream event is activation of the arachidonic acid pathway . PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase . These enzymes ultimately mediate the synthesis and release of PGE2. [ citation needed ] PGE2 is the ultimate mediator of the febrile response. The setpoint temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa), and the paraventricular nucleus (PVN) of the hypothalamus. Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs . [ citation needed ]Fever does not necessarily need to be treated, and most people with a fever recover without specific medical attention. Although it is unpleasant, fever rarely rises to a dangerous level even if untreated. Damage to the brain generally does not occur until temperatures reach 42.0 °C (107.6 °F) , and it is rare for an untreated fever to exceed 40.6 °C (105.1 °F) . Treating fever in people with sepsis does not affect outcomes. Small trials have shown no benefit of treating fevers of 38.5 °C (101.3 °F) or higher of critically ill patients in ICUs, and one trial was terminated early because patients receiving aggressive fever treatment were dying more often. According to the NIH, the two assumptions which are generally used to argue in favor of treating fevers have not been experimentally validated. These are that (1) a fever is noxious, and (2) suppression of a fever will reduce its noxious effect. Most of the other studies supporting the association of fever with poorer outcomes have been observational in nature. In theory, these critically ill patients and those faced with additional physiologic stress may benefit from fever reduction, but the evidence on both sides of the argument appears to be mostly equivocal. Limited evidence supports sponging or bathing feverish children with tepid water. The use of a fan or air conditioning may somewhat reduce the temperature and increase comfort. If the temperature reaches the extremely high level of hyperpyrexia , aggressive cooling is required (generally produced mechanically via conduction by applying numerous ice packs across most of the body or direct submersion in ice water). In general, people are advised to keep adequately hydrated. Whether increased fluid intake improves symptoms or shortens respiratory illnesses such as the common cold is not known. Medications that lower fevers are called antipyretics . The antipyretic ibuprofen is effective in reducing fevers in children. It is more effective than acetaminophen (paracetamol) in children. Ibuprofen and acetaminophen may be safely used together in children with fevers. The efficacy of acetaminophen by itself in children with fevers has been questioned. Ibuprofen is also superior to aspirin in children with fevers. Additionally, aspirin is not recommended in children and young adults (those under the age of 16 or 19 depending on the country) due to the risk of Reye's syndrome . Using both paracetamol and ibuprofen at the same time or alternating between the two is more effective at decreasing fever than using only paracetamol or ibuprofen. It is not clear if it increases child comfort. Response or nonresponse to medications does not predict whether or not a child has a serious illness. With respect to the effect of antipyretics on the risk of death in those with infection, studies have found mixed results as of 2019. Animal models have found increased mortality with the use of antipyretics in influenza but as of 2010 there have been no randomized placebo-controlled trials in humans that gave data on mortality. Limited evidence supports sponging or bathing feverish children with tepid water. The use of a fan or air conditioning may somewhat reduce the temperature and increase comfort. If the temperature reaches the extremely high level of hyperpyrexia , aggressive cooling is required (generally produced mechanically via conduction by applying numerous ice packs across most of the body or direct submersion in ice water). In general, people are advised to keep adequately hydrated. Whether increased fluid intake improves symptoms or shortens respiratory illnesses such as the common cold is not known. Medications that lower fevers are called antipyretics . The antipyretic ibuprofen is effective in reducing fevers in children. It is more effective than acetaminophen (paracetamol) in children. Ibuprofen and acetaminophen may be safely used together in children with fevers. The efficacy of acetaminophen by itself in children with fevers has been questioned. Ibuprofen is also superior to aspirin in children with fevers. Additionally, aspirin is not recommended in children and young adults (those under the age of 16 or 19 depending on the country) due to the risk of Reye's syndrome . Using both paracetamol and ibuprofen at the same time or alternating between the two is more effective at decreasing fever than using only paracetamol or ibuprofen. It is not clear if it increases child comfort. Response or nonresponse to medications does not predict whether or not a child has a serious illness. With respect to the effect of antipyretics on the risk of death in those with infection, studies have found mixed results as of 2019. Animal models have found increased mortality with the use of antipyretics in influenza but as of 2010 there have been no randomized placebo-controlled trials in humans that gave data on mortality. Fever is one of the most common medical signs . It is part of about 30% of healthcare visits by children, and occurs in up to 75% of adults who are seriously sick. About 5% of people who go to an emergency room have a fever. A number of types of fever were known as early as 460 BC to 370 BC when Hippocrates was practicing medicine including that due to malaria (tertian or every 2 days and quartan or every 3 days). It also became clear around this time that fever was a symptom of disease rather than a disease in and of itself. Infections presenting with fever were a major source of mortality in humans for about 200,000 years. Until the late nineteenth century, approximately half of all humans died from infections before the age of fifteen. An older term, febricula (a diminutive form of the Latin word for fever), was once used to refer to a low-grade fever lasting only a few days. This term fell out of use in the early 20th century, and the symptoms it referred to are now thought to have been caused mainly by various minor viral respiratory infections . Fever is often viewed with greater concern by parents and healthcare professionals than might be deserved, a phenomenon known as fever phobia, which is based in both caregiver's and parents' misconceptions about fever in children. Among them, many parents incorrectly believe that fever is a disease rather than a medical sign , that even low fevers are harmful, and that any temperature even briefly or slightly above the oversimplified "normal" number marked on a thermometer is a clinically significant fever. They are also afraid of harmless side effects like febrile seizures and dramatically overestimate the likelihood of permanent damage from typical fevers. The underlying problem, according to professor of pediatrics Barton D. Schmitt, is that "as parents we tend to suspect that our children's brains may melt." As a result of these misconceptions parents are anxious, give the child fever-reducing medicine when the temperature is technically normal or only slightly elevated, and interfere with the child's sleep to give the child more medicine. Fever is often viewed with greater concern by parents and healthcare professionals than might be deserved, a phenomenon known as fever phobia, which is based in both caregiver's and parents' misconceptions about fever in children. Among them, many parents incorrectly believe that fever is a disease rather than a medical sign , that even low fevers are harmful, and that any temperature even briefly or slightly above the oversimplified "normal" number marked on a thermometer is a clinically significant fever. They are also afraid of harmless side effects like febrile seizures and dramatically overestimate the likelihood of permanent damage from typical fevers. The underlying problem, according to professor of pediatrics Barton D. Schmitt, is that "as parents we tend to suspect that our children's brains may melt." As a result of these misconceptions parents are anxious, give the child fever-reducing medicine when the temperature is technically normal or only slightly elevated, and interfere with the child's sleep to give the child more medicine. Fever is an important metric for the diagnosis of disease in domestic animals . The body temperature of animals, which is taken rectally, is different from one species to another. For example, a horse is said to have a fever above 101 °F ( 38.3 °C ). In species that allow the body to have a wide range of "normal" temperatures, such as camels , whose body temperature varies as the environmental temperature varies, the body temperature which constitutes a febrile state differs depending on the environmental temperature. Fever can also be behaviorally induced by invertebrates that do not have immune-system based fever. For instance, some species of grasshopper will thermoregulate to achieve body temperatures that are 2–5 °C higher than normal in order to inhibit the growth of fungal pathogens such as Beauveria bassiana and Metarhizium acridum . Honeybee colonies are also able to induce a fever in response to a fungal parasite Ascosphaera apis .
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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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Sonja Buckley
Sonja Buckley (June 13, 1918 – February 2, 2005 ) was a Swiss -born virologist . She was the first person to culture Lassa virus , the causative agent of Lassa fever , a potentially deadly disease that originated in Africa. Sonja Grob was born in Zürich , Switzerland. In 1941, she married Dr. John J. Buckley, a pathologist who was also studying in Zürich. Sonja Buckley was awarded her medical degree in 1944 from the University of Zurich , and she was later a microbiology instructor there. With her husband, she emigrated to the United States in 1947, as both of them had already arranged to work at Johns Hopkins University in Baltimore . Her first research "assignment was to study the spread of the polio virus in East Baltimore neighborhoods". After working as a research assistant at Johns Hopkins for a short time, she joined the Sloan-Kettering Institute in New York City where she was chosen to head the solid tumor program in 1949. In 1957, she joined the Rockefeller Foundation to work in the foundation's virus laboratories. In 1964, those labs were transferred to Yale University in New Haven, Connecticut , and became known as the Arbovirus Research Unit. Buckley became interested in Lassa fever ( Lassa mammarenavirus ) after an outbreak of the unknown virus occurred in Nigeria in Africa in 1969 that was responsible for outbreaks of hemorrhagic fever. Specimens were sent to four different laboratories, including the Arbovirus Research Unit, where virologists attempted to isolate the causative agent, but Buckley was the first to do so, working with her team, which included Wilbur Downs and Jordi Casals-Ariet , Sonja Buckley retired from Yale in 1994, and died February 2, 2005, at the age of 86. A daughter, Sonja Mary Buckley, died as a youmg child in 1943, and her husband died in 1987. Buckley, Sonja M., Elinor Whitney, and Fred Rapp. "Identification by fluorescent antibody of developmental forms of psittacosis virus in tissue culture." Proceedings of the Society for Experimental Biology and Medicine 90.1 (1955): 226-230. Buckley, Sonja M. "Propagation, Cytopathogenicity, and Hemagglutination-Hemadsorption of Some Arthropodborne Viruses in Tissue Culture." NYASA 81.1 (1959): 172-187. Buckley, Sonja M. "Susceptibility of the Aedes albopictus and A. aegypti cell lines to infection with arboviruses." Proceedings of the Society for Experimental Biology and Medicine 131.2 (1969): 625-630. Buckley, Sonja M., and Jordi Casals. "Lassa fever, a new virus disease of man from West Africa." The American journal of tropical medicine and hygiene 19.4 (1970): 680-691. Buckley, Sonja M., Jordi Casals, and Wilbur G. Downs. "Isolation and antigenic characterization of Lassa virus." Nature 227.5254 (1970): 174-174. Cunningham, Ann, et al. "Isolation of chikungunya virus contaminating an Aedes albopictus cell line." Journal of General Virology 27.1 (1975): 97-100. Buckley, Sonja M. "Arbovirus infection of vertebrate and insect cell cultures, with special emphasis on Mokola, Obodhiang, and kotonkan viruses of the rabies serogroup." Annals of the New York Academy of Sciences 266 (1975): 241-250.
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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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Social history of viruses
The social history of viruses describes the influence of viruses and viral infections on human history. Epidemics caused by viruses began when human behaviour changed during the Neolithic period , around 12,000 years ago, when humans developed more densely populated agricultural communities. This allowed viruses to spread rapidly and subsequently to become endemic . Viruses of plants and livestock also increased, and as humans became dependent on agriculture and farming, diseases such as potyviruses of potatoes and rinderpest of cattle had devastating consequences. Smallpox and measles viruses are among the oldest that infect humans. Having evolved from viruses that infected other animals, they first appeared in humans in Europe and North Africa thousands of years ago. The viruses were later carried to the New World by Europeans during the time of the Spanish Conquests , but the indigenous people had no natural resistance to the viruses and millions of them died during epidemics. Influenza pandemics have been recorded since 1580, and they have occurred with increasing frequency in subsequent centuries. The pandemic of 1918–19 , in which 40–50 million died in less than a year, was one of the most devastating in history. Louis Pasteur and Edward Jenner were the first to develop vaccines to protect against viral infections. The nature of viruses remained unknown until the invention of the electron microscope in the 1930s, when the science of virology gained momentum. In the 20th century many diseases both old and new were found to be caused by viruses. There were epidemics of poliomyelitis that were only controlled following the development of a vaccine in the 1950s. HIV is one of the most pathogenic new viruses to have emerged in centuries. Although scientific interest in them arose because of the diseases they cause, most viruses are beneficial. Retroviruses drive evolution by transferring genes across species and bacteriophages play important roles in ecosystems and are essential to life.Over the past 50,000–100,000 years, as modern humans increased in numbers and dispersed throughout the world, new infectious diseases emerged, including those caused by viruses. Earlier, humans lived in small, isolated communities, and most epidemic diseases did not exist. Smallpox , which is the most lethal and devastating viral infection in history, first emerged among agricultural communities in India about 11,000 years ago. The virus, which only infected humans, probably descended from the poxviruses of rodents. Humans probably came into contact with these rodents, and some people became infected by the viruses they carried. When viruses cross this so-called "species barrier", their effects can be severe, and humans may have had little natural resistance . Contemporary humans lived in small communities, and those who succumbed to infection either died or developed immunity. This acquired immunity is only passed down to offspring temporarily, by antibodies in breast milk and other antibodies that cross the placenta from the mother's blood to the unborn child's. Therefore, sporadic outbreaks probably occurred in each generation. In about 9000 BC, when many people began to settle on the fertile flood plains of the River Nile , the population became dense enough for the virus to maintain a constant presence because of the high concentration of susceptible people. Other epidemics of viral diseases that depend on large concentrations of people, such as mumps , rubella and polio , also first occurred at this time. The Neolithic age, which began in the Middle East in about 9500 BC, was a time when humans became farmers. This agricultural revolution embraced the development of monoculture and presented an opportunity for the rapid spread of several species of plant viruses . The divergence and spread of sobemoviruses – southern bean mosaic virus – date from this time. The spread of the potyviruses of potatoes, and other fruits and vegetables, began about 6,600 years ago. About 10,000 years ago the humans who inhabited the lands around the Mediterranean basin began to domesticate wild animals. Pigs, cattle, goats, sheep, horses, camels, cats and dogs were all kept and bred in captivity. These animals would have brought their viruses with them. The transmission of viruses from animals to humans can occur, but such zoonotic infections are rare and subsequent human-to-human transmission of animal viruses is even rarer, although there are notable exceptions such as influenza . Most viruses are species-specific and would have posed no threat to humans. The rare epidemics of viral diseases originating in animals would have been short-lived because the viruses were not fully adapted to humans and the human populations were too small to maintain the chains of infection. Other, more ancient, viruses have been less of a threat. Herpes viruses first infected the ancestors of modern humans over 80 million years ago. Humans have developed a tolerance to these viruses, and most are infected with at least one species. Records of these milder virus infections are rare, but it is likely that early hominids suffered from colds, influenza and diarrhoea caused by viruses just as humans do today. More recently evolved viruses cause epidemics and pandemics – and it is these that history records. Among the earliest records of a viral infection is an Egyptian stele thought to depict an Egyptian priest from the 18th Dynasty (1580–1350 BC) with a foot drop deformity characteristic of a poliovirus infection. The mummy of Siptah – a ruler during the 19th Dynasty – shows signs of poliomyelitis , and that of Ramesses V and some other Egyptian mummies buried over 3000 years ago show evidence of smallpox. There was an epidemic of smallpox in Athens in 430 BC, in which a quarter of the Athenian army and many of the city's civilians died from the infection. The Antonine Plague of 165–180 CE, a probable smallpox pandemic, wiped out around five million people in the Roman Empire , which included Britain, Europe, the Middle East and North Africa. The pandemic began after Roman soldiers who were sent to suppress an uprising in what is now Iraq, plundered the city of Seleucia on the river Tigris and at the same time were infected. They brought the disease back to Rome and Europe where up to 5,000 people a day were fatally infected. At its height, the pandemic reached India and China. Measles is an old disease, but it was not until the 10th century that the Persian physician Muhammad ibn Zakariya al-Razi (865–925) – known as "Rhazes" – first identified it. Rhazes used the Arabic name hasbah (حصبة) for measles. It has had many other names including rubeola from the Latin word rubeus , "red", and morbilli , "small plague". The close similarities between measles virus, canine distemper virus and rinderpest virus have given rise to speculation that measles was first transmitted to humans from domesticated dogs or cattle. The measles virus appears to have fully diverged from the then-widespread rinderpest virus by the 12th century. A measles infection confers lifelong immunity. Therefore, the virus requires a high population density to become endemic , and this probably did not occur in the Neolithic age . Following the emergence of the virus in the Middle East , it reached India by 2500 BC. Measles was so common in children at the time that it was not recognised as a disease. In Egyptian hieroglyphs it was described as a normal stage of human development. One of the earliest descriptions of a virus-infected plant can be found in a poem written by the Japanese Empress Kōken (718–770), in which she describes a plant in summer with yellowing leaves. The plant, later identified as Eupatorium lindleyanum , is often infected with tomato yellow leaf curl virus . The rapidly growing population of Europe and the rising concentrations of people in its towns and cities became a fertile ground for many infectious and contagious diseases, of which the Black Death – a bacterial infection – is probably the most notorious. Except for smallpox and influenza, documented outbreaks of infections now known to be caused by viruses were rare. Rabies , a disease that had been recognised for over 4000 years, was rife in Europe, and continued to be so until the development of a vaccine by Louis Pasteur in 1886. The average life expectancy in Europe during the Middle Ages was 35 years; 60% of children died before the age of 16, many of them during their first 6 years of life. Physicians – what few there were – relied as much on astrology as they did on their limited medical knowledge. Some treatments for infections consisted of ointments prepared from cats that had been roasted in hedgehog fat. Among the plethora of diseases that caused childhood death were measles, influenza and smallpox. The Crusades and the Muslim conquests aided the spread of smallpox, which was the cause of frequent epidemics in Europe following its introduction to the continent between the fifth and seventh centuries. Measles was endemic throughout the highly populated countries of Europe, North Africa and the Middle East. In England the disease, then called "mezils", was first described in the 13th century, and it was probably one of the 49 plagues that occurred between 526 and 1087. Rinderpest, which is caused by a virus closely related to measles virus, is a disease of cattle known since Roman times. The disease, which originated in Asia, was first brought to Europe by the invading Huns in 370. Later invasions of Mongols , led by Genghis Khan and his army, started pandemics in Europe in 1222, 1233 and 1238. The infection subsequently reached England following the importation of cattle from the continent. At the time rinderpest was a devastating disease with a mortality rate of 80–90%. The resulting loss of cattle caused famine. A short time after Henry Tudor 's victory at the Battle of Bosworth on 22 August 1485, his army suddenly went down with "the English sweat ", which contemporary observers described as a new disease. The disease, which was unusual in that it mainly affected the affluent, might have originated in France where Henry VII had recruited soldiers for his army. An epidemic hit London in the hot summer of 1508. Affected people died within a day, and there were deaths throughout the city. The streets were deserted apart from carts transporting bodies, and King Henry declared the city off limits except for physicians and apothecaries. The disease spread to Europe, arriving in Hamburg in July 1529 where one to two thousand people died within the first few weeks. During the following months it wreaked havoc in Prussia, Switzerland, and northern Europe. The last outbreak was in England in 1556. The disease – which killed tens of thousands of people – was probably influenza or a similar viral infection, but records from the time when medicine was not a science can be unreliable. As medicine became a science, the descriptions of disease became less vague. Although medicine could do little at the time to alleviate the suffering of those infected, measures to control the spread of diseases were used. Restrictions on trade and travel were implemented, stricken families were isolated from their communities, buildings were fumigated and livestock killed. References to influenza infections date from the late 15th and early 16th centuries, but infections almost certainly occurred long before then. In 1173, an epidemic occurred that was possibly the first in Europe, and in 1493, an outbreak of what is now thought to be swine influenza , struck Native Americans in Hispaniola . There is some evidence to suggest that source of the infection was pigs on Columbus 's ships. During an influenza epidemic that occurred in England between 1557 and 1559, five per cent of the population – about 150,000 – died from the infection. The mortality rate was nearly five times that of the 1918–19 pandemic. The first pandemic that was reliably recorded began in July 1580 and swept across Europe, Africa, and Asia. The mortality rate was high – 8,000 died in Rome. The next three pandemics occurred in the 18th century, including that during 1781–82, which was probably the most devastating in history. This began in November 1781 in China and reached Moscow in December. In February 1782 it hit Saint Petersburg , and by May it had reached Denmark. Within six weeks, 75 per cent of the British population were infected and the pandemic soon spread to the Americas. The Americas and Australia remained free of measles and smallpox until the arrival of European colonists between the 15th and 18th centuries. Along with measles and influenza, smallpox was taken to the Americas by the Spanish. Smallpox was endemic in Spain, having been introduced by the Moors from Africa. In 1519, an epidemic of smallpox broke out in the Aztec capital Tenochtitlan in Mexico. This was started by the army of Pánfilo de Narváez , who followed Hernán Cortés from Cuba and had an African slave with smallpox aboard his ship. When the Spanish finally entered the capital in the summer of 1521, they saw it strewn with the bodies of smallpox victims. The epidemic, and those that followed during 1545–1548 and 1576–1581, eventually killed more than half of the native population. Most of the Spanish were immune; with his army of fewer than 900 men it would not have been possible for Cortés to defeat the Aztecs and conquer Mexico without the help of smallpox. Many Native American populations were devastated later by the inadvertent spread of diseases introduced by Europeans. In the 150 years that followed Columbus's arrival in 1492, the Native American population of North America was reduced by 80 per cent from diseases, including measles, smallpox and influenza. The damage done by these viruses significantly aided European attempts to displace and conquer the native population. By the 18th century, smallpox was endemic in Europe. There were five epidemics in London between 1719 and 1746, and large outbreaks occurred in other major European cities. By the end of the century about 400,000 Europeans were dying from the disease each year. It reached South Africa in 1713, having been carried by ships from India, and in 1789 the disease struck Australia. In the 19th century, smallpox became the single most important cause of death of the Australian Aborigines . In 1546 Girolamo Fracastoro (1478–1553) wrote a classic description of measles. He thought the disease was caused by "seeds" ( seminaria ) that were spread from person to person. An epidemic hit London in 1670, recorded by Thomas Sydenham (1624–1689), who thought it was caused by toxic vapours emanating from the earth. His theory was wrong but he was a skilled observer and kept meticulous records. Yellow fever is an often lethal disease caused by a flavivirus . The virus is transmitted to humans by mosquitoes ( Aedes aegypti ) and first appeared over 3,000 years ago. In 1647, the first recorded epidemic occurred on Barbados and was called "Barbados distemper" by John Winthrop , who was the governor of the island at the time. He passed quarantine laws to protect the people – the first ever such laws in North America. Further epidemics of the disease occurred in North America in the 17th, 18th and 19th centuries. The first known cases of dengue fever occurred in Indonesia and Egypt in 1779. Trade ships brought the disease to the US, where an epidemic occurred in Philadelphia in 1780. Newly emerging infectious diseases (EIDs) have been posing an increasingly significant threat to human health. The majority of EIDs are of zoonotic origin, for which human population increase and the intensification of animal farming as well as of wild animal environments are causative in part. Many paintings can be found in the museums of Europe depicting tulips with attractive coloured stripes. Most, such as the still life studies of Johannes Bosschaert , were painted during the 17th century. These flowers were particularly popular and became sought after by those who could afford them. At the peak of this tulip mania in the 1630s, one bulb could cost as much as a house. It was not known at the time that the stripes were caused by a plant virus , which became known as the tulip breaking virus , accidentally transferred by humans to tulips from jasmine . Weakened by the virus, the plants turned out to be a poor investment. Only a few bulbs produced flowers with the attractive characteristics of their parent plants. Until the Irish Great Famine of 1845–1852, the commonest cause of disease in potatoes was not the mould that causes blight, it was a virus. The disease, called "curl", is caused by potato leafroll virus , and it was widespread in England in the 1770s, where it destroyed 75 per cent of the potato crop. At that time, the Irish potato crop remained relatively unscathed. Lady Mary Wortley Montagu (1689–1762) was an aristocrat, a writer and the wife of a Member of Parliament . In 1716, her husband, Edward Wortley Montagu, was appointed British Ambassador in Istanbul. She followed him there and two weeks after her arrival discovered the local practice of protection against smallpox by variolation – the injection of pus from people with smallpox into the skin. Her younger brother had died of smallpox, and she too had had the disease. Determined to spare her five-year-old son Edward from similar suffering, she ordered the embassy surgeon Charles Maitland to variolate him. On her return to London, she asked Maitland to variolate her four-year-old daughter in the presence of the king's physicians. Later, Montagu persuaded the Prince and Princess of Wales to sponsor a public demonstration of the procedure. Six prisoners who had been condemned to death and were awaiting execution at Newgate Prison were offered a full pardon for serving as the subjects of the public experiment. They accepted and were variolated in 1721. All the prisoners recovered from the procedure. To test its protective effect one of them, a nineteen-year-old woman, was ordered to sleep in the same bed as a ten-year-old with smallpox for six weeks. She did not contract the disease. The experiment was repeated on eleven orphan children, all of whom survived the ordeal, and by 1722 even King George I 's grandchildren had been inoculated. The practice was not entirely safe and there was a one in fifty chance of death. The procedure was expensive; some medical practitioners charged between £5 and £10 and some sold the method to other practitioners for fees between £50 and £100, or for half of the profits. Variolation became a lucrative franchise, but it remained beyond the means of many until the late 1770s. At the time nothing was known about viruses or the immune system , and no one knew how the procedure afforded protection. Edward Jenner (1749–1823), a British rural physician, was variolated as a boy. He had suffered greatly from the ordeal but survived fully protected from smallpox. Jenner knew of a local belief that dairy workers who had contracted a relatively mild infection called cowpox were immune to smallpox. He decided to test the theory (although he was probably not the first to do so). On 14 May 1796 he selected "a healthy boy, about eight years old for the purpose of inoculation for the Cow Pox". The boy, James Phipps (1788–1853), survived the experimental inoculation with cowpox virus and developed only a mild fever. On 1 July 1796, Jenner took some "smallpox matter" (probably infected pus) and repeatedly inoculated Phipps's arms with it. Phipps survived and was subsequently inoculated with smallpox more than 20 times without succumbing to the disease. Vaccination – the word is derived from the Latin vacca meaning "cow" – had been invented. Jenner's method was soon shown to be safer than variolation, and by 1801 more than 100,000 people had been vaccinated. Despite objections from those medical practitioners who still practised variolation, and who foresaw a decline in their income, free vaccination of the poor was introduced in the UK in 1840. Because of associated deaths, variolation was declared illegal in the same year. Vaccination was made compulsory in England and Wales by the 1853 Vaccination Act , and parents could be fined £1 if their children were not vaccinated before they were three months of age. The law was not adequately enforced, and the system for providing vaccinations, unchanged since 1840, was ineffective. After an early compliance by the population only a small proportion were vaccinated. Compulsory vaccination was not well received and, following protests, the Anti-Vaccination League and the Anti-Compulsory Vaccination League were formed in 1866. Following the anti-vaccination campaigns there was a severe outbreak of smallpox in Gloucester in 1895, the city's first in twenty years; 434 people died, including 281 children. Despite this, the British government conceded to the protesters and the Vaccination Act of 1898 abolished fines and made provision for a " conscientious objector " clause – the first use of the term – for parents who did not believe in vaccination. During the following year, 250,000 objections were granted, and by 1912 less than half of the population of newborns were being vaccinated. By 1948, smallpox vaccination was no longer compulsory in the UK. Rabies is an often fatal disease caused by the infection of mammals with rabies virus . In the 21st century it is mainly a disease that affects wild mammals such as foxes and bats, but it is one of the oldest known virus diseases: rabies is a Sanskrit word ( rabhas ) that dates from 3000 BC, which means "madness" or "rage", and the disease has been known for over 4000 years. Descriptions of rabies can be found in Mesopotamian texts, and the ancient Greeks called it "lyssa" or "lytta", meaning "madness". References to rabies can be found in the Laws of Eshnunna , which date from 2300 BC. Aristotle (384–322 BC) wrote one of the earliest undisputed descriptions of the disease and how it was passed to humans. Celsus , in the first century AD, first recorded the symptom called hydrophobia and suggested that the saliva of infected animals and humans contained a slime or poison – to describe this he invented the word "virus". Rabies does not cause epidemics, but the infection was greatly feared because of its terrible symptoms, which include insanity, hydrophobia and death. In France during the time of Louis Pasteur (1822–1895) there were only a few hundred rabies infections in humans each year, but cures were desperately sought. Aware of the possible danger, Pasteur began to look for the "microbe" in mad dogs. Pasteur showed that when the dried spinal cords from dogs that had died from rabies were crushed and injected into healthy dogs they did not become infected. He repeated the experiment several times on the same dog with tissue that had been dried for fewer and fewer days, until the dog survived even after injections of fresh rabies-infected spinal tissue. Pasteur had immunised the dog against rabies, as he later did with 50 more. Although Pasteur had little idea how his method worked, he tested it on a boy, Joseph Meister (1876–1940), who was brought to Pasteur by his mother on 6 July 1885. He was covered in bites, having been set upon by a mad dog. Meister's mother begged Pasteur to help her son. Pasteur was a scientist, not a physician, and he was well aware of the consequences for him if things were to go wrong. He nevertheless decided to help the boy and injected him with increasingly virulent rabid rabbit spinal tissue over the following 10 days. Later Pasteur wrote, "as the death of this child appeared inevitable, I decided, not without deep and severe unease ... to try out on Joseph Meister the procedure, which had consistently worked on dogs". Meister recovered and returned home with his mother on 27 July. Pasteur successfully treated a second boy in October that same year; Jean-Baptiste Jupille (1869–1923) was a 15-year-old shepherd boy who had been severely bitten as he tried to protect other children from a rabid dog. Pasteur's method of treatment remained in use for over 50 years. Little was known about the cause of the disease until 1903 when Adelchi Negri (1876–1912) first saw microscopic lesions – now called Negri bodies – in the brains of rabid animals. He wrongly thought they were protozoan parasites. Paul Remlinger (1871–1964) soon showed by filtration experiments that they were much smaller than protozoa, and even smaller than bacteria. Thirty years later, Negri bodies were shown to be accumulations of particles 100–150 nanometres long, now known to be the size of rhabdovirus particles – the virus that causes rabies. Lady Mary Wortley Montagu (1689–1762) was an aristocrat, a writer and the wife of a Member of Parliament . In 1716, her husband, Edward Wortley Montagu, was appointed British Ambassador in Istanbul. She followed him there and two weeks after her arrival discovered the local practice of protection against smallpox by variolation – the injection of pus from people with smallpox into the skin. Her younger brother had died of smallpox, and she too had had the disease. Determined to spare her five-year-old son Edward from similar suffering, she ordered the embassy surgeon Charles Maitland to variolate him. On her return to London, she asked Maitland to variolate her four-year-old daughter in the presence of the king's physicians. Later, Montagu persuaded the Prince and Princess of Wales to sponsor a public demonstration of the procedure. Six prisoners who had been condemned to death and were awaiting execution at Newgate Prison were offered a full pardon for serving as the subjects of the public experiment. They accepted and were variolated in 1721. All the prisoners recovered from the procedure. To test its protective effect one of them, a nineteen-year-old woman, was ordered to sleep in the same bed as a ten-year-old with smallpox for six weeks. She did not contract the disease. The experiment was repeated on eleven orphan children, all of whom survived the ordeal, and by 1722 even King George I 's grandchildren had been inoculated. The practice was not entirely safe and there was a one in fifty chance of death. The procedure was expensive; some medical practitioners charged between £5 and £10 and some sold the method to other practitioners for fees between £50 and £100, or for half of the profits. Variolation became a lucrative franchise, but it remained beyond the means of many until the late 1770s. At the time nothing was known about viruses or the immune system , and no one knew how the procedure afforded protection. Edward Jenner (1749–1823), a British rural physician, was variolated as a boy. He had suffered greatly from the ordeal but survived fully protected from smallpox. Jenner knew of a local belief that dairy workers who had contracted a relatively mild infection called cowpox were immune to smallpox. He decided to test the theory (although he was probably not the first to do so). On 14 May 1796 he selected "a healthy boy, about eight years old for the purpose of inoculation for the Cow Pox". The boy, James Phipps (1788–1853), survived the experimental inoculation with cowpox virus and developed only a mild fever. On 1 July 1796, Jenner took some "smallpox matter" (probably infected pus) and repeatedly inoculated Phipps's arms with it. Phipps survived and was subsequently inoculated with smallpox more than 20 times without succumbing to the disease. Vaccination – the word is derived from the Latin vacca meaning "cow" – had been invented. Jenner's method was soon shown to be safer than variolation, and by 1801 more than 100,000 people had been vaccinated. Despite objections from those medical practitioners who still practised variolation, and who foresaw a decline in their income, free vaccination of the poor was introduced in the UK in 1840. Because of associated deaths, variolation was declared illegal in the same year. Vaccination was made compulsory in England and Wales by the 1853 Vaccination Act , and parents could be fined £1 if their children were not vaccinated before they were three months of age. The law was not adequately enforced, and the system for providing vaccinations, unchanged since 1840, was ineffective. After an early compliance by the population only a small proportion were vaccinated. Compulsory vaccination was not well received and, following protests, the Anti-Vaccination League and the Anti-Compulsory Vaccination League were formed in 1866. Following the anti-vaccination campaigns there was a severe outbreak of smallpox in Gloucester in 1895, the city's first in twenty years; 434 people died, including 281 children. Despite this, the British government conceded to the protesters and the Vaccination Act of 1898 abolished fines and made provision for a " conscientious objector " clause – the first use of the term – for parents who did not believe in vaccination. During the following year, 250,000 objections were granted, and by 1912 less than half of the population of newborns were being vaccinated. By 1948, smallpox vaccination was no longer compulsory in the UK. Rabies is an often fatal disease caused by the infection of mammals with rabies virus . In the 21st century it is mainly a disease that affects wild mammals such as foxes and bats, but it is one of the oldest known virus diseases: rabies is a Sanskrit word ( rabhas ) that dates from 3000 BC, which means "madness" or "rage", and the disease has been known for over 4000 years. Descriptions of rabies can be found in Mesopotamian texts, and the ancient Greeks called it "lyssa" or "lytta", meaning "madness". References to rabies can be found in the Laws of Eshnunna , which date from 2300 BC. Aristotle (384–322 BC) wrote one of the earliest undisputed descriptions of the disease and how it was passed to humans. Celsus , in the first century AD, first recorded the symptom called hydrophobia and suggested that the saliva of infected animals and humans contained a slime or poison – to describe this he invented the word "virus". Rabies does not cause epidemics, but the infection was greatly feared because of its terrible symptoms, which include insanity, hydrophobia and death. In France during the time of Louis Pasteur (1822–1895) there were only a few hundred rabies infections in humans each year, but cures were desperately sought. Aware of the possible danger, Pasteur began to look for the "microbe" in mad dogs. Pasteur showed that when the dried spinal cords from dogs that had died from rabies were crushed and injected into healthy dogs they did not become infected. He repeated the experiment several times on the same dog with tissue that had been dried for fewer and fewer days, until the dog survived even after injections of fresh rabies-infected spinal tissue. Pasteur had immunised the dog against rabies, as he later did with 50 more. Although Pasteur had little idea how his method worked, he tested it on a boy, Joseph Meister (1876–1940), who was brought to Pasteur by his mother on 6 July 1885. He was covered in bites, having been set upon by a mad dog. Meister's mother begged Pasteur to help her son. Pasteur was a scientist, not a physician, and he was well aware of the consequences for him if things were to go wrong. He nevertheless decided to help the boy and injected him with increasingly virulent rabid rabbit spinal tissue over the following 10 days. Later Pasteur wrote, "as the death of this child appeared inevitable, I decided, not without deep and severe unease ... to try out on Joseph Meister the procedure, which had consistently worked on dogs". Meister recovered and returned home with his mother on 27 July. Pasteur successfully treated a second boy in October that same year; Jean-Baptiste Jupille (1869–1923) was a 15-year-old shepherd boy who had been severely bitten as he tried to protect other children from a rabid dog. Pasteur's method of treatment remained in use for over 50 years. Little was known about the cause of the disease until 1903 when Adelchi Negri (1876–1912) first saw microscopic lesions – now called Negri bodies – in the brains of rabid animals. He wrongly thought they were protozoan parasites. Paul Remlinger (1871–1964) soon showed by filtration experiments that they were much smaller than protozoa, and even smaller than bacteria. Thirty years later, Negri bodies were shown to be accumulations of particles 100–150 nanometres long, now known to be the size of rhabdovirus particles – the virus that causes rabies. At the turn of the 20th century, evidence for the existence of viruses was obtained from experiments with filters that had pores too small for bacteria to pass through; the term "filterable virus" was coined to describe them. Until the 1930s most scientists believed that viruses were small bacteria, but following the invention of the electron microscope in 1931 they were shown to be completely different, to a degree that not all scientists were convinced they were anything other than accumulations of toxic proteins . The situation changed radically when it was discovered that viruses contain genetic material in the form of DNA or RNA . Once they were recognised as distinct biological entities they were soon shown to be the cause of numerous infections of plants, animals and even bacteria. Of the many diseases of humans that were found to be caused by viruses in the 20th century one, smallpox, has been eradicated. The diseases caused by viruses such as HIV and influenza virus have proved to be more difficult to control. Other diseases, such as those caused by arboviruses , are presenting new challenges. As humans have changed their behaviour during history, so have viruses. In ancient times the human population was too small for pandemics to occur and, in the case of some viruses, too small for them to survive. In the 20th and 21st century increasing population densities, revolutionary changes in agriculture and farming methods, and high speed travel have contributed to the spread of new viruses and the re-appearance of old ones. Like smallpox, some viral diseases might be conquered, but new ones, such as severe acute respiratory syndrome ( SARS ), will continue to emerge. Although vaccines are still the most powerful weapon against viruses, in recent decades antiviral drugs have been developed to specifically target viruses as they replicate in their hosts . The 2009 influenza pandemic showed how rapidly new strains of viruses continue to spread around the world, despite efforts to contain them. Advances in virus discovery and control continue to be made. Human metapneumovirus , which is a cause of respiratory infections including pneumonia , was discovered in 2001. A vaccine for the papillomaviruses that cause cervical cancer was developed between 2002 and 2006. In 2005, human T lymphotropic viruses 3 and 4 were discovered. In 2008 the WHO Global Polio Eradication Initiative was re-launched with a plan to eradicate poliomyelitis by 2015. In 2010, the largest virus, Megavirus chilensis was discovered to infect amoebae . These giant viruses have renewed interest in the role viruses play in evolution. Smallpox virus was a major cause of death in the 20th century, killing about 300 million people. It has probably killed more humans than any other virus. In 1966 an agreement was reached by the World Health Assembly (the decision-making body of the World Health Organization ) to start an "intensified smallpox eradication programme" and attempt to eradicate the disease within ten years. At the time, smallpox was still endemic in 31 countries including Brazil, the whole of the Indian sub-continent, Indonesia and sub-Saharan Africa. This ambitious goal was considered achievable for several reasons: the vaccine afforded exceptional protection; there was only one type of the virus; there were no animals that naturally carried it; the incubation period of the infection was known and rarely varied from 12 days; and infections always gave rise to symptoms, so it was clear who had the disease. Following mass vaccinations, disease detection and containment were central to the eradication campaign. As soon as cases were detected, they were isolated as were their close contacts, who were vaccinated. Successes came quickly; by 1970 smallpox was no longer endemic in western Africa, nor, by 1971, in Brazil . By 1973, smallpox remained endemic only in the Indian sub-continent, Botswana and Ethiopia . Finally, after 13 years of coordinated disease surveillance and vaccination campaigns throughout the world, the World Health Organization declared smallpox eradicated in 1979. Although the main weapon used was vaccinia virus , which was used as the vaccine, no one seems to know exactly where vaccinia virus came from; it is not the strain of cowpox that Edward Jenner used, and it is not a weakened form of smallpox. The eradication campaign led to the death of Janet Parker (c. 1938–1978) and the subsequent suicide of the smallpox expert Henry Bedson (1930–1978). Parker was an employee of the University of Birmingham who worked in the same building as Bedson's smallpox laboratory. She was infected by a strain of smallpox virus that Bedson's team had been investigating. Ashamed of the accident and having blamed himself for it, Bedson committed suicide. Before the September 11 attacks on the United States in 2001, the World Health Organization proposed the destruction of all the known remaining stocks of smallpox virus that were kept in laboratories in the US and Russia. Fears of bioterrorism using smallpox virus and the possible need for the virus in the development of drugs to treat the infection have put an end to this plan. Had the destruction gone ahead, smallpox virus might have been the first to be made extinct by human intervention. Measles was a rare – although most often fatal – infection in South Africa in the early nineteenth century but epidemics increased in frequency from the 1850s. During the Second Boer War (1899−1902) measles was rife among the prisoners in the British concentration camps and accounted for thousands of deaths. This fatality rate in the camps was ten times greater than among British casualties. Before the introduction of vaccination in the US in the 1960s there were more than 500,000 cases each year resulting in about 400 deaths. In developed countries children were mainly infected between the ages of three and five years old, but in developing countries half the children were infected before the age of two. In the US and the UK, there were regular annual or biannual epidemics of the disease, which depended on the number of children born each year. The current epidemic strain evolved in the first part of the 20th century – probably between 1908 and 1943. In London between 1950 and 1968 there were epidemics every two years, but in Liverpool , which had a higher birth rate, there was an annual cycle of epidemics. During the Great Depression in the US before the Second World War the birth rate was low, and epidemics of measles were sporadic. After the war the birth rate increased, and epidemics occurred regularly every two years. In developing countries with very high birth rates, epidemics occurred every year. Measles is still a major problem in densely populated, less-developed countries with high birth rates and lacking effective vaccination campaigns. By the mid-1970s, following a mass vaccination programme that was known as "make measles a memory", the incidence of measles in the US had fallen by 90 per cent. Similar vaccination campaigns in other countries have reduced the levels of infection by 99 per cent over the past 50 years. Susceptible individuals remain a source of infection and include those who have migrated from countries with ineffective vaccination schedules, or who refuse the vaccine or choose not to have their children vaccinated. Humans are the only natural host of measles virus. Immunity to the disease following an infection is lifelong; that afforded by vaccination is long term but eventually wanes. The use of the vaccine has been controversial . In 1998, Andrew Wakefield and his colleagues published a fraudulent research paper and he claimed to link the MMR vaccine with autism . The study was widely reported and fed concern about the safety of vaccinations. Wakefield's research was identified as fraudulent and in 2010, he was struck off the UK medical register and can no longer practise medicine in the UK. In the wake of the controversy, the MMR vaccination rate in the UK fell from 92 per cent in 1995, to less than 80 per cent in 2003. Cases of measles rose from 56 in 1998 to 1370 in 2008, and similar increases occurred throughout Europe. In April 2013, an epidemic of measles in Wales in the UK broke out, which mainly affected teenagers who had not been vaccinated. Despite this controversy, measles has been eliminated from Finland, Sweden and Cuba. Japan abolished mandatory vaccination in 1992, and in 1995–1997 more than 200,000 cases were reported in the country. Measles remains a public health problem in Japan, where it is now endemic; a National Measles Elimination Plan was established in December 2007, with a view to eliminating the disease from the country. The possibility of global elimination of measles has been debated in medical literature since the introduction of the vaccine in the 1960s. Should the current campaign to eradicate poliomyelitis be successful, it is likely that the debate will be renewed. During the summers of the mid-20th century, parents in the US and Europe dreaded the annual appearance of poliomyelitis (or polio), which was commonly known as "infantile paralysis". The disease was rare at the beginning of the century, and worldwide there were only a few thousand cases per year, but by the 1950s there were 60,000 cases each year in the US alone and an average of 2,300 in England and Wales. During 1916 and 1917 there had been a major epidemic in the US; 27,000 cases and 6,000 deaths were recorded, with 9,000 cases in New York City . At the time nobody knew how the virus was spreading. Many of the city's inhabitants, including scientists, thought that impoverished slum-dwelling immigrants were to blame even though the prevalence of the disease was higher in the more prosperous districts such as Staten Island – a pattern that had also been seen in cities like Philadelphia. Many other industrialised countries were affected at the same time. In particular, before the outbreaks in the US, large epidemics had occurred in Sweden. The reason for the rise of polio in industrialised countries in the 20th century has never been fully explained. The disease is caused by a virus that is passed from person to person by the faecal-oral route , and naturally infects only humans. It is a paradox that it became a problem during times of improved sanitation and increasing affluence. Although the virus was discovered at the beginning of the 20th century, its ubiquity was unrecognised until the 1950s. It is now known that fewer than two per cent of individuals who are infected develop the disease, and most infections are mild. During epidemics the virus was effectively everywhere, which explains why public health officials were unable to isolate a source. Following the development of vaccines in the mid-1950s, mass vaccination campaigns took place in many countries. In the US, after a campaign promoted by the March of Dimes , the annual number of polio cases fell dramatically; the last outbreak was in 1979. In 1988 the World Health Organization along with others launched the Global Polio Eradication Initiative, and by 1994 the Americas were declared to be free of disease, followed by the Pacific region in 2000 and Europe in 2003. At the end of 2012, only 223 cases were reported by the World Health Organization. Mainly poliovirus type 1 infections, 122 occurred in Nigeria , one in Chad , 58 in Pakistan and 37 in Afghanistan . Vaccination teams often face danger; seven vaccinators were murdered in Pakistan and nine in Nigeria at the beginning of 2013. In Pakistan, the campaign was further hampered by the murder on 26 February 2013 of a police officer who was providing security. The human immunodeficiency virus ( HIV ) is the virus that – when the infection is not treated – can cause AIDS (acquired immunodeficiency syndrome). Most virologists believe that HIV originated in Kinshasa in the Democratic Republic of Congo during the 20th century, and over 70 million individuals have been infected by the virus. By 2011, an estimated 35 million had died from AIDS, making it one of the most destructive epidemics in recorded history. HIV-1 is one of the most significant viruses to have emerged in the last quarter of the 20th century. When, in 1981, a scientific article was published that reported the deaths of five young gay men, no one knew that they had died from AIDS. The full scale of the epidemic – and that the virus had been silently emerging over several decades – was not known. HIV crossed the species barrier between chimpanzees and humans in Africa in the early decades of the 20th century. During the years that followed there were enormous social changes and turmoil in Africa. Population shifts were unprecedented as vast numbers of people moved from rural farms to the expanding cities, and the virus was spread from remote regions to densely populated urban conurbations. The incubation period for AIDS is around 10 years, so a global epidemic starting in the early 1980s is credible. At this time there was much scapegoating and stigmatisation. The "out of Africa" theory for the origin of the HIV pandemic was not well received by Africans, who felt that the "blame" was misplaced. This led the World Health Assembly to pass a 1987 resolution, which stated that HIV is "a naturally occurring [virus] of undetermined geographic origin". The HIV pandemic has challenged communities and brought about social changes throughout the world. Opinions on sexuality are more openly discussed. Advice on sexual practices and drug use – which were once taboo – is sponsored by many governments and their healthcare providers. Debates on the ethics of provision and cost of anti-retroviral drugs , particularly in poorer countries, have highlighted inequalities in healthcare and stimulated far-reaching legislative changes. In developing countries the impact of HIV/AIDS has been profound; key organisations such as healthcare, defense and civil services have been severely disrupted. Life expectancy has fallen. In Zimbabwe, for example, life expectancy was 79 years in 1991 but by 2001 it had fallen to 39 years. When influenza virus undergoes a genetic shift many humans have no immunity to the new strain, and if the population of susceptible individuals is high enough to maintain the chain of infection, pandemics occur. The genetic changes usually happen when different strains of the virus co-infect animals, particularly birds and swine. Although many viruses of vertebrates are restricted to one species, influenza virus is an exception. The last pandemic of the 19th century occurred in 1899 and resulted in the deaths of 250,000 people in Europe. The virus, which originated in Russia or Asia, was the first to be rapidly spread by people on trains and steamships. A new strain of the virus emerged in 1918, and the subsequent pandemic of Spanish flu was one of the worst natural disasters in history. The death toll was enormous; throughout the world around 50 million people died from the infection. There were 550,000 reported deaths caused by the disease in the US, ten times the country's losses during the First World War, and 228,000 deaths in the UK. In India there were more than 20 million deaths, and in Western Samoa 22 per cent of the population died. Although cases of influenza occurred every winter, there were only two other pandemics in the 20th century. In 1957 another new strain of the virus emerged and caused a pandemic of Asian flu ; although the virus was not as virulent as the 1918 strain, over one million died worldwide. The next pandemic occurred when Hong Kong flu emerged in 1968, a new strain of the virus that replaced the 1957 strain. Affecting mainly the elderly, the 1968 pandemic was the least severe, but 33,800 were killed in the US. New strains of influenza virus often originate in East Asia; in rural China the concentration of ducks, pigs, and humans in close proximity is the highest in the world. The most recent pandemic occurred in 2009, but none of the last three has caused anything near the devastation seen in 1918. Exactly why the strain of influenza that emerged in 1918 was so devastating is a question that still remains unanswered. Arboviruses are viruses that are transmitted to humans and other vertebrates by blood-sucking insects. These viruses are diverse; the term "arbovirus" – which was derived from "arthropod-borne virus" – is no longer used in formal taxonomy because many species of virus are known to be spread in this way. There are more than 500 species of arboviruses, but in the 1930s only three were known to cause disease in humans: yellow fever virus , dengue virus and Pappataci fever virus . More than 100 of such viruses are now known to cause human diseases including encephalitis . Yellow fever is the most notorious disease caused by a flavivirus. The last major epidemic in the US occurred in 1905. During the building of the Panama Canal thousands of workers died from the disease. Yellow fever originated in Africa and the virus was brought to the Americas on cargo ships, which were harbouring the Aedes aegypti mosquito that carries the virus. The first recorded epidemic in Africa occurred in Ghana , in West Africa, in 1926. In the 1930s the disease re-emerged in Brazil. Fred Soper , an American epidemiologist (1893–1977), discovered the importance of the sylvatic cycle of infection in non-human hosts, and that infection of humans was a "dead end" that broke this cycle. Although the yellow fever vaccine is one of the most successful ever developed, epidemics continue to occur. In 1986–91 in West Africa, over 20,000 people were infected, 4,000 of whom died. In the 1930s, St. Louis encephalitis , eastern equine encephalitis and western equine encephalitis emerged in the US. The virus that causes La Crosse encephalitis was discovered in the 1960s, and West Nile virus arrived in New York in 1999. As of 2010, dengue virus is the most prevalent arbovirus and increasingly virulent strains of the virus have spread across Asia and the Americas. Hepatitis is a disease of the liver that has been recognised since antiquity. Symptoms include jaundice , a yellowing of the skin, eyes and body fluids. There are numerous causes, including viruses – particularly hepatitis A virus , hepatitis B virus and hepatitis C virus . Throughout history epidemics of jaundice have been reported, mainly affecting soldiers at war. This "campaign jaundice" was common in the Middle Ages. It occurred among Napoleon 's armies and during most of the major conflicts of the 19th and 20th centuries, including the American Civil War , where over 40,000 cases and around 150 deaths were reported. The viruses that cause epidemic jaundice were not discovered until the middle of the 20th century. The names for epidemic jaundice, hepatitis A, and for blood-borne infectious jaundice, hepatitis B, were first used in 1947, following a publication in 1946 giving evidence that the two diseases were distinct. In the 1960s, the first virus that could cause hepatitis was discovered. This was hepatitis B virus, which was named after the disease it causes. Hepatitis A virus was discovered in 1974. The discovery of hepatitis B virus and the invention of tests to detect it have radically changed many medical, and some cosmetic procedures. The screening of donated blood , which was introduced in the early 1970s, has dramatically reduced the transmission of the virus. Donations of human blood plasma and Factor VIII collected before 1975 often contained infectious levels of hepatitis B virus. Until the late 1960s, hypodermic needles were often reused by medical professionals, and tattoo artists' needles were a common source of infection. In the late 1990s, needle exchange programmes were established in Europe and the US to prevent the spread of infections by intravenous drug users . These measures also helped to reduce the subsequent impact of HIV and hepatitis C virus. Epizootics are outbreaks (epidemics) of disease among non-human animals. During the 20th century significant epizootics of viral diseases in animals, particularly livestock, occurred worldwide. The many diseases caused by viruses included foot-and-mouth disease , rinderpest of cattle, avian and swine influenza, swine fever and bluetongue of sheep. Viral diseases of livestock can be devastating both to farmers and the wider community, as the outbreak of foot-and-mouth disease in the UK in 2001 showed. First appearing in East Africa in 1891, rinderpest, a disease of cattle, spread rapidly across Africa. By 1892, 95 per cent of the cattle in East Africa had died. This resulted in a famine that devastated the farmers and nomadic people, some of whom were entirely dependent on their cattle. Two thirds of the population of Maasai people died. The situation was made worse by epidemics of smallpox that followed in the wake of the famine. In the early years of the 20th century rinderpest was common in Asia and parts of Europe. The prevalence of the disease was steadily reduced during the century by control measures that included vaccination. By 1908 Europe was free from the disease. Outbreaks did occur following the Second World War, but these were quickly controlled. The prevalence of the disease increased in Asia, and in 1957 Thailand had to appeal for aid because so many buffaloes had died that the paddy fields could not be prepared for rice growing. Russia west of the Ural Mountains remained free from the disease – Lenin approved several laws on the control of the disease – but cattle in eastern Russia were constantly infected with rinderpest that originated in Mongolia and China where the prevalence remained high. India controlled the spread of the disease, which had retained a foothold in the southern states of Tamil Nadu and Kerala , throughout the 20th century, and had eradicated the disease by 1995. Africa suffered two major panzootics in the 1920s and 1980s. There was a severe outbreak in Somalia in 1928 and the disease was widespread in the country until 1953. In the 1980s, outbreaks in Tanzania and Kenya were controlled by the use of 26 million doses of vaccine, and a recurrence of the disease in 1997 was suppressed by an intensive vaccination campaign. By the end of the century rinderpest had been eradicated from most countries. A few pockets of infection remained in Ethiopia and Sudan, and in 1994 the Global Rinderpest Eradication Programme was launched by the Food and Agriculture Organization (FAO) with the aim of global eradication by 2010. In May 2011, the FAO and the World Organisation for Animal Health announced that "rinderpest as a freely circulating viral disease has been eliminated from the world." Foot-and-mouth disease is a highly contagious infection caused by an aphthovirus , and is classified in the same family as poliovirus. The virus has infected animals, mainly ungulates , in Africa since ancient times and was probably brought to the Americas in the 19th century by imported livestock. Foot-and-mouth disease is rarely fatal, but the economic losses incurred by outbreaks in sheep and cattle herds can be high. The last occurrence of the disease in the US was in 1929, but as recently as 2001, several large outbreaks occurred throughout the UK and thousands of animals were killed and burnt. The natural hosts of influenza viruses are pigs and birds, although it has probably infected humans since antiquity. The virus can cause mild to severe epizootics in wild and domesticated animals. Many species of wild birds migrate and this has spread influenza across the continents throughout the ages. The virus has evolved into numerous strains and continues to do so, posing an ever-present threat. In the early years of the 21st century epizootics in livestock caused by viruses continue to have serious consequences. Bluetongue disease , a disease caused by an orbivirus broke out in sheep in France in 2007. Until then the disease had been mainly confined to the Americas, Africa, southern Asia and northern Australia, but it is now an emerging disease around the Mediterranean. During the 20th century, many "old" diseases of plants were found to be caused by viruses. These included maize streak and cassava mosaic disease . As with humans, when plants thrive in close proximity, so do their viruses. This can cause huge economic losses and human tragedies. In Jordan during the 1970s, where tomatoes and cucurbits (cucumbers, melons and gourds) were extensively grown, entire fields were infected with viruses. Similarly, in Côte d'Ivoire , thirty different viruses infected crops such as legumes and vegetables. In Kenya cassava mosaic virus, maize streak virus and groundnut viral diseases caused the loss of up to 70 per cent of the crop. Cassava is the most abundant crop that is grown in eastern Africa and it is a staple crop for more than 200 million people. It was introduced to Africa from South America and grows well in soils with poor fertility. The most important disease of cassava is caused by cassava mosaic virus, a geminivirus , which is transmitted between plants by whiteflies . The disease was first recorded in 1894 and outbreaks of the disease occurred in eastern Africa throughout the 20th century, often resulting in famine. In the 1920s the sugarbeet growers in the western US suffered huge economic loss caused by damage done to their crops by the leafhopper -transmitted beet curly top virus . In 1956, between 25 and 50 per cent of the rice crop in Cuba and Venezuela was destroyed by rice hoja blanca virus . In 1958, it caused the loss of many rice fields in Colombia. Outbreaks recurred in 1981, which caused losses of up to 100 per cent. In Ghana between 1936 and 1977, the mealybug-transmitted cacao swollen-shoot virus caused the loss of 162 million cacao trees , and additional trees were lost at the rate of 15 million each year. In 1948, in Kansas , US, seven per cent of the wheat crop was destroyed by wheat streak mosaic virus , spread by the wheat curl mite (Aceria tulipae) . In the 1950s papaya ringspot virus – a potyvirus – caused a devastating loss of solo papaya crops on Oahu , Hawaii. Solo papaya had been introduced to the island in the previous century but the disease had not been seen on the island before the 1940s. Such disasters occurred when human intervention caused ecological changes by the introduction of crops to new vectors and viruses. Cacao is native to South America and was introduced to West Africa in the late 19th century. In 1936, swollen root disease had been transmitted to plantations by mealybugs from indigenous trees. New habitats can trigger outbreaks of plant virus diseases. Before 1970, the rice yellow mottle virus was only found in the Kisumu district of Kenya, but following the irrigation of large areas of East Africa and extensive rice cultivation, the virus spread throughout East Africa. Human activity introduced plant viruses to native crops. The citrus tristeza virus (CTV) was introduced to South America from Africa between 1926 and 1930. At the same time, the aphid Toxoptera citricidus was carried from Asia to South America and this accelerated the transmission of the virus. By 1950, more than six million citrus trees had been killed by the virus in São Paulo , Brazil. CTV and citrus trees probably coevolved for centuries in their original countries. The dispersal of CTV to other regions and its interaction with new citrus varieties resulted in devastating outbreaks of plant diseases. Because of the problems caused by the introduction – by humans – of plant viruses, many countries have strict importation controls on any materials that can harbour dangerous plant viruses or their insect vectors. Smallpox virus was a major cause of death in the 20th century, killing about 300 million people. It has probably killed more humans than any other virus. In 1966 an agreement was reached by the World Health Assembly (the decision-making body of the World Health Organization ) to start an "intensified smallpox eradication programme" and attempt to eradicate the disease within ten years. At the time, smallpox was still endemic in 31 countries including Brazil, the whole of the Indian sub-continent, Indonesia and sub-Saharan Africa. This ambitious goal was considered achievable for several reasons: the vaccine afforded exceptional protection; there was only one type of the virus; there were no animals that naturally carried it; the incubation period of the infection was known and rarely varied from 12 days; and infections always gave rise to symptoms, so it was clear who had the disease. Following mass vaccinations, disease detection and containment were central to the eradication campaign. As soon as cases were detected, they were isolated as were their close contacts, who were vaccinated. Successes came quickly; by 1970 smallpox was no longer endemic in western Africa, nor, by 1971, in Brazil . By 1973, smallpox remained endemic only in the Indian sub-continent, Botswana and Ethiopia . Finally, after 13 years of coordinated disease surveillance and vaccination campaigns throughout the world, the World Health Organization declared smallpox eradicated in 1979. Although the main weapon used was vaccinia virus , which was used as the vaccine, no one seems to know exactly where vaccinia virus came from; it is not the strain of cowpox that Edward Jenner used, and it is not a weakened form of smallpox. The eradication campaign led to the death of Janet Parker (c. 1938–1978) and the subsequent suicide of the smallpox expert Henry Bedson (1930–1978). Parker was an employee of the University of Birmingham who worked in the same building as Bedson's smallpox laboratory. She was infected by a strain of smallpox virus that Bedson's team had been investigating. Ashamed of the accident and having blamed himself for it, Bedson committed suicide. Before the September 11 attacks on the United States in 2001, the World Health Organization proposed the destruction of all the known remaining stocks of smallpox virus that were kept in laboratories in the US and Russia. Fears of bioterrorism using smallpox virus and the possible need for the virus in the development of drugs to treat the infection have put an end to this plan. Had the destruction gone ahead, smallpox virus might have been the first to be made extinct by human intervention. Measles was a rare – although most often fatal – infection in South Africa in the early nineteenth century but epidemics increased in frequency from the 1850s. During the Second Boer War (1899−1902) measles was rife among the prisoners in the British concentration camps and accounted for thousands of deaths. This fatality rate in the camps was ten times greater than among British casualties. Before the introduction of vaccination in the US in the 1960s there were more than 500,000 cases each year resulting in about 400 deaths. In developed countries children were mainly infected between the ages of three and five years old, but in developing countries half the children were infected before the age of two. In the US and the UK, there were regular annual or biannual epidemics of the disease, which depended on the number of children born each year. The current epidemic strain evolved in the first part of the 20th century – probably between 1908 and 1943. In London between 1950 and 1968 there were epidemics every two years, but in Liverpool , which had a higher birth rate, there was an annual cycle of epidemics. During the Great Depression in the US before the Second World War the birth rate was low, and epidemics of measles were sporadic. After the war the birth rate increased, and epidemics occurred regularly every two years. In developing countries with very high birth rates, epidemics occurred every year. Measles is still a major problem in densely populated, less-developed countries with high birth rates and lacking effective vaccination campaigns. By the mid-1970s, following a mass vaccination programme that was known as "make measles a memory", the incidence of measles in the US had fallen by 90 per cent. Similar vaccination campaigns in other countries have reduced the levels of infection by 99 per cent over the past 50 years. Susceptible individuals remain a source of infection and include those who have migrated from countries with ineffective vaccination schedules, or who refuse the vaccine or choose not to have their children vaccinated. Humans are the only natural host of measles virus. Immunity to the disease following an infection is lifelong; that afforded by vaccination is long term but eventually wanes. The use of the vaccine has been controversial . In 1998, Andrew Wakefield and his colleagues published a fraudulent research paper and he claimed to link the MMR vaccine with autism . The study was widely reported and fed concern about the safety of vaccinations. Wakefield's research was identified as fraudulent and in 2010, he was struck off the UK medical register and can no longer practise medicine in the UK. In the wake of the controversy, the MMR vaccination rate in the UK fell from 92 per cent in 1995, to less than 80 per cent in 2003. Cases of measles rose from 56 in 1998 to 1370 in 2008, and similar increases occurred throughout Europe. In April 2013, an epidemic of measles in Wales in the UK broke out, which mainly affected teenagers who had not been vaccinated. Despite this controversy, measles has been eliminated from Finland, Sweden and Cuba. Japan abolished mandatory vaccination in 1992, and in 1995–1997 more than 200,000 cases were reported in the country. Measles remains a public health problem in Japan, where it is now endemic; a National Measles Elimination Plan was established in December 2007, with a view to eliminating the disease from the country. The possibility of global elimination of measles has been debated in medical literature since the introduction of the vaccine in the 1960s. Should the current campaign to eradicate poliomyelitis be successful, it is likely that the debate will be renewed. During the summers of the mid-20th century, parents in the US and Europe dreaded the annual appearance of poliomyelitis (or polio), which was commonly known as "infantile paralysis". The disease was rare at the beginning of the century, and worldwide there were only a few thousand cases per year, but by the 1950s there were 60,000 cases each year in the US alone and an average of 2,300 in England and Wales. During 1916 and 1917 there had been a major epidemic in the US; 27,000 cases and 6,000 deaths were recorded, with 9,000 cases in New York City . At the time nobody knew how the virus was spreading. Many of the city's inhabitants, including scientists, thought that impoverished slum-dwelling immigrants were to blame even though the prevalence of the disease was higher in the more prosperous districts such as Staten Island – a pattern that had also been seen in cities like Philadelphia. Many other industrialised countries were affected at the same time. In particular, before the outbreaks in the US, large epidemics had occurred in Sweden. The reason for the rise of polio in industrialised countries in the 20th century has never been fully explained. The disease is caused by a virus that is passed from person to person by the faecal-oral route , and naturally infects only humans. It is a paradox that it became a problem during times of improved sanitation and increasing affluence. Although the virus was discovered at the beginning of the 20th century, its ubiquity was unrecognised until the 1950s. It is now known that fewer than two per cent of individuals who are infected develop the disease, and most infections are mild. During epidemics the virus was effectively everywhere, which explains why public health officials were unable to isolate a source. Following the development of vaccines in the mid-1950s, mass vaccination campaigns took place in many countries. In the US, after a campaign promoted by the March of Dimes , the annual number of polio cases fell dramatically; the last outbreak was in 1979. In 1988 the World Health Organization along with others launched the Global Polio Eradication Initiative, and by 1994 the Americas were declared to be free of disease, followed by the Pacific region in 2000 and Europe in 2003. At the end of 2012, only 223 cases were reported by the World Health Organization. Mainly poliovirus type 1 infections, 122 occurred in Nigeria , one in Chad , 58 in Pakistan and 37 in Afghanistan . Vaccination teams often face danger; seven vaccinators were murdered in Pakistan and nine in Nigeria at the beginning of 2013. In Pakistan, the campaign was further hampered by the murder on 26 February 2013 of a police officer who was providing security. The human immunodeficiency virus ( HIV ) is the virus that – when the infection is not treated – can cause AIDS (acquired immunodeficiency syndrome). Most virologists believe that HIV originated in Kinshasa in the Democratic Republic of Congo during the 20th century, and over 70 million individuals have been infected by the virus. By 2011, an estimated 35 million had died from AIDS, making it one of the most destructive epidemics in recorded history. HIV-1 is one of the most significant viruses to have emerged in the last quarter of the 20th century. When, in 1981, a scientific article was published that reported the deaths of five young gay men, no one knew that they had died from AIDS. The full scale of the epidemic – and that the virus had been silently emerging over several decades – was not known. HIV crossed the species barrier between chimpanzees and humans in Africa in the early decades of the 20th century. During the years that followed there were enormous social changes and turmoil in Africa. Population shifts were unprecedented as vast numbers of people moved from rural farms to the expanding cities, and the virus was spread from remote regions to densely populated urban conurbations. The incubation period for AIDS is around 10 years, so a global epidemic starting in the early 1980s is credible. At this time there was much scapegoating and stigmatisation. The "out of Africa" theory for the origin of the HIV pandemic was not well received by Africans, who felt that the "blame" was misplaced. This led the World Health Assembly to pass a 1987 resolution, which stated that HIV is "a naturally occurring [virus] of undetermined geographic origin". The HIV pandemic has challenged communities and brought about social changes throughout the world. Opinions on sexuality are more openly discussed. Advice on sexual practices and drug use – which were once taboo – is sponsored by many governments and their healthcare providers. Debates on the ethics of provision and cost of anti-retroviral drugs , particularly in poorer countries, have highlighted inequalities in healthcare and stimulated far-reaching legislative changes. In developing countries the impact of HIV/AIDS has been profound; key organisations such as healthcare, defense and civil services have been severely disrupted. Life expectancy has fallen. In Zimbabwe, for example, life expectancy was 79 years in 1991 but by 2001 it had fallen to 39 years. When influenza virus undergoes a genetic shift many humans have no immunity to the new strain, and if the population of susceptible individuals is high enough to maintain the chain of infection, pandemics occur. The genetic changes usually happen when different strains of the virus co-infect animals, particularly birds and swine. Although many viruses of vertebrates are restricted to one species, influenza virus is an exception. The last pandemic of the 19th century occurred in 1899 and resulted in the deaths of 250,000 people in Europe. The virus, which originated in Russia or Asia, was the first to be rapidly spread by people on trains and steamships. A new strain of the virus emerged in 1918, and the subsequent pandemic of Spanish flu was one of the worst natural disasters in history. The death toll was enormous; throughout the world around 50 million people died from the infection. There were 550,000 reported deaths caused by the disease in the US, ten times the country's losses during the First World War, and 228,000 deaths in the UK. In India there were more than 20 million deaths, and in Western Samoa 22 per cent of the population died. Although cases of influenza occurred every winter, there were only two other pandemics in the 20th century. In 1957 another new strain of the virus emerged and caused a pandemic of Asian flu ; although the virus was not as virulent as the 1918 strain, over one million died worldwide. The next pandemic occurred when Hong Kong flu emerged in 1968, a new strain of the virus that replaced the 1957 strain. Affecting mainly the elderly, the 1968 pandemic was the least severe, but 33,800 were killed in the US. New strains of influenza virus often originate in East Asia; in rural China the concentration of ducks, pigs, and humans in close proximity is the highest in the world. The most recent pandemic occurred in 2009, but none of the last three has caused anything near the devastation seen in 1918. Exactly why the strain of influenza that emerged in 1918 was so devastating is a question that still remains unanswered. Arboviruses are viruses that are transmitted to humans and other vertebrates by blood-sucking insects. These viruses are diverse; the term "arbovirus" – which was derived from "arthropod-borne virus" – is no longer used in formal taxonomy because many species of virus are known to be spread in this way. There are more than 500 species of arboviruses, but in the 1930s only three were known to cause disease in humans: yellow fever virus , dengue virus and Pappataci fever virus . More than 100 of such viruses are now known to cause human diseases including encephalitis . Yellow fever is the most notorious disease caused by a flavivirus. The last major epidemic in the US occurred in 1905. During the building of the Panama Canal thousands of workers died from the disease. Yellow fever originated in Africa and the virus was brought to the Americas on cargo ships, which were harbouring the Aedes aegypti mosquito that carries the virus. The first recorded epidemic in Africa occurred in Ghana , in West Africa, in 1926. In the 1930s the disease re-emerged in Brazil. Fred Soper , an American epidemiologist (1893–1977), discovered the importance of the sylvatic cycle of infection in non-human hosts, and that infection of humans was a "dead end" that broke this cycle. Although the yellow fever vaccine is one of the most successful ever developed, epidemics continue to occur. In 1986–91 in West Africa, over 20,000 people were infected, 4,000 of whom died. In the 1930s, St. Louis encephalitis , eastern equine encephalitis and western equine encephalitis emerged in the US. The virus that causes La Crosse encephalitis was discovered in the 1960s, and West Nile virus arrived in New York in 1999. As of 2010, dengue virus is the most prevalent arbovirus and increasingly virulent strains of the virus have spread across Asia and the Americas. Hepatitis is a disease of the liver that has been recognised since antiquity. Symptoms include jaundice , a yellowing of the skin, eyes and body fluids. There are numerous causes, including viruses – particularly hepatitis A virus , hepatitis B virus and hepatitis C virus . Throughout history epidemics of jaundice have been reported, mainly affecting soldiers at war. This "campaign jaundice" was common in the Middle Ages. It occurred among Napoleon 's armies and during most of the major conflicts of the 19th and 20th centuries, including the American Civil War , where over 40,000 cases and around 150 deaths were reported. The viruses that cause epidemic jaundice were not discovered until the middle of the 20th century. The names for epidemic jaundice, hepatitis A, and for blood-borne infectious jaundice, hepatitis B, were first used in 1947, following a publication in 1946 giving evidence that the two diseases were distinct. In the 1960s, the first virus that could cause hepatitis was discovered. This was hepatitis B virus, which was named after the disease it causes. Hepatitis A virus was discovered in 1974. The discovery of hepatitis B virus and the invention of tests to detect it have radically changed many medical, and some cosmetic procedures. The screening of donated blood , which was introduced in the early 1970s, has dramatically reduced the transmission of the virus. Donations of human blood plasma and Factor VIII collected before 1975 often contained infectious levels of hepatitis B virus. Until the late 1960s, hypodermic needles were often reused by medical professionals, and tattoo artists' needles were a common source of infection. In the late 1990s, needle exchange programmes were established in Europe and the US to prevent the spread of infections by intravenous drug users . These measures also helped to reduce the subsequent impact of HIV and hepatitis C virus. Epizootics are outbreaks (epidemics) of disease among non-human animals. During the 20th century significant epizootics of viral diseases in animals, particularly livestock, occurred worldwide. The many diseases caused by viruses included foot-and-mouth disease , rinderpest of cattle, avian and swine influenza, swine fever and bluetongue of sheep. Viral diseases of livestock can be devastating both to farmers and the wider community, as the outbreak of foot-and-mouth disease in the UK in 2001 showed. First appearing in East Africa in 1891, rinderpest, a disease of cattle, spread rapidly across Africa. By 1892, 95 per cent of the cattle in East Africa had died. This resulted in a famine that devastated the farmers and nomadic people, some of whom were entirely dependent on their cattle. Two thirds of the population of Maasai people died. The situation was made worse by epidemics of smallpox that followed in the wake of the famine. In the early years of the 20th century rinderpest was common in Asia and parts of Europe. The prevalence of the disease was steadily reduced during the century by control measures that included vaccination. By 1908 Europe was free from the disease. Outbreaks did occur following the Second World War, but these were quickly controlled. The prevalence of the disease increased in Asia, and in 1957 Thailand had to appeal for aid because so many buffaloes had died that the paddy fields could not be prepared for rice growing. Russia west of the Ural Mountains remained free from the disease – Lenin approved several laws on the control of the disease – but cattle in eastern Russia were constantly infected with rinderpest that originated in Mongolia and China where the prevalence remained high. India controlled the spread of the disease, which had retained a foothold in the southern states of Tamil Nadu and Kerala , throughout the 20th century, and had eradicated the disease by 1995. Africa suffered two major panzootics in the 1920s and 1980s. There was a severe outbreak in Somalia in 1928 and the disease was widespread in the country until 1953. In the 1980s, outbreaks in Tanzania and Kenya were controlled by the use of 26 million doses of vaccine, and a recurrence of the disease in 1997 was suppressed by an intensive vaccination campaign. By the end of the century rinderpest had been eradicated from most countries. A few pockets of infection remained in Ethiopia and Sudan, and in 1994 the Global Rinderpest Eradication Programme was launched by the Food and Agriculture Organization (FAO) with the aim of global eradication by 2010. In May 2011, the FAO and the World Organisation for Animal Health announced that "rinderpest as a freely circulating viral disease has been eliminated from the world." Foot-and-mouth disease is a highly contagious infection caused by an aphthovirus , and is classified in the same family as poliovirus. The virus has infected animals, mainly ungulates , in Africa since ancient times and was probably brought to the Americas in the 19th century by imported livestock. Foot-and-mouth disease is rarely fatal, but the economic losses incurred by outbreaks in sheep and cattle herds can be high. The last occurrence of the disease in the US was in 1929, but as recently as 2001, several large outbreaks occurred throughout the UK and thousands of animals were killed and burnt. The natural hosts of influenza viruses are pigs and birds, although it has probably infected humans since antiquity. The virus can cause mild to severe epizootics in wild and domesticated animals. Many species of wild birds migrate and this has spread influenza across the continents throughout the ages. The virus has evolved into numerous strains and continues to do so, posing an ever-present threat. In the early years of the 21st century epizootics in livestock caused by viruses continue to have serious consequences. Bluetongue disease , a disease caused by an orbivirus broke out in sheep in France in 2007. Until then the disease had been mainly confined to the Americas, Africa, southern Asia and northern Australia, but it is now an emerging disease around the Mediterranean. During the 20th century, many "old" diseases of plants were found to be caused by viruses. These included maize streak and cassava mosaic disease . As with humans, when plants thrive in close proximity, so do their viruses. This can cause huge economic losses and human tragedies. In Jordan during the 1970s, where tomatoes and cucurbits (cucumbers, melons and gourds) were extensively grown, entire fields were infected with viruses. Similarly, in Côte d'Ivoire , thirty different viruses infected crops such as legumes and vegetables. In Kenya cassava mosaic virus, maize streak virus and groundnut viral diseases caused the loss of up to 70 per cent of the crop. Cassava is the most abundant crop that is grown in eastern Africa and it is a staple crop for more than 200 million people. It was introduced to Africa from South America and grows well in soils with poor fertility. The most important disease of cassava is caused by cassava mosaic virus, a geminivirus , which is transmitted between plants by whiteflies . The disease was first recorded in 1894 and outbreaks of the disease occurred in eastern Africa throughout the 20th century, often resulting in famine. In the 1920s the sugarbeet growers in the western US suffered huge economic loss caused by damage done to their crops by the leafhopper -transmitted beet curly top virus . In 1956, between 25 and 50 per cent of the rice crop in Cuba and Venezuela was destroyed by rice hoja blanca virus . In 1958, it caused the loss of many rice fields in Colombia. Outbreaks recurred in 1981, which caused losses of up to 100 per cent. In Ghana between 1936 and 1977, the mealybug-transmitted cacao swollen-shoot virus caused the loss of 162 million cacao trees , and additional trees were lost at the rate of 15 million each year. In 1948, in Kansas , US, seven per cent of the wheat crop was destroyed by wheat streak mosaic virus , spread by the wheat curl mite (Aceria tulipae) . In the 1950s papaya ringspot virus – a potyvirus – caused a devastating loss of solo papaya crops on Oahu , Hawaii. Solo papaya had been introduced to the island in the previous century but the disease had not been seen on the island before the 1940s. Such disasters occurred when human intervention caused ecological changes by the introduction of crops to new vectors and viruses. Cacao is native to South America and was introduced to West Africa in the late 19th century. In 1936, swollen root disease had been transmitted to plantations by mealybugs from indigenous trees. New habitats can trigger outbreaks of plant virus diseases. Before 1970, the rice yellow mottle virus was only found in the Kisumu district of Kenya, but following the irrigation of large areas of East Africa and extensive rice cultivation, the virus spread throughout East Africa. Human activity introduced plant viruses to native crops. The citrus tristeza virus (CTV) was introduced to South America from Africa between 1926 and 1930. At the same time, the aphid Toxoptera citricidus was carried from Asia to South America and this accelerated the transmission of the virus. By 1950, more than six million citrus trees had been killed by the virus in São Paulo , Brazil. CTV and citrus trees probably coevolved for centuries in their original countries. The dispersal of CTV to other regions and its interaction with new citrus varieties resulted in devastating outbreaks of plant diseases. Because of the problems caused by the introduction – by humans – of plant viruses, many countries have strict importation controls on any materials that can harbour dangerous plant viruses or their insect vectors. Even without mutation, it is always possible that some hitherto obscure parasitic organism may escape its accustomed ecological niche and expose the dense populations that have become so conspicuous a feature of the earth to some fresh and perchance devastating mortality. McNeill (1998) p. 293 Emerging viruses are those that have only relatively recently infected the host species. In humans, many emerging viruses have come from other animals. When viruses jump to other species the diseases caused in humans are called zoonoses or zoonotic infections . Severe acute respiratory syndrome (SARS) is caused by a new type of coronavirus . Other coronaviruses were known to cause mild infections in humans, so the virulence and rapid spread of this novel virus strain caused alarm among health professionals as well as public fear. The fears of a major pandemic were not realised, and by July 2003, after causing around 8,000 cases and 800 deaths, the outbreak had ended. The exact origin of the SARS virus is not known, but evidence suggests that it came from bats. A related coronavirus emerged in Wuhan , China in November 2019 and spread rapidly around the world. Subsequently, named severe acute respiratory syndrome coronavirus 2 , infections with the virus caused a pandemic with a case fatality rate of around 2% in healthy people under the age of 50, to around 15% in those aged over 80 particularly those with pre-existing comorbidities. The fatality rate was lower than SARS but the infection was more contagious. Measures to curtail the impact of the pandemic were hampered by fear and prejudice and stigmatisation of infected people. Unprecedented restrictions in peacetime were placed on international travel, and curfews imposed in several major cities worldwide. Many countries and regions to imposed quarantine, entry bans, or other restrictions. The effectiveness of these measure was questioned as the virus spread across the world. Governments were not prepared for the scale of the pandemic and worldwide, virology and epidemiology experts were complacent with regards to the efficiency of existing testing and monitoring systems. As of 10 March 2023 , the pandemic had caused more than 676 million cases and 6.88 million confirmed deaths , making it one of the deadliest in history . West Nile virus, a flavivirus, was first identified in 1937 when it was found in the blood of a feverish woman. The virus, which is carried by mosquitoes and birds, caused outbreaks of infection in North Africa and the Middle East in the 1950s and by the 1960s horses in Europe were also affected. The largest outbreak in humans occurred in 1974 in Cape Province , South Africa and 10,000 people became ill. An increasing frequency of epidemics and epizootics (in horses) began in 1996, around the Mediterranean basin, and by 1999 the virus had reached New York City. Since then the virus has spread throughout the US. In the US, mosquitoes carry the highest amounts of virus in late summer, and the number of cases of the disease increases in mid July to early September. When the weather becomes colder, the mosquitoes die and the risk of disease decreases. In Europe, many outbreaks have occurred; in 2000 a surveillance programme began in the UK to monitor the incidence of the virus in humans, dead birds, mosquitoes and horses. The mosquito ( Culex modestus ) that can carry the virus breeds on the marshes of north Kent . This mosquito species was not previously thought to be present in the UK, but it is widespread in southern Europe where it carries West Nile virus. In 1997 an outbreak of respiratory disease occurred in Malaysian farmers and their pigs. More than 265 cases of encephalitis, of which 105 were fatal, were recorded. A new paramyxovirus was discovered in an individual's brain; it was named Nipah virus , after the village where he had lived. The infection was caused by a virus from fruit bats, after their colony had been disrupted by deforestation. The bats had moved to trees nearer the pig farm and the pigs caught the virus from their droppings. Several highly lethal viral pathogens are members of the Filoviridae . Filoviruses are filament-like viruses that cause viral haemorrhagic fever , and include the Ebola and Marburg viruses . The Marburg virus attracted widespread press attention in April 2005 after an outbreak in Angola . Beginning in October 2004 and continuing into 2005, there were 252 cases including 227 deaths. The Ebola virus epidemic in West Africa , which began in 2013, is the most devastating since the emergence of HIV. The initial outbreak occurred in December 2013 in Meliandou, a village in southern Guinea . Among the first cases were a two-year-old boy, his three-year-old sister, their mother and grandmother. After the grandmother's funeral, which was attended by her family and caregivers, the disease spread to neighbouring villages. By March 2014 the outbreak was severe enough to raise the concern of local health officials who reported it to the Guinean Ministry of Health. By the middle of the year the epidemic had spread to Liberia and Sierra Leone. As of June 2015, the World Health Organization reported over 27,000 cases of the disease, which had resulted in more than 11,000 deaths. The natural source of Ebola virus is probably bats. Marburg viruses are transmitted to humans by monkeys, and Lassa fever by rats ( Mastomys natalensis ). Zoonotic infections can be severe because humans often have no natural resistance to the infection and it is only when viruses become well-adapted to new host that their virulence decreases. Some zoonotic infections are often "dead ends", in that after the initial outbreak the rate of subsequent infections subsides because the viruses are not efficient at spreading from person to person. The beginning of the 21st century saw an increase in the global awareness of devastating epidemics in developing countries, which, in previous decades had passed relatively unnoticed by the international health community. Severe acute respiratory syndrome (SARS) is caused by a new type of coronavirus . Other coronaviruses were known to cause mild infections in humans, so the virulence and rapid spread of this novel virus strain caused alarm among health professionals as well as public fear. The fears of a major pandemic were not realised, and by July 2003, after causing around 8,000 cases and 800 deaths, the outbreak had ended. The exact origin of the SARS virus is not known, but evidence suggests that it came from bats. A related coronavirus emerged in Wuhan , China in November 2019 and spread rapidly around the world. Subsequently, named severe acute respiratory syndrome coronavirus 2 , infections with the virus caused a pandemic with a case fatality rate of around 2% in healthy people under the age of 50, to around 15% in those aged over 80 particularly those with pre-existing comorbidities. The fatality rate was lower than SARS but the infection was more contagious. Measures to curtail the impact of the pandemic were hampered by fear and prejudice and stigmatisation of infected people. Unprecedented restrictions in peacetime were placed on international travel, and curfews imposed in several major cities worldwide. Many countries and regions to imposed quarantine, entry bans, or other restrictions. The effectiveness of these measure was questioned as the virus spread across the world. Governments were not prepared for the scale of the pandemic and worldwide, virology and epidemiology experts were complacent with regards to the efficiency of existing testing and monitoring systems. As of 10 March 2023 , the pandemic had caused more than 676 million cases and 6.88 million confirmed deaths , making it one of the deadliest in history . West Nile virus, a flavivirus, was first identified in 1937 when it was found in the blood of a feverish woman. The virus, which is carried by mosquitoes and birds, caused outbreaks of infection in North Africa and the Middle East in the 1950s and by the 1960s horses in Europe were also affected. The largest outbreak in humans occurred in 1974 in Cape Province , South Africa and 10,000 people became ill. An increasing frequency of epidemics and epizootics (in horses) began in 1996, around the Mediterranean basin, and by 1999 the virus had reached New York City. Since then the virus has spread throughout the US. In the US, mosquitoes carry the highest amounts of virus in late summer, and the number of cases of the disease increases in mid July to early September. When the weather becomes colder, the mosquitoes die and the risk of disease decreases. In Europe, many outbreaks have occurred; in 2000 a surveillance programme began in the UK to monitor the incidence of the virus in humans, dead birds, mosquitoes and horses. The mosquito ( Culex modestus ) that can carry the virus breeds on the marshes of north Kent . This mosquito species was not previously thought to be present in the UK, but it is widespread in southern Europe where it carries West Nile virus. In 1997 an outbreak of respiratory disease occurred in Malaysian farmers and their pigs. More than 265 cases of encephalitis, of which 105 were fatal, were recorded. A new paramyxovirus was discovered in an individual's brain; it was named Nipah virus , after the village where he had lived. The infection was caused by a virus from fruit bats, after their colony had been disrupted by deforestation. The bats had moved to trees nearer the pig farm and the pigs caught the virus from their droppings. Several highly lethal viral pathogens are members of the Filoviridae . Filoviruses are filament-like viruses that cause viral haemorrhagic fever , and include the Ebola and Marburg viruses . The Marburg virus attracted widespread press attention in April 2005 after an outbreak in Angola . Beginning in October 2004 and continuing into 2005, there were 252 cases including 227 deaths. The Ebola virus epidemic in West Africa , which began in 2013, is the most devastating since the emergence of HIV. The initial outbreak occurred in December 2013 in Meliandou, a village in southern Guinea . Among the first cases were a two-year-old boy, his three-year-old sister, their mother and grandmother. After the grandmother's funeral, which was attended by her family and caregivers, the disease spread to neighbouring villages. By March 2014 the outbreak was severe enough to raise the concern of local health officials who reported it to the Guinean Ministry of Health. By the middle of the year the epidemic had spread to Liberia and Sierra Leone. As of June 2015, the World Health Organization reported over 27,000 cases of the disease, which had resulted in more than 11,000 deaths. The natural source of Ebola virus is probably bats. Marburg viruses are transmitted to humans by monkeys, and Lassa fever by rats ( Mastomys natalensis ). Zoonotic infections can be severe because humans often have no natural resistance to the infection and it is only when viruses become well-adapted to new host that their virulence decreases. Some zoonotic infections are often "dead ends", in that after the initial outbreak the rate of subsequent infections subsides because the viruses are not efficient at spreading from person to person. The beginning of the 21st century saw an increase in the global awareness of devastating epidemics in developing countries, which, in previous decades had passed relatively unnoticed by the international health community. Sir Peter Medawar (1915–1987) described a virus as "a piece of bad news wrapped in a protein coat". With the exception of the bacteriophages , viruses had a well-deserved reputation for being nothing but the cause of diseases and death. The discovery of the abundance of viruses and their overwhelming presence in many ecosystems has led modern virologists to reconsider their role in the biosphere . It is estimated that there are about 10 31 viruses on Earth. Most of them are bacteriophages, and most are in the oceans. Microorganisms constitute more than 90 per cent of the biomass in the sea, and it has been estimated that viruses kill approximately 20 per cent of this biomass each day and that there are fifteen times as many viruses in the oceans as there are bacteria and archaea . Viruses are the main agents responsible for the rapid destruction of harmful algal blooms , which often kill other marine life, and help maintain the ecological balance of different species of marine blue-green algae , and thus adequate oxygen production for life on Earth. The emergence of strains of bacteria that are resistant to a broad range of antibiotics has become a problem in the treatment of bacterial infections. Only two new classes of antibiotics have been developed in the past 30 years, and novel ways of combating bacterial infections are being sought. Bacteriophages were first used to control bacteria in the 1920s, and a large clinical trial was conducted by Soviet scientists in 1963. This work was unknown outside the Soviet Union until the results of the trial were published in the West in 1989. The recent and escalating problems caused by antibiotic-resistant bacteria has stimulated a renewed interest in the use of bacteriophages and phage therapy . The Human Genome Project has revealed the presence of numerous viral DNA sequences scattered throughout the human genome . These sequences make up around eight per cent of human DNA, and appear to be the remains of ancient retrovirus infections of human ancestors. These pieces of DNA have firmly established themselves in human DNA. Most of this DNA is no longer functional, but some of these viruses have brought with them novel genes that are important in human development, and could aid the immune system's B cells destroy tumours. Viruses have transferred important genes to plants. About ten per cent of all photosynthesis uses the products of genes that have been transferred to plants from blue-green algae by viruses.
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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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https://api.wikimedia.org/core/v1/wikipedia/en/page/1967_Marburg_virus_outbreak/html
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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Viral_hepatitis/html
Viral hepatitis
Viral hepatitis is liver inflammation due to a viral infection . It may present in acute form as a recent infection with relatively rapid onset, or in chronic form, typically progressing from a long-lasting asymptomatic condition up to a decompensated hepatic disease and hepatocellular carcinoma (HCC). The most common causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A , B , C , D , and E . Other viruses can also cause liver inflammation, including cytomegalovirus , Epstein–Barr virus , and yellow fever . There also have been scores of recorded cases of viral hepatitis caused by herpes simplex virus. Viral hepatitis is either transmitted through contaminated food or water (A, E) or via blood and body fluids (B, C). The viruses transmitted through water and food are mostly self-limited, resulting in acute illness with full resolution. The blood borne viruses (B, C) can cause both acute and chronic liver disease and can be transmitted from mother to child during birth, through contact with body fluids during sex, unsafe injections and through unscreened blood transfusions. The most common types of hepatitis can be prevented or treated. Hepatitis A and hepatitis B can be prevented by vaccination. Effective treatments for hepatitis C are available but costly. In 2013, about 1.5 million people died from viral hepatitis, most commonly due to hepatitis B and C. East Asia, in particular Mongolia , is the region most affected. The most common cause of hepatitis is viral. Although the effects of various viruses are all classified under the disease hepatitis , these viruses are not all related. [ citation needed ]Hepatitis A or infectious jaundice is caused by hepatitis A virus (HAV), a picornavirus transmitted by the fecal-oral route often associated with ingestion of contaminated food . It causes an acute form of hepatitis and does not have a chronic stage. A patient's immune system makes antibodies against HAV that confer immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent HAV infection for up to 10 years. Hepatitis A can be spread through personal contact, consumption of raw sea food, or drinking contaminated water . This occurs primarily in third world countries . Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an infection. Infected people excrete HAV with their feces two weeks before and one week after the appearance of jaundice . The time between the infection and the start of the illness averages 28 days. (ranging from 15 to 50 days), Most patients recover fully within 2 months, although approximately 15% of affected people may experience continuous or relapsing symptoms from six months to a year following initial diagnosis . Hepatitis B is caused by the hepatitis B virus, a hepadnavirus that can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus after an initial infection. Identified methods of transmission include contact with blood, blood transfusion (now rare), unsanitary tattoos, sex (through sexual intercourse or contact with bodily fluids), or mother-to-child by breast feeding ; [ citation needed ] there is minimal evidence of transplacental crossing . However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention. [ citation needed ] Patients with chronic hepatitis B have antibodies against the virus, but not enough to clear the infected liver cells . The continued production of virus and countervailing antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available to prevent infection for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis , and hepatocellular carcinoma (HCC). Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are eight treatment options approved by the U.S. Food and Drug Administration (FDA) available for persons with a chronic hepatitis B infection: alpha-interferon , pegylated interferon , adefovir , entecavir , telbivudine , lamivudine , tenofovir disoproxil and tenofovir alafenamide with a 65% rate of sustained response. [ citation needed ] Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus of the family Flaviviridae . HCV can be transmitted through contact with blood (including through sexual contact if the two parties' blood is mixed) and can also cross the placenta . Hepatitis C usually leads to chronic hepatitis, culminating in cirrhosis in some people. It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. HCV can lead to the development of hepatocellular carcinoma , however, only a minority of HCV-infected individuals develop cancer (1–4% annually), suggesting a complex interplay between viral gene expression and host and environmental factors to promote carcinogenesis. The risk is increased two-fold with active HBV coinfection and a 21% increase in mortality compared to those with latent HBV and HCV. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin . The genotype of the virus is the primary determinant of the rate of response to this treatment regimen, with genotype 1 being the most resistant. [ citation needed ] Hepatitis C is the most common chronic bloodborne infection in the United States, and the leading cause of liver tranplants. Hepatitis D is caused by the hepatitis D virus (HDV), or hepatitis delta virus; it belongs to the genus Deltavirus . HDV is similar to a satellite virus as it can only propagate in the presence of the hepatitis B virus, depending on the helper function of HBV for its replication and expression. It has no independent life cycle, but can survive and replicate as long as HBV infection persists in the host body. It can only cause infection when encapsulated by hepatitis B virus surface antigens. The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate. Hepatitis E is caused by the Hepatitis E virus (HEV), from the family Hepeviridae. It produces symptoms similar to hepatitis A , although it can take a fulminant course in some patients, particularly pregnant women (mortality rate about 20%); chronic infections may occur in immune-compromised patients. It is more prevalent in the Indian subcontinent . The virus is feco-orally transmitted and is usually self-limited. [ citation needed ] Hepatitis F virus (HFV) is a hypothetical virus linked to certain cases of hepatitis. Several hepatitis F virus candidates emerged in the 1990s, but none of these reports have been substantiated. [ citation needed ] The GB virus C is a virus that is probably spread by blood and sexual contact. It was initially identified as Hepatitis G virus. There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver. It is now classified as GB virus C. In 2022, several hundred cases of acute hepatitis of probable infectious origin were reported worldwide. As of May 2023, the virus causing these cases has not been identified, but an adenovirus is suspected. Hepatitis A or infectious jaundice is caused by hepatitis A virus (HAV), a picornavirus transmitted by the fecal-oral route often associated with ingestion of contaminated food . It causes an acute form of hepatitis and does not have a chronic stage. A patient's immune system makes antibodies against HAV that confer immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent HAV infection for up to 10 years. Hepatitis A can be spread through personal contact, consumption of raw sea food, or drinking contaminated water . This occurs primarily in third world countries . Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an infection. Infected people excrete HAV with their feces two weeks before and one week after the appearance of jaundice . The time between the infection and the start of the illness averages 28 days. (ranging from 15 to 50 days), Most patients recover fully within 2 months, although approximately 15% of affected people may experience continuous or relapsing symptoms from six months to a year following initial diagnosis . Hepatitis B is caused by the hepatitis B virus, a hepadnavirus that can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of adults who are unable to eliminate the virus after an initial infection. Identified methods of transmission include contact with blood, blood transfusion (now rare), unsanitary tattoos, sex (through sexual intercourse or contact with bodily fluids), or mother-to-child by breast feeding ; [ citation needed ] there is minimal evidence of transplacental crossing . However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention. [ citation needed ] Patients with chronic hepatitis B have antibodies against the virus, but not enough to clear the infected liver cells . The continued production of virus and countervailing antibodies is a likely cause of the immune complex disease seen in these patients. A vaccine is available to prevent infection for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis , and hepatocellular carcinoma (HCC). Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are eight treatment options approved by the U.S. Food and Drug Administration (FDA) available for persons with a chronic hepatitis B infection: alpha-interferon , pegylated interferon , adefovir , entecavir , telbivudine , lamivudine , tenofovir disoproxil and tenofovir alafenamide with a 65% rate of sustained response. [ citation needed ]Hepatitis C (originally "non-A non-B hepatitis") is caused by hepatitis C virus (HCV), an RNA virus of the family Flaviviridae . HCV can be transmitted through contact with blood (including through sexual contact if the two parties' blood is mixed) and can also cross the placenta . Hepatitis C usually leads to chronic hepatitis, culminating in cirrhosis in some people. It usually remains asymptomatic for decades. Patients with hepatitis C are susceptible to severe hepatitis if they contract either hepatitis A or B, so all persons with hepatitis C should be immunized against hepatitis A and hepatitis B if they are not already immune, and avoid alcohol. HCV can lead to the development of hepatocellular carcinoma , however, only a minority of HCV-infected individuals develop cancer (1–4% annually), suggesting a complex interplay between viral gene expression and host and environmental factors to promote carcinogenesis. The risk is increased two-fold with active HBV coinfection and a 21% increase in mortality compared to those with latent HBV and HCV. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin . The genotype of the virus is the primary determinant of the rate of response to this treatment regimen, with genotype 1 being the most resistant. [ citation needed ] Hepatitis C is the most common chronic bloodborne infection in the United States, and the leading cause of liver tranplants. Hepatitis D is caused by the hepatitis D virus (HDV), or hepatitis delta virus; it belongs to the genus Deltavirus . HDV is similar to a satellite virus as it can only propagate in the presence of the hepatitis B virus, depending on the helper function of HBV for its replication and expression. It has no independent life cycle, but can survive and replicate as long as HBV infection persists in the host body. It can only cause infection when encapsulated by hepatitis B virus surface antigens. The vaccine for hepatitis B protects against hepatitis D virus because of the latter's dependence on the presence of hepatitis B virus for it to replicate. Hepatitis E is caused by the Hepatitis E virus (HEV), from the family Hepeviridae. It produces symptoms similar to hepatitis A , although it can take a fulminant course in some patients, particularly pregnant women (mortality rate about 20%); chronic infections may occur in immune-compromised patients. It is more prevalent in the Indian subcontinent . The virus is feco-orally transmitted and is usually self-limited. [ citation needed ]Hepatitis F virus (HFV) is a hypothetical virus linked to certain cases of hepatitis. Several hepatitis F virus candidates emerged in the 1990s, but none of these reports have been substantiated. [ citation needed ]The GB virus C is a virus that is probably spread by blood and sexual contact. It was initially identified as Hepatitis G virus. There is very little evidence that this virus causes hepatitis, as it does not appear to replicate primarily in the liver. It is now classified as GB virus C. In 2022, several hundred cases of acute hepatitis of probable infectious origin were reported worldwide. As of May 2023, the virus causing these cases has not been identified, but an adenovirus is suspected. Hepatitis C virus (HCV) can cause acute and chronic infections that are a major cause of hepatocellular carcinoma (HCC), advanced hepatic fibrosis and cirrhosis. [ citation needed ] HCC is a major cause of death in patients with chronic HCV infection. Regarding the pathogenesis of HCC associated with HCV, that virus may play direct or indirect roles. A major risk for the development of HCC is persistent infection with HCV, and the highest risk for HCC development is associated with co-infection of HBV with HDV, HCV or HIV. Risk factors that can lead to the development of HCC in those with chronic HCV include synchronous liver diseases, viral genotype, diabetes mellitus, and obesity. Lifestyle factors such as liver steatosis, smoking, and alcohol use can accelerate progression to HCC and liver decompensation in patients with HCV. The purpose of HCV treatment is to eliminate the infection, reduce the transmission to other people and decrease the risk of HCC development. The virus first known to cause hepatitis was the yellow fever virus , a mosquito-borne flavivirus . Other viruses than can cause hepatitis include: Additionally, a casual role between the virus KIs-V and hepatitis is suspected based on a 2011 study that isolated KIs-V from four patients with raised serum alanine transferases without other known cause.
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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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Ebola virus epidemic in Sierra Leone
An Ebola virus epidemic in Sierra Leone occurred in 2014, along with the neighbouring countries of Guinea and Liberia . At the time it was discovered, it was thought that Ebola virus was not endemic to Sierra Leone or to the West African region and that the epidemic represented the first time the virus was discovered there. However, US researchers pointed to lab samples used for Lassa fever testing to suggest that Ebola had been in Sierra Leone as early as 2006. In 2014, it was discovered that samples of suspected Lassa fever showed evidence of the Zaire strain of Ebola virus in Sierra Leone as early as 2006. Prior to the current Zaire strain outbreak in 2014, Ebola had not really been seen in Sierra Leone, or even in West Africa among humans. It is suspected that fruit bats are natural carriers of disease, native to this region of Africa including Sierra Leone and also a popular food source for both humans and wildlife. The Gola forests in south-east Sierra Leone are a noted source of bushmeat. Bats are known to be carriers of at least 90 different viruses that can make transition to a human host. However, the virus has different symptoms in humans. It takes one to ten viruses to infect a human but there can be millions in a drop of blood from someone very sick from the disease. Transmission is believed to be by contact with the blood and body fluids of those infected with the virus, as well as by handling raw bushmeat such as bats and monkeys, which are important sources of protein in West Africa. Infectious body fluids include blood, sweat, semen, breast milk, saliva, tears, feces, urine, vaginal secretions, vomit, and diarrhea. Even after a successful recovery from an Ebola infection, semen may contain the virus for at least two months. Breast milk may contain the virus for two weeks after recovery, and transmission of the disease to a consumer of the breast milk may be possible. By October 2014, it was suspected that handling a piece of contaminated paper may be enough to contract the disease. Contamination on paper makes it harder to keep records in Ebola clinics, as data about patients written on paper that gets written down in a "hot" zone is hard to pass to a "safe" zone, because if there is any contamination it may bring Ebola into that area. One aspect of Sierra Leone that is alleged to have aided the disease, is the strong desire of many to have very involved funeral practices. For example, for the Kissi people who inhabit part of Sierra Leone, it is important to bury the bodies of the dead near them. Funeral practices include rubbing the corpses down with oil, dressing them in fine clothes, then having those at the funeral hug and kiss the dead body. This may aid the transmission of Ebola, because those that die from Ebola disease are thought to have high concentrations of the virus in their body, even after they have died. For the 2001 outbreak of Sudan virus in Uganda, attending a funeral of an Ebola victim was rated by the Centers for Disease Control and Prevention (CDC) as one of the top three risk factors for contracting Ebola, along with contact with a family member with Ebola or providing medical care to someone with a case of Ebola virus disease. The main start of the outbreak in Sierra Leone was linked to a single funeral in which the World Health Organization (WHO) estimates as many as 365 died from Ebola disease after getting the disease at the funeral. Bushmeat has also been implicated in spreading Ebola disease, either by handling the raw meat or through droppings from the animals. It is the raw blood and meat that is thought to be more dangerous, so it is those that hunt and butcher the raw meat that are more at risk as opposed to cooked meat sold at market. Health care workers in Sierra Leone have been warned not to go to markets. In late March 2014, there were suspected but not confirmed cases in Sierra Leone. The government announced on 31 March 2014, that there were no cases in Sierra Leone. Cases initially started appearing soon after the arrival of US researchers into the area. "After Ebola was first confirmed by laboratory tests in mid-March 2014, persistent rumours in the region linked the outbreak to a US-run research laboratory in Kenema, Sierra Leone (Wilkinson, 2017) ." Two U.S. doctors who "followed all CDC and WHO protocols to the letter" contracted Ebola, and it is not clear how they got infected. By 27 May 2014, it was reported 5 people died from the Ebola virus and there were 16 new cases of the disease. Between 27 May 2014, and 30 May the number of confirmed, probable, or suspected cases of Ebola went from 16 to 50. By 9 June, the number of cases had risen to 42 known and 113 being tested, with a total of 16 known to have died from the disease by that time. The disease spread rapidly in Kenema, and the local government hospital was overwhelmed. At that hospital, 12 nurses died despite having the world's only Lassa fever isolation ward, according to the U.N. Many health are workers were infected at the state hospital, including beloved physician and hemorrhagic fever expert, Dr. Sheik Humarr Khan, and chief nurse Mbalu Fonnie. Khan and his colleagues had bravely provided care to patients with this devastating illness. On 12 June, the country declared a state of emergency in the Kailahun District , where it announced the closure of schools, cinemas, and nightlife places; the district borders both Guinea and Liberia, and all vehicles would be subject to screening at checkpoints. The government declared on 11 June, that its country's borders would be closed to Guinea and Liberia; but many local people cross the borders on unofficial routes which were difficult for authorities to control. Seasonal rains that fall between June and August interfered with the fight against Ebola, and in some cases caused flooding in Sierra Leone. By 11 July 2014, the first case was reported in the capital of Sierra Leone, Freetown, however the person had traveled to the capital from another area of the country. By this time there were over 300 confirmed cases and 99 were confirmed to have died from Ebola. There was another case before the end of the month. On 29 July, well-known physician Sheik Umar Khan , Sierra Leone's only expert on hemorrhagic fever, died after contracting Ebola at his clinic in Kenema . Khan had long worked with Lassa fever , a disease that kills over 5,000 a year in Africa. He had expanded his clinic to accept Ebola patients. Sierra Leone's president, Ernest Bai Koroma, celebrated Khan as a "national hero". On 30 July, Sierra Leone declared a state of emergency and deployed troops to quarantine hot spots. In August, awareness campaigns in Freetown , Sierra Leone's capital, were delivered over the radio and through loudspeakers. Also in August, Sierra Leone passed a law that subjected anyone hiding someone believed to be infected to two years in jail. At the time the law was enacted, a top parliamentarian was critical of failures by neighboring countries to stop the outbreak. Also in early August Sierra Leone cancelled league football (soccer) matches. Within 2 days of 12 September 2014, there were 20 lab-confirmed cases discovered in Freetown, Sierra Leone. One issue was that residents were leaving dead bodies in the street. By 6 September 2014, there were 60 cases of Ebola in Freetown, out of about 1100 nationwide at this time. However, not everyone was bringing cases to doctors, and they were not always being treated. One doctor said the Freetown health system was not functioning, and during this time, respected Freetown Doctor Olivette Buck fell ill and died from Ebola by 14 September 2014. The population of Freetown in 2011 was 941,000. By 18 September 2014, teams of people that buried the dead were struggling to keep up, as 20–30 bodies needed to be buried each day. The teams drove on motor-bikes to collect samples from corpses to see if they died from Ebola. Freetown, Sierra Leone had one laboratory that could do Ebola testing. WHO estimated on 21 September, that Sierra Leone's capacity to treat Ebola cases fell short by the equivalent of 532 beds. Experts pushed for a greater response at this time noting that it could destroy Sierra Leone and Liberia. At that time it was estimated that if it spread through both Liberia and Sierra Leone up to 5 million could be killed; the population of Liberia is about 4.3 million and Sierra Leone is about 6.1 million. In an attempt to control the disease, Sierra Leone imposed a three-day lockdown on its population from 19 to 21 September. During this period 28,500 trained community workers and volunteers went door-to-door providing information on how to prevent infection, as well as setting up community Ebola surveillance teams. The campaign was called the Ouse to Ouse Tock in Krio language . There was concern the 72-hour lock-down could backfire. On 22 September, Stephen Gaojia said that the three-day lock down had obtained its objective and would not be extended. Eighty percent of targeted households were reached in the operation. A total of around 150 new cases were uncovered, but the exact figures would only be known on the following Thursday as the health ministry was still awaiting reports from remote locations. One incident during the lock-down was when a burial team was attacked. On 24 September, President Ernest Bai Koroma added three more districts under "isolation", in an effort to contain the spread. The districts included Port Loko , Bombali , and Moyamba . In the capital, Freetown, all homes with identified cases would be quarantined. This brought the total areas under isolation to 5, including the outbreak "hot spots" Kenema and Kailahun which were already in isolation. Only deliveries and essential services would be allowed in and out. A sharp rise in cases in these areas was also noted by WHO. As of late September, about 2 million people were in areas of restricted travel, which included Kailahun, Kenema, Bombali, Tonkolili, and Port Loko Districts. The number of cases seemed to be doubling every 20 days, which led to the estimate that by January 2015 the number of cases in Liberia and Sierra Leone could grow to 1.4 million. On 25 September, there were 1940 cases and 587 deaths officially, however, many acknowledged under-reporting and there was an increasing number of cases in Freetown (the capital of Sierra Leone). WHO estimated on 21 September, that Sierra Leone's capacity to treat Ebola cases fell short by the equivalent of 532 beds. There were reports that political interference and administrative incompetence had hindered the flow of medical supplies into the country. By 2 October 2014, an estimated 5 people per hour were being infected with the Ebola virus in Sierra Leone. By this time it was estimated the number of infected had been doubling every 20 days. On 4 October, Sierra Leone recorded 121 fatalities, the largest number in a single day. On 8 October, Sierra Leone burial crews went on strike. On 12 October, it was reported that the UK would begin providing military support to Sierra Leone in addition to a major UK civilian operation in support of the Government of Sierra Leone. In October, it was noted hospitals were running out of supplies in Sierra Leone. There were reports that political interference and administrative incompetence hindered the flow of medical supplies into the country. In the week prior to 2 October there were 765 new cases, and Ebola was spreading rapidly. At the start of October, there were nearly 2200 laboratory confirmed cases of Ebola and over 600 had died from it. The epidemic also had claimed the life of 4 doctors and at least 60 nurses by the end of September 2014. Sierra Leone limited its reported deaths to laboratory confirmed cases in facilities, so the actual number of losses was known to be higher. Sierra Leone was considering making reduced care clinics, to stop those sick with Ebola from getting their families sick with the disease and to provide something in between home-care and the full-care clinics. These "isolation centers" would provide an alternative to the overwhelmed clinics. The problem the country was facing was 726 new Ebola cases but less than 330 beds available. More than 160 additional medical personnel from Cuba arrived in early October, building on about 60 that had been there since September. At that time there were about 327 beds for patients in Sierra Leone. Canada announced it was sending a 2nd mobile lab and more staff to Sierra Leone on 4 October 2014. There were reports of drunken grave-diggers making graves for Ebola patients too shallow, and as a result wildlife came and dug up and ate at the corpses. In addition, in some cases bodies were not buried for days, because no one came to collect them. One problem was that it was hard to care for local health care workers, and there was not enough money to evacuate them. Meanwhile, other diseases like malaria, pneumonia, and diarrhea were not being treated properly because the health system was trying to deal with Ebola patients. On 7 October 2014, Canada sent a C-130 loaded with 128,000 face shields to Freetown. In early October 2014, a burial team leader said there were piles of corpses south of Freetown. On 9 October, the International Charter on Space and Major Disasters was activated on Sierra Leone's behalf, the first time that its charitably repurposed satellite imaging assets had been deployed in an epidemiological role. On 14 October 2014, 800 Sierra Leone peacekeepers due to relieve a contingent deployed in Somalia , were placed under quarantine when one of the soldiers tested positive for Ebola. The last district in Sierra Leone untouched by the Ebola virus declared Ebola cases. According to Abdul Sesay, a local health official, 15 suspected deaths with 2 confirmed cases of the deadly disease were reported on 16 October, in the village of Fakonya. The village is 60 miles from the town of Kabala in the center of the mountainous region of the Koinadugu district. This was the last district free from the virus in Sierra Leone. All of the districts in this country had then confirmed cases of Ebola. In late October 2014, the United Kingdom sent one of their hospital ships, the Royal Navy's Argus , to help Sierra Leone. By late October Sierra Leone was experiencing more than twenty deaths a day from Ebola. In October 2014, officials reported that very few pregnant women were surviving Ebola disease. In previous outbreaks pregnant women were noted to have a higher rate of death with Ebola. Officials struggled to maintain order in one town after a medical team trying to take a blood sample from a corpse were blocked by an angry machete-wielding mob. They allegedly believed the person had died from high-blood pressure and did not want the body being tested for Ebola. When security forces tried to defend the medical team, a riot ensued leaving two dead. The town was placed on a 24-hour curfew and authorities tried to calm the situation down. Despite this several buildings were attacked. On 30 October, the ship Argus arrived in Sierra Leone. It carried 32 off-road vehicles to support Ebola treatment units. The ship also carried three transport helicopters to support operations against the epidemic. By the end of October 2014 there were over 5200 laboratory confirmed cases of Ebola virus disease in Sierra Leone. [ citation needed ] On 31 October 2014, an ambulance driver in Bo District died of Ebola. His ambulance picked up Ebola patients (or suspected Ebola cases) and took them to treatment centers. On 1 November, the United Kingdom announced plans to build three more Ebola laboratories in Sierra Leone. The labs helped to determine if a patient had been infected by the Ebola virus. At that time, it took as much as five days to test a sample because of the volume of samples that needed to be tested. On 2 November, a person with Ebola employed by the United Nations was evacuated from Sierra Leone to France for treatment. On 4 November, it was reported that thousands violated quarantine in search for food, in the town of Kenema. On 6 November, it was reported that the situation was "getting worse" due to "intense transmission" in Freetown as a contributing factor; the capital city reported 115 cases in the previous week alone. Food shortages and aggressive quarantines were reported to be making the situation worse, according to the Disaster Emergency Committee. Sierra Leone established call centers in Port Loko and Kambia, according to MSSL Communications as reported on 21 November; this was in addition to the June hotline originally established. On 12 November, more than 400 health workers went on strike over salary issues at one of the few Ebola treatment centers in the country. On 18 November, the supply ship Karel Doorman of the Royal Netherlands Navy ( Koninklijke Marine ) arrived in Freetown, with supplies. Its Captain-Commander, Peter van den Berg, took steps to reduce the chance of the crew contracting Ebola virus disease. The Neini Chiefdom in Koinadugu District was subject to isolation after Ebola cases. On 19 November, it was reported that the Ebola virus was spreading intensely; "much of this was driven by intense transmission in the country's west and north", the WHO said. A British-built Ebola Treatment Centre which started in Kerry Town during November, generated some controversy because of its initially limited capacity. However, this was because they were following guidelines of how to safely open an Ebola treatment unit. This was the first of six planned treatment centres which, when completed, would be staffed by a number of NGOs . In mid-November the WHO reported that while all cases and deaths continued to be under-reported, "there is some evidence that case incidence is no longer increasing nationally in Guinea and Liberia, but steep increases persist in Sierra Leone". On 19 November, it was reported that the Ebola virus was spreading intensely; "much of this was driven by intense transmission in the country's west and north", the WHO said. The first Cuban doctor to be infected with the virus was flown to Geneva. On 26 November, it was reported that due to Sierra Leone's increased Ebola transmission, the country would surpass Liberia in the total cases count. On 27 November, Canada announced it would deploy military health staff to the infected region. On 29 November, the President of Sierra Leone canceled a planned three-day shutdown in Freetown to curb the virus. On 2 December, it was reported that the Tonkolili district had begun a two-week lockdown, "which was agreed in a key stakeholders meeting of cabinet ministers, parliamentarians and paramount chiefs of the district as part of efforts to stem the spread of the disease", according to a ministry spokesman. The move meant that a total of six districts, containing more than half of the population, were locked down. Sierra Leone indicated, in a report on 5 December, that about 100 cases of the virus were now being reported daily. On the same day, it was further reported that families caught taking part in burial washing rituals, which can spread the virus, would be taken to jail. On 6 December, a report indicated that the Canadian Armed Forces would send a medical team to the country of Sierra Leone to help combat the Ebola virus epidemic. On 8 December, the doctors in Sierra Leone went on strike, demanding better treatment for health care workers, according to Health Ministry spokesman Jonathan Abass Kamara. On 9 December, Sierra Leone authorities placed the Eastern Kono District in a two-week lock-down following the alarming rate of infection and deaths there. The lock down lasted until 23 December. This followed the grim discovery of bodies piling up in the district. The WHO reported fear of a major breakout in the area. The district with 350,000 inhabitants buried 87 bodies in 11 days, with 25 patients dying in 5 days before the WHO arrived. On 12 December, Sierra Leone banned all public festivities for Christmas or New Year, because of the outbreak. On 13 December, it was reported that the first Australian facility had been opened; "operations will be gradually scaled up to full capacity at 100 beds under strict guidelines to ensure infection control procedures are working effectively and trained staff ... are in place", one source indicated. Médecins Sans Frontières /Doctors Without Borders, in partnership with the Ministry of Health, carried out during December the largest-ever distribution of antimalarials in Sierra Leone. Teams distributed 1.5 million antimalarial treatments in Freetown and surrounding districts with the aim of protecting people from malaria during the disease's peak season. A spokesman said "In the context of Ebola, malaria is a major concern, because people who are sick with malaria have the same symptoms as people sick with Ebola. As a result, most people turn up at Ebola treatment centres thinking that they have Ebola, when actually they have malaria. It's a huge load on the system, as well as being a huge stress on patients and their families." Between 14 and 17 December Sierra Leone reported 403 new cases with a total of 8,759 cases on the latter date. On 25 December, Sierra Leone put the north area of the country on lockdown. By the end of December Sierra Leone again reported a surge in numbers, with 9,446 cases reported. On 29 December 2014, Pauline Cafferkey , a British aid worker who had just returned to Glasgow from working at the treatment centre in Kerry Town, was diagnosed with Ebola at Glasgow's Gartnavel General Hospital . Two U.S. doctors who "followed all CDC and WHO protocols to the letter" contracted Ebola, and it is not clear how they got infected. By 27 May 2014, it was reported 5 people died from the Ebola virus and there were 16 new cases of the disease. Between 27 May 2014, and 30 May the number of confirmed, probable, or suspected cases of Ebola went from 16 to 50. By 9 June, the number of cases had risen to 42 known and 113 being tested, with a total of 16 known to have died from the disease by that time. The disease spread rapidly in Kenema, and the local government hospital was overwhelmed. At that hospital, 12 nurses died despite having the world's only Lassa fever isolation ward, according to the U.N. Many health are workers were infected at the state hospital, including beloved physician and hemorrhagic fever expert, Dr. Sheik Humarr Khan, and chief nurse Mbalu Fonnie. Khan and his colleagues had bravely provided care to patients with this devastating illness. On 12 June, the country declared a state of emergency in the Kailahun District , where it announced the closure of schools, cinemas, and nightlife places; the district borders both Guinea and Liberia, and all vehicles would be subject to screening at checkpoints. The government declared on 11 June, that its country's borders would be closed to Guinea and Liberia; but many local people cross the borders on unofficial routes which were difficult for authorities to control. Seasonal rains that fall between June and August interfered with the fight against Ebola, and in some cases caused flooding in Sierra Leone. By 11 July 2014, the first case was reported in the capital of Sierra Leone, Freetown, however the person had traveled to the capital from another area of the country. By this time there were over 300 confirmed cases and 99 were confirmed to have died from Ebola. There was another case before the end of the month. On 29 July, well-known physician Sheik Umar Khan , Sierra Leone's only expert on hemorrhagic fever, died after contracting Ebola at his clinic in Kenema . Khan had long worked with Lassa fever , a disease that kills over 5,000 a year in Africa. He had expanded his clinic to accept Ebola patients. Sierra Leone's president, Ernest Bai Koroma, celebrated Khan as a "national hero". On 30 July, Sierra Leone declared a state of emergency and deployed troops to quarantine hot spots. In August, awareness campaigns in Freetown , Sierra Leone's capital, were delivered over the radio and through loudspeakers. Also in August, Sierra Leone passed a law that subjected anyone hiding someone believed to be infected to two years in jail. At the time the law was enacted, a top parliamentarian was critical of failures by neighboring countries to stop the outbreak. Also in early August Sierra Leone cancelled league football (soccer) matches. Within 2 days of 12 September 2014, there were 20 lab-confirmed cases discovered in Freetown, Sierra Leone. One issue was that residents were leaving dead bodies in the street. By 6 September 2014, there were 60 cases of Ebola in Freetown, out of about 1100 nationwide at this time. However, not everyone was bringing cases to doctors, and they were not always being treated. One doctor said the Freetown health system was not functioning, and during this time, respected Freetown Doctor Olivette Buck fell ill and died from Ebola by 14 September 2014. The population of Freetown in 2011 was 941,000. By 18 September 2014, teams of people that buried the dead were struggling to keep up, as 20–30 bodies needed to be buried each day. The teams drove on motor-bikes to collect samples from corpses to see if they died from Ebola. Freetown, Sierra Leone had one laboratory that could do Ebola testing. WHO estimated on 21 September, that Sierra Leone's capacity to treat Ebola cases fell short by the equivalent of 532 beds. Experts pushed for a greater response at this time noting that it could destroy Sierra Leone and Liberia. At that time it was estimated that if it spread through both Liberia and Sierra Leone up to 5 million could be killed; the population of Liberia is about 4.3 million and Sierra Leone is about 6.1 million. In an attempt to control the disease, Sierra Leone imposed a three-day lockdown on its population from 19 to 21 September. During this period 28,500 trained community workers and volunteers went door-to-door providing information on how to prevent infection, as well as setting up community Ebola surveillance teams. The campaign was called the Ouse to Ouse Tock in Krio language . There was concern the 72-hour lock-down could backfire. On 22 September, Stephen Gaojia said that the three-day lock down had obtained its objective and would not be extended. Eighty percent of targeted households were reached in the operation. A total of around 150 new cases were uncovered, but the exact figures would only be known on the following Thursday as the health ministry was still awaiting reports from remote locations. One incident during the lock-down was when a burial team was attacked. On 24 September, President Ernest Bai Koroma added three more districts under "isolation", in an effort to contain the spread. The districts included Port Loko , Bombali , and Moyamba . In the capital, Freetown, all homes with identified cases would be quarantined. This brought the total areas under isolation to 5, including the outbreak "hot spots" Kenema and Kailahun which were already in isolation. Only deliveries and essential services would be allowed in and out. A sharp rise in cases in these areas was also noted by WHO. As of late September, about 2 million people were in areas of restricted travel, which included Kailahun, Kenema, Bombali, Tonkolili, and Port Loko Districts. The number of cases seemed to be doubling every 20 days, which led to the estimate that by January 2015 the number of cases in Liberia and Sierra Leone could grow to 1.4 million. On 25 September, there were 1940 cases and 587 deaths officially, however, many acknowledged under-reporting and there was an increasing number of cases in Freetown (the capital of Sierra Leone). WHO estimated on 21 September, that Sierra Leone's capacity to treat Ebola cases fell short by the equivalent of 532 beds. There were reports that political interference and administrative incompetence had hindered the flow of medical supplies into the country. By 2 October 2014, an estimated 5 people per hour were being infected with the Ebola virus in Sierra Leone. By this time it was estimated the number of infected had been doubling every 20 days. On 4 October, Sierra Leone recorded 121 fatalities, the largest number in a single day. On 8 October, Sierra Leone burial crews went on strike. On 12 October, it was reported that the UK would begin providing military support to Sierra Leone in addition to a major UK civilian operation in support of the Government of Sierra Leone. In October, it was noted hospitals were running out of supplies in Sierra Leone. There were reports that political interference and administrative incompetence hindered the flow of medical supplies into the country. In the week prior to 2 October there were 765 new cases, and Ebola was spreading rapidly. At the start of October, there were nearly 2200 laboratory confirmed cases of Ebola and over 600 had died from it. The epidemic also had claimed the life of 4 doctors and at least 60 nurses by the end of September 2014. Sierra Leone limited its reported deaths to laboratory confirmed cases in facilities, so the actual number of losses was known to be higher. Sierra Leone was considering making reduced care clinics, to stop those sick with Ebola from getting their families sick with the disease and to provide something in between home-care and the full-care clinics. These "isolation centers" would provide an alternative to the overwhelmed clinics. The problem the country was facing was 726 new Ebola cases but less than 330 beds available. More than 160 additional medical personnel from Cuba arrived in early October, building on about 60 that had been there since September. At that time there were about 327 beds for patients in Sierra Leone. Canada announced it was sending a 2nd mobile lab and more staff to Sierra Leone on 4 October 2014. There were reports of drunken grave-diggers making graves for Ebola patients too shallow, and as a result wildlife came and dug up and ate at the corpses. In addition, in some cases bodies were not buried for days, because no one came to collect them. One problem was that it was hard to care for local health care workers, and there was not enough money to evacuate them. Meanwhile, other diseases like malaria, pneumonia, and diarrhea were not being treated properly because the health system was trying to deal with Ebola patients. On 7 October 2014, Canada sent a C-130 loaded with 128,000 face shields to Freetown. In early October 2014, a burial team leader said there were piles of corpses south of Freetown. On 9 October, the International Charter on Space and Major Disasters was activated on Sierra Leone's behalf, the first time that its charitably repurposed satellite imaging assets had been deployed in an epidemiological role. On 14 October 2014, 800 Sierra Leone peacekeepers due to relieve a contingent deployed in Somalia , were placed under quarantine when one of the soldiers tested positive for Ebola. The last district in Sierra Leone untouched by the Ebola virus declared Ebola cases. According to Abdul Sesay, a local health official, 15 suspected deaths with 2 confirmed cases of the deadly disease were reported on 16 October, in the village of Fakonya. The village is 60 miles from the town of Kabala in the center of the mountainous region of the Koinadugu district. This was the last district free from the virus in Sierra Leone. All of the districts in this country had then confirmed cases of Ebola. In late October 2014, the United Kingdom sent one of their hospital ships, the Royal Navy's Argus , to help Sierra Leone. By late October Sierra Leone was experiencing more than twenty deaths a day from Ebola. In October 2014, officials reported that very few pregnant women were surviving Ebola disease. In previous outbreaks pregnant women were noted to have a higher rate of death with Ebola. Officials struggled to maintain order in one town after a medical team trying to take a blood sample from a corpse were blocked by an angry machete-wielding mob. They allegedly believed the person had died from high-blood pressure and did not want the body being tested for Ebola. When security forces tried to defend the medical team, a riot ensued leaving two dead. The town was placed on a 24-hour curfew and authorities tried to calm the situation down. Despite this several buildings were attacked. On 30 October, the ship Argus arrived in Sierra Leone. It carried 32 off-road vehicles to support Ebola treatment units. The ship also carried three transport helicopters to support operations against the epidemic. By the end of October 2014 there were over 5200 laboratory confirmed cases of Ebola virus disease in Sierra Leone. [ citation needed ] On 31 October 2014, an ambulance driver in Bo District died of Ebola. His ambulance picked up Ebola patients (or suspected Ebola cases) and took them to treatment centers. On 1 November, the United Kingdom announced plans to build three more Ebola laboratories in Sierra Leone. The labs helped to determine if a patient had been infected by the Ebola virus. At that time, it took as much as five days to test a sample because of the volume of samples that needed to be tested. On 2 November, a person with Ebola employed by the United Nations was evacuated from Sierra Leone to France for treatment. On 4 November, it was reported that thousands violated quarantine in search for food, in the town of Kenema. On 6 November, it was reported that the situation was "getting worse" due to "intense transmission" in Freetown as a contributing factor; the capital city reported 115 cases in the previous week alone. Food shortages and aggressive quarantines were reported to be making the situation worse, according to the Disaster Emergency Committee. Sierra Leone established call centers in Port Loko and Kambia, according to MSSL Communications as reported on 21 November; this was in addition to the June hotline originally established. On 12 November, more than 400 health workers went on strike over salary issues at one of the few Ebola treatment centers in the country. On 18 November, the supply ship Karel Doorman of the Royal Netherlands Navy ( Koninklijke Marine ) arrived in Freetown, with supplies. Its Captain-Commander, Peter van den Berg, took steps to reduce the chance of the crew contracting Ebola virus disease. The Neini Chiefdom in Koinadugu District was subject to isolation after Ebola cases. On 19 November, it was reported that the Ebola virus was spreading intensely; "much of this was driven by intense transmission in the country's west and north", the WHO said. A British-built Ebola Treatment Centre which started in Kerry Town during November, generated some controversy because of its initially limited capacity. However, this was because they were following guidelines of how to safely open an Ebola treatment unit. This was the first of six planned treatment centres which, when completed, would be staffed by a number of NGOs . In mid-November the WHO reported that while all cases and deaths continued to be under-reported, "there is some evidence that case incidence is no longer increasing nationally in Guinea and Liberia, but steep increases persist in Sierra Leone". On 19 November, it was reported that the Ebola virus was spreading intensely; "much of this was driven by intense transmission in the country's west and north", the WHO said. The first Cuban doctor to be infected with the virus was flown to Geneva. On 26 November, it was reported that due to Sierra Leone's increased Ebola transmission, the country would surpass Liberia in the total cases count. On 27 November, Canada announced it would deploy military health staff to the infected region. On 29 November, the President of Sierra Leone canceled a planned three-day shutdown in Freetown to curb the virus. On 2 December, it was reported that the Tonkolili district had begun a two-week lockdown, "which was agreed in a key stakeholders meeting of cabinet ministers, parliamentarians and paramount chiefs of the district as part of efforts to stem the spread of the disease", according to a ministry spokesman. The move meant that a total of six districts, containing more than half of the population, were locked down. Sierra Leone indicated, in a report on 5 December, that about 100 cases of the virus were now being reported daily. On the same day, it was further reported that families caught taking part in burial washing rituals, which can spread the virus, would be taken to jail. On 6 December, a report indicated that the Canadian Armed Forces would send a medical team to the country of Sierra Leone to help combat the Ebola virus epidemic. On 8 December, the doctors in Sierra Leone went on strike, demanding better treatment for health care workers, according to Health Ministry spokesman Jonathan Abass Kamara. On 9 December, Sierra Leone authorities placed the Eastern Kono District in a two-week lock-down following the alarming rate of infection and deaths there. The lock down lasted until 23 December. This followed the grim discovery of bodies piling up in the district. The WHO reported fear of a major breakout in the area. The district with 350,000 inhabitants buried 87 bodies in 11 days, with 25 patients dying in 5 days before the WHO arrived. On 12 December, Sierra Leone banned all public festivities for Christmas or New Year, because of the outbreak. On 13 December, it was reported that the first Australian facility had been opened; "operations will be gradually scaled up to full capacity at 100 beds under strict guidelines to ensure infection control procedures are working effectively and trained staff ... are in place", one source indicated. Médecins Sans Frontières /Doctors Without Borders, in partnership with the Ministry of Health, carried out during December the largest-ever distribution of antimalarials in Sierra Leone. Teams distributed 1.5 million antimalarial treatments in Freetown and surrounding districts with the aim of protecting people from malaria during the disease's peak season. A spokesman said "In the context of Ebola, malaria is a major concern, because people who are sick with malaria have the same symptoms as people sick with Ebola. As a result, most people turn up at Ebola treatment centres thinking that they have Ebola, when actually they have malaria. It's a huge load on the system, as well as being a huge stress on patients and their families." Between 14 and 17 December Sierra Leone reported 403 new cases with a total of 8,759 cases on the latter date. On 25 December, Sierra Leone put the north area of the country on lockdown. By the end of December Sierra Leone again reported a surge in numbers, with 9,446 cases reported. On 29 December 2014, Pauline Cafferkey , a British aid worker who had just returned to Glasgow from working at the treatment centre in Kerry Town, was diagnosed with Ebola at Glasgow's Gartnavel General Hospital . On 4 January, the lockdown was extended for two weeks. On this day the country reported 9780 cases with 2943 deaths. Among healthcare workers there were 296 cases with 221 fatalities reported. On 8 January, MSF admitted its first patients to a Treatment Centre (ETC) in Kissy , an Ebola hotspot on the outskirts of Freetown. Once the ETC is fully operational it will include specialist facilities for pregnant women. By 9 January, the case load in the country exceeded 10,000, with 10,074 cases and 3,029 deaths reported. On 9 January, it was reported that South Korea would send a medical team to Goderich . On 10 January, Sierra Leone declared its first Ebola-free district. The Pujehun district in the south east of the country reported no new cases for 42 days. A worker at Kerry Town clinic was evacuated to the United Kingdom on 2 February 2015, after a needlestick injury . On 5 February, it was reported that there was a rise in weekly cases for the first time this year. The U.N. indicated that the sharp drop in cases had "flattened out" raising concern about the virus. On 5 March, a report indicated cases in Sierra Leone continued to rise. The government of Sierra Leone declared a three-day country-wide lock-down including 2.5 million people on 18 March. The U.N. indicates the outbreak will be over by August of this year. The 3-day lock-down of over 6 million inhabitants revealed a 191% increase in possible Ebola cases. In Freetown alone 173 patients meeting the criteria for Ebola were discovered according to Obi Sesay from the National Ebola Response Center. As of 12 May, Sierra Leone had gone 8 days without an Ebola case, and was down to two confirmed cases of Ebola. The WHO weekly update for 29 July reported a total of only three new cases, the lowest total in more than a year. On 17 August, the country had its first week with no new cases, and one week later the last patients were released. A new death was reported on 1 September after a patient from Sella Kafta village in Kambia District was tested positive for the disease after her death. On 5 September, another case of Ebola was identified in the village among the approximately 1000 people currently under quarantine. A woman tested positive for the virus. The " Guinea ring vaccine " has been administered by a WHO team in the village since Friday 5 September. On 8 September the head of the National Ebola Response Center confirmed new cases of Ebola. This brought the total from the village to four cases, with all of them being under the "high risk" contact cases with the death of the new index case in the village. In total four cases were then confirmed including the dead woman. On 14 September, the National Ebola Response Center confirmed the death of a 16-year-old in a village in the Bombali district. Swabs taken from the body tested positive for the disease. The village was placed under quarantine. She had no history of traveling outside the village, and it is suspected that she contracted the disease from the semen of an Ebola survivor who was discharged in March 2015. Seven of her immediate contacts were taken to an Ebola treatment center, with a further three patients she had contact with at a health clinic. A new study to be published in the New England Journal of Medicine indicates the possibility that the virus may lurk in the semen of survivors for up to six months. Nearly half of 200 patients tested had traces of the virus in their semen six months after surviving the disease. On 7 November, the World Health Organization declared Sierra Leone Ebola-free. Sierra Leone entered a 90-day period of enhanced surveillance which was scheduled to conclude on 5 February 2016, but due to a new case in mid-January it did not. On 14 January, it was reported there had been a fatality linked to the Ebola virus. The case occurred in the Tonkolili district. Prior to this case WHO had advised, "we anticipate more flare-ups and must be prepared for them ... massive effort is underway to ensure robust prevention, surveillance and response capacity across all three countries by the end of March." On 16 January, it was reported that the woman who died of the virus may have exposed several individuals; the government announced that 100 people had been quarantined. On the same day, WHO released a statement, indicating that originally the 90-day enhanced surveillance period was to end on 5 February. Investigations indicate the female case was a student at Lunsar in Port Loko district, who had gone to Kambia district on December the 28th until returning symptomatic. Bombali district was visited by the individual, for consultation with an herbalist, later going to a government hospital in Magburaka. WHO indicates there are 109 contacts, 28 of which are high risk, furthermore, there are three missing contacts.The source or route of transmission which caused the fatality is still unknown. A second new case was confirmed on 20 January; the patient had contact with the previous fatality. On 17 March, the WHO declared the country Ebola-free. On 4 January, the lockdown was extended for two weeks. On this day the country reported 9780 cases with 2943 deaths. Among healthcare workers there were 296 cases with 221 fatalities reported. On 8 January, MSF admitted its first patients to a Treatment Centre (ETC) in Kissy , an Ebola hotspot on the outskirts of Freetown. Once the ETC is fully operational it will include specialist facilities for pregnant women. By 9 January, the case load in the country exceeded 10,000, with 10,074 cases and 3,029 deaths reported. On 9 January, it was reported that South Korea would send a medical team to Goderich . On 10 January, Sierra Leone declared its first Ebola-free district. The Pujehun district in the south east of the country reported no new cases for 42 days. A worker at Kerry Town clinic was evacuated to the United Kingdom on 2 February 2015, after a needlestick injury . On 5 February, it was reported that there was a rise in weekly cases for the first time this year. The U.N. indicated that the sharp drop in cases had "flattened out" raising concern about the virus. On 5 March, a report indicated cases in Sierra Leone continued to rise. The government of Sierra Leone declared a three-day country-wide lock-down including 2.5 million people on 18 March. The U.N. indicates the outbreak will be over by August of this year. The 3-day lock-down of over 6 million inhabitants revealed a 191% increase in possible Ebola cases. In Freetown alone 173 patients meeting the criteria for Ebola were discovered according to Obi Sesay from the National Ebola Response Center. As of 12 May, Sierra Leone had gone 8 days without an Ebola case, and was down to two confirmed cases of Ebola. The WHO weekly update for 29 July reported a total of only three new cases, the lowest total in more than a year. On 17 August, the country had its first week with no new cases, and one week later the last patients were released. A new death was reported on 1 September after a patient from Sella Kafta village in Kambia District was tested positive for the disease after her death. On 5 September, another case of Ebola was identified in the village among the approximately 1000 people currently under quarantine. A woman tested positive for the virus. The " Guinea ring vaccine " has been administered by a WHO team in the village since Friday 5 September. On 8 September the head of the National Ebola Response Center confirmed new cases of Ebola. This brought the total from the village to four cases, with all of them being under the "high risk" contact cases with the death of the new index case in the village. In total four cases were then confirmed including the dead woman. On 14 September, the National Ebola Response Center confirmed the death of a 16-year-old in a village in the Bombali district. Swabs taken from the body tested positive for the disease. The village was placed under quarantine. She had no history of traveling outside the village, and it is suspected that she contracted the disease from the semen of an Ebola survivor who was discharged in March 2015. Seven of her immediate contacts were taken to an Ebola treatment center, with a further three patients she had contact with at a health clinic. A new study to be published in the New England Journal of Medicine indicates the possibility that the virus may lurk in the semen of survivors for up to six months. Nearly half of 200 patients tested had traces of the virus in their semen six months after surviving the disease. On 7 November, the World Health Organization declared Sierra Leone Ebola-free. Sierra Leone entered a 90-day period of enhanced surveillance which was scheduled to conclude on 5 February 2016, but due to a new case in mid-January it did not. On 14 January, it was reported there had been a fatality linked to the Ebola virus. The case occurred in the Tonkolili district. Prior to this case WHO had advised, "we anticipate more flare-ups and must be prepared for them ... massive effort is underway to ensure robust prevention, surveillance and response capacity across all three countries by the end of March." On 16 January, it was reported that the woman who died of the virus may have exposed several individuals; the government announced that 100 people had been quarantined. On the same day, WHO released a statement, indicating that originally the 90-day enhanced surveillance period was to end on 5 February. Investigations indicate the female case was a student at Lunsar in Port Loko district, who had gone to Kambia district on December the 28th until returning symptomatic. Bombali district was visited by the individual, for consultation with an herbalist, later going to a government hospital in Magburaka. WHO indicates there are 109 contacts, 28 of which are high risk, furthermore, there are three missing contacts.The source or route of transmission which caused the fatality is still unknown. A second new case was confirmed on 20 January; the patient had contact with the previous fatality. On 17 March, the WHO declared the country Ebola-free. Long-term political factors contributed to the Ebola crisis including the acute dependency on external health assistance, patron-client politics, corruption and a weak state capacity . Prior to the Ebola epidemic Sierra Leone had about 136 doctors and 1,017 nurses/midwives for a population of about 6 million people. On 26 August, the WHO (World Health Organisation) shut down one of two laboratories after a health worker became infected. The laboratory was situated in the Kailahun district, one of the worst-affected areas. It was thought by some that this move would disrupt efforts to increase the global response to the outbreak of the disease in the district. "It's a temporary measure to take care of the welfare of our remaining workers", WHO spokesperson Christy Feig announced. He did not specify how long the closure would last, but said they would return after an assessment of the situation by the WHO. The medical worker, one of the first WHO staff infected by the Ebola Virus, was treated at a hospital in Kenema and then evacuated to Germany . By 4 October 2014, it was announced he has recovered and left Germany. As the Ebola epidemic grew it damaged the health care infrastructure, leading to increased deaths from other health issues including malaria, diarrhoea, and pneumonia because they were not being treated. The WHO estimated on 21 September that Sierra Leone's capacity to treat Ebola cases fell short by the equivalent of 532 beds. On 27 August 2014, Dr. Sahr Rogers died from Ebola after contracting it working in Kenema. Sierra Leone lost three of its top doctors by the end of August to Ebola. A fourth doctor, Dr. Olivette Buck, became ill with Ebola in September and died later that month. Dr. Olivette Buck was a Sierra Leone doctor who worked in Freetown, who tested positive for Ebola on 9 September 2014, and died on 14 September 2014. Her staff believes she was exposed in August. She eventually went to Lumley Hospital on 1 September 2014, with a fever, thinking it was malaria. After a few more days of illness she was admitted to Connaught Hospital . By 23 September 2014, out of 91 health workers known to have been infected with Ebola in Sierra Leone, approximately 61 had died. On 19 October, the WHO reported 129 cases with 95 deaths of healthcare workers (125 / 91 confirmed). On 2 November 2014, a fifth doctor, Dr. Godfrey George, a medical superintendent of Kambia Government Hospital died as a result of Ebola infection. On 17 November 2014, a sixth doctor, Dr Martin Salia, died as a result of Ebola infection, after being transported by medevac to Nebraska Medical Center in the United States. On 18 November 2014, a seventh doctor, Dr Michael Kargbo, died in Sierra Leone. He worked at the Magburaka Government Hospital . Dr. Aiah Solomon Konoyeima was reported to have Ebola in late November 2014, which would make him the eighth physician to contract Ebola. He was reported to have died from the disease on 7 December 2014, becoming what was reported as the tenth doctor to die from Ebola. On 26 November 2014, a ninth doctor, Dr. Songo Mbriwa, was reported to be sick with Ebola disease. He was working at an Ebola treatment centre in Freetown. He was one of the doctors that cared for the late Dr Martin Salia, who experienced a false-negative Ebola test, but did indeed have it and may have exposed others. On Friday 5 December, a senior health official announced the death of two of the country's doctors in one day. This brings the total number of doctors who have died from the disease in Sierra Leone to ten. Dr Dauda Koroma and Dr Thomas Rogers are the latest deaths among healthcare workers. The two doctors were not in the front line of the Ebola battle and did not work in an Ebola treatment hospital. On 18 December, Dr. Victor Willoughby died from the disease after being tested positive for the disease on Saturday 6 December. The doctor died hours before he was to receive ZMAb, an experimental treatment from Canada, according to Dr. Brima Kargbo the country's chief medical officer. Dr. Victor Willoughby is the 11th doctor, and a top physician, to succumb to the disease. On 27 August 2014, Dr. Sahr Rogers died from Ebola after contracting it working in Kenema. Sierra Leone lost three of its top doctors by the end of August to Ebola. A fourth doctor, Dr. Olivette Buck, became ill with Ebola in September and died later that month. Dr. Olivette Buck was a Sierra Leone doctor who worked in Freetown, who tested positive for Ebola on 9 September 2014, and died on 14 September 2014. Her staff believes she was exposed in August. She eventually went to Lumley Hospital on 1 September 2014, with a fever, thinking it was malaria. After a few more days of illness she was admitted to Connaught Hospital . By 23 September 2014, out of 91 health workers known to have been infected with Ebola in Sierra Leone, approximately 61 had died. On 19 October, the WHO reported 129 cases with 95 deaths of healthcare workers (125 / 91 confirmed). On 2 November 2014, a fifth doctor, Dr. Godfrey George, a medical superintendent of Kambia Government Hospital died as a result of Ebola infection. On 17 November 2014, a sixth doctor, Dr Martin Salia, died as a result of Ebola infection, after being transported by medevac to Nebraska Medical Center in the United States. On 18 November 2014, a seventh doctor, Dr Michael Kargbo, died in Sierra Leone. He worked at the Magburaka Government Hospital . Dr. Aiah Solomon Konoyeima was reported to have Ebola in late November 2014, which would make him the eighth physician to contract Ebola. He was reported to have died from the disease on 7 December 2014, becoming what was reported as the tenth doctor to die from Ebola. On 26 November 2014, a ninth doctor, Dr. Songo Mbriwa, was reported to be sick with Ebola disease. He was working at an Ebola treatment centre in Freetown. He was one of the doctors that cared for the late Dr Martin Salia, who experienced a false-negative Ebola test, but did indeed have it and may have exposed others. On Friday 5 December, a senior health official announced the death of two of the country's doctors in one day. This brings the total number of doctors who have died from the disease in Sierra Leone to ten. Dr Dauda Koroma and Dr Thomas Rogers are the latest deaths among healthcare workers. The two doctors were not in the front line of the Ebola battle and did not work in an Ebola treatment hospital. On 18 December, Dr. Victor Willoughby died from the disease after being tested positive for the disease on Saturday 6 December. The doctor died hours before he was to receive ZMAb, an experimental treatment from Canada, according to Dr. Brima Kargbo the country's chief medical officer. Dr. Victor Willoughby is the 11th doctor, and a top physician, to succumb to the disease. Since the beginning of the outbreak in Sierra Leone in late May 2014, several people have been evacuated. An increasing lack of hospital beds , medical equipment, and health care personnel made treatment difficult. [ citation needed ] On 24 August William Pooley , a British nurse, was evacuated from Sierra Leone. He was released on 3 September 2014. In October 2014, he announced he would return to Sierra Leone. On 21 September 2014, Spain evacuated a Catholic priest who had contracted Ebola while working in Sierra Leone with Hospital Order of San Juan de Dios. He died on 25 September in Madrid. On 6 October 2014, a nurse who treated the priest tested positive for Ebola. By 20 October 2014, the nurse seemed to have recovered after many days battling the disease in the hospital, with tests coming back negative. A doctor from Senegal contracted Ebola while working in Sierra Leone for the WHO, and was evacuated to Germany at the end of August 2014. By 4 October 2014, it was announced he has recovered and returned to Senegal. In late September, a doctor working for an International Aid organization in Sierra Leone, was evacuated to Switzerland after potentially being exposed. He later tested negative for the disease. In late September 2014, an American doctor working in Sierra Leone was evacuated to Maryland, USA, after being exposed to Ebola. "Just because someone is exposed to the deadly virus, it doesn't necessarily mean they are infected", said Anthony S. Fauci , director of the National Institute of Allergy and Infectious Diseases at the NIH . He was evacuated after a needle sticking accident and even developed a fever, but he was determined not to have Ebola and was released the first week in October 2014. After being discharged he remained at home under medical observation, checking his temperature twice a day for 21 days. In early October, a Ugandan doctor who contracted Ebola while working in Sierra Leone was evacuated for treatment to Frankfurt, Germany. The doctor was working at Lakaa Hospital and flown out from Lungi Airport . On 6 October 2014, a female Norwegian MSF worker tested positive for Ebola virus and was subsequently evacuated to Norway. Norwegian authorities reported that they had been granted a dose of the experimental biopharmaceutical drug ZMAb , a variant of ZMapp . ZMapp has previously been used on 3 Liberian health workers, of which 2 survived. It was also used on 4 evacuated westerners, of which 3 survived. A U.N. employee was evacuated to France in early November 2014 after contracting Ebola. On 12 November 2014, Dr Martin Salia, a permanent resident of the United States, tested positive for Ebola while working as a specialist surgeon at the Connaught Hospital in Freetown . He is the sixth Sierra Leone doctor to have contracted Ebola virus disease. Initially he preferred to be treated at the Hastings Holding Centre by Sierra Leonean medical personnel, however on 15 November 2014, he was evacuated to the Nebraska Medical Center where his condition was reported as "still extremely critical" on 16 November. On 16 November the hospital released a statement that he "passed away as a result of the advanced symptoms of the disease". On 18 November a Cuban doctor, Felix Baez, tested positive for Ebola and was due to be sent to Geneva for treatment. He later recovered. Baez was one of 165 Cuban doctors and nurses in Sierra Leone helping treat Ebola patients. There were a further 53 Cubans in Liberia and 38 in Guinea, making this the largest single country medical team mobilized during the outbreak. On 5 October, The New York Times reported that a shipping container full of protective gowns, gloves, stretchers, mattresses and other medical supplies had been allowed to sit unopened on the docks in Freetown, Sierra Leone, since 9 August. The $140,000 worth of equipment included 100 bags and boxes of hospital linens, 100 cases of protective suits, 80 cases of face masks and other items, and were donated by individuals and institutions in the United States. The shipment was organised by Mr Chernoh Alpha Bah, a Sierra Leonean opposition politician, who comes from Sierra Leonean President Ernest Bai Koroma 's hometown, Makeni . The New York Times reported that political tensions may have contributed to the government delay in clearing the shipping container, to prevent the political opposition from trumpeting the donations. Government officials stated that the shipping container could not be cleared through customs, as proper procedures had not been followed. The Sierra Leonean government refused to pay the shipping fee of $6,500. The New York Times noted that the government had already received well over $40 million in cash from international donors to fight Ebola. The New York Times noted that in the 2 months that the shipping container remained on the docks in Freetown, health workers in Sierra Leone endured severe shortages of protective supplies, with some nurses having to wear street clothes. David Tam-Baryoh, a radio journalist , was held for 11 days when he and a talk show guest, an opposition party spokesperson, criticised how President Ernest Bai Koroma handled the Ebola outbreak in a live broadcast on 1 November 2014. The weekly show Monologue was taken off-air mid-show from the independently run Citizen FM. He was arrested on 3 November and sent to the Pademba Road jail, after an executive order was signed by the president. On 14 November Sierra Leone's Deputy Information Minister Theo Nicol gave a statement that Baryoh had "been put on a ten thousand dollar bail by the Criminal Investigation Department after a statement has been taken from him". Amid concerns for his health, Tam-Baryoh apparently signed a confession to ensure his release from the prison, engineered by a committee made up of his lawyer, 2 journalists and a peace studies lecturer of the University of Sierra Leone . Rightsway International, an independent human rights group, has condemned President Koroma for allegedly dictating to the committee about obtaining the confession. A statement later released by the group read: Rightsway is disappointed that Tam Baryoh's forced confession has been published widely by pro-government media outlets and social networks. The publication of forced confessions is often used to discredit dissident news and information providers. This is a media propaganda tool used by dictatorial regimes, to avoid being exposed, investigated and punished for the grave violations of human rights. On 21 October, there was Ebola related violence and rioting in the eastern town of Koidu , with police imposing a curfew. Local youth fired at police with shotguns after a former youth leader refused health authorities permission to take her relative for an Ebola test. Several buildings were attacked and youth gangs roamed the streets shouting "No more Ebola!" A local leader reported seeing two bodies with gunshot wounds in the aftermath. Police denied that anyone had been killed. Doctors reported two dead. The local district medical officer said he had been forced to abandon the local hospital because of the rioting. On 5 October, The New York Times reported that a shipping container full of protective gowns, gloves, stretchers, mattresses and other medical supplies had been allowed to sit unopened on the docks in Freetown, Sierra Leone, since 9 August. The $140,000 worth of equipment included 100 bags and boxes of hospital linens, 100 cases of protective suits, 80 cases of face masks and other items, and were donated by individuals and institutions in the United States. The shipment was organised by Mr Chernoh Alpha Bah, a Sierra Leonean opposition politician, who comes from Sierra Leonean President Ernest Bai Koroma 's hometown, Makeni . The New York Times reported that political tensions may have contributed to the government delay in clearing the shipping container, to prevent the political opposition from trumpeting the donations. Government officials stated that the shipping container could not be cleared through customs, as proper procedures had not been followed. The Sierra Leonean government refused to pay the shipping fee of $6,500. The New York Times noted that the government had already received well over $40 million in cash from international donors to fight Ebola. The New York Times noted that in the 2 months that the shipping container remained on the docks in Freetown, health workers in Sierra Leone endured severe shortages of protective supplies, with some nurses having to wear street clothes. David Tam-Baryoh, a radio journalist , was held for 11 days when he and a talk show guest, an opposition party spokesperson, criticised how President Ernest Bai Koroma handled the Ebola outbreak in a live broadcast on 1 November 2014. The weekly show Monologue was taken off-air mid-show from the independently run Citizen FM. He was arrested on 3 November and sent to the Pademba Road jail, after an executive order was signed by the president. On 14 November Sierra Leone's Deputy Information Minister Theo Nicol gave a statement that Baryoh had "been put on a ten thousand dollar bail by the Criminal Investigation Department after a statement has been taken from him". Amid concerns for his health, Tam-Baryoh apparently signed a confession to ensure his release from the prison, engineered by a committee made up of his lawyer, 2 journalists and a peace studies lecturer of the University of Sierra Leone . Rightsway International, an independent human rights group, has condemned President Koroma for allegedly dictating to the committee about obtaining the confession. A statement later released by the group read: Rightsway is disappointed that Tam Baryoh's forced confession has been published widely by pro-government media outlets and social networks. The publication of forced confessions is often used to discredit dissident news and information providers. This is a media propaganda tool used by dictatorial regimes, to avoid being exposed, investigated and punished for the grave violations of human rights.On 21 October, there was Ebola related violence and rioting in the eastern town of Koidu , with police imposing a curfew. Local youth fired at police with shotguns after a former youth leader refused health authorities permission to take her relative for an Ebola test. Several buildings were attacked and youth gangs roamed the streets shouting "No more Ebola!" A local leader reported seeing two bodies with gunshot wounds in the aftermath. Police denied that anyone had been killed. Doctors reported two dead. The local district medical officer said he had been forced to abandon the local hospital because of the rioting. There are various restrictions and quarantines within Sierra Leone, and a state of emergency was declared on 31 July 2014. Countries at higher risk for Ebola in Africa include Benin, Burkina Faso, Côte d'Ivoire, Guinea-Bissau, Mali, and Senegal. [ citation needed ] The outbreak was noted for increasing hand washing stations, and reducing the prevalence of physical greetings such as hand-shakes between members of society. In June 2014 all schools were closed because of the spread of Ebola. In August 2014 the S.L. Health Minister was removed from that office. (see Cabinet of Sierra Leone ) In October 2014 the Defense Minister was placed in charge of the anti-Ebola efforts. The president at this time was Ernest Bai Koroma . On 13 October, the UN's International Fund for Agricultural Development stated up to 40% of farms had been abandoned in the worst Ebola-hit areas of Sierra Leone. In October 2014 Sierra Leone launched a school by radio program, that will be transmitted on 41 of the local radio stations as well as on the only local TV station. (See Cultural effects of the Ebola crisis ) September through October is the malaria season, which may complicate efforts to treat Ebola. For example, one Freetown doctor did not immediately quarantine herself because she thought she had malaria not Ebola. The doctor was eventually diagnosed with Ebola and died in September 2014. There are various restrictions and quarantines within Sierra Leone, and a state of emergency was declared on 31 July 2014. Countries at higher risk for Ebola in Africa include Benin, Burkina Faso, Côte d'Ivoire, Guinea-Bissau, Mali, and Senegal. [ citation needed ]The outbreak was noted for increasing hand washing stations, and reducing the prevalence of physical greetings such as hand-shakes between members of society. In June 2014 all schools were closed because of the spread of Ebola. In August 2014 the S.L. Health Minister was removed from that office. (see Cabinet of Sierra Leone ) In October 2014 the Defense Minister was placed in charge of the anti-Ebola efforts. The president at this time was Ernest Bai Koroma . On 13 October, the UN's International Fund for Agricultural Development stated up to 40% of farms had been abandoned in the worst Ebola-hit areas of Sierra Leone. In October 2014 Sierra Leone launched a school by radio program, that will be transmitted on 41 of the local radio stations as well as on the only local TV station. (See Cultural effects of the Ebola crisis ) September through October is the malaria season, which may complicate efforts to treat Ebola. For example, one Freetown doctor did not immediately quarantine herself because she thought she had malaria not Ebola. The doctor was eventually diagnosed with Ebola and died in September 2014.
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Mpox
Mpox (formerly known as monkeypox ) is an infectious viral disease that can occur in humans and a wide range of other animals. Symptoms include a rash that forms blisters and then crusts over, fever, and swollen lymph nodes . The illness is usually mild and most of those infected will recover within a few weeks without treatment. The time from exposure to onset of symptoms ranges from five to twenty-one days and symptoms typically last from two to four weeks. Cases may be severe, especially in children, pregnant women or people with suppressed immune systems. The disease is caused by the monkeypox virus , [lower-alpha 1] a zoonotic virus in the genus Orthopoxvirus . The variola virus , the causative agent of the disease smallpox , is also in this genus. Human-to-human transmission can occur through direct contact with infected skin or body fluids, including sexual contact. People remain infectious from the onset of symptoms until all the lesions have scabbed and healed. It may spread from infected animals by handling infected meat or via bites or scratches. Diagnosis can be confirmed by PCR testing a lesion for the virus' DNA . Vaccination is recommended for those at high risk of infection. Evidence shows that the MVA-BN [lower-alpha 2] vaccine is 86% effective at reducing the risk of mpox illness. The aim of treatment is to manage the symptoms and prevent complications as there is no specific treatment for the disease. Antiviral drugs such as tecovirimat can be used to treat mpox, although their effectiveness has not been proved. Mpox is endemic in central and western Africa , where several species of mammals are suspected to act as a natural reservoir of the virus. The first human cases were diagnosed in 1970 in Basankusu , Democratic Republic of the Congo . Since then the frequency and severity of outbreaks has significantly increased, possibly as a result of waning immunity since the cessation of routine smallpox vaccination. The 2022–2023 mpox outbreak represents the first incidence of widespread community transmission outside of Africa. This was initially identified in the United Kingdom in May 2022, with subsequent cases confirmed in 111 countries as of May 2023. The World Health Organization (WHO) declared the outbreak a Public Health Emergency of International Concern (PHEIC) between 23 July 2022 and 10 May 2023. The name monkeypox was originally coined because the disease was first identified in laboratory monkeys. This was subsequently criticised as a misnomer, because monkeys are not the main host or reservoir. It was also criticized because the name reinforced stigma about African countries as a source of disease. After requests by a number of public health organisations and scientists, who argued that these issues were harming the fight to contain the disease outbreak, the subtypes of monkeypox virus were renamed Clade I and Clade II in August 2022. The World Health Organization announced in November 2022 that it "will adopt the term mpox in its communications, and encourages others to follow these recommendations". Initial symptoms of mpox infection are fever, muscle pains , and sore throat, followed by an itchy or painful rash, headache, swollen lymph nodes, and fatigue . Not everyone will exhibit the complete range of symptoms. Most mpox patients become symptomatic 4–11 days after infection. However, the incubation period can be as short as 1 day. The 2022–2023 outbreak revealed that incubation periods of up to 4 weeks are possible, with 5% of cases having incubation periods longer than the previously assumed 21 days. The rash comprises many small lesions which may appear on the palms and soles, face, mouth and throat, genitals or anus. They begin as small flat spots , before becoming small bumps which then fill with fluid and subsequently burst and scab over, persisting for around ten days. Some patients may manifest only a single sore from the disease while others may have hundreds. It is possible for a person to be infected with monkeypox virus without showing any symptoms . Symptoms typically last for two to four weeks, but may last longer if the patient has a weakened immune system. Complications include secondary infections , pneumonia , sepsis , encephalitis , and loss of vision following corneal infection. Persons with weakened immune systems, whether due to medication, medical conditions, or HIV, are more likely to develop severe disease. If infection occurs during pregnancy, this may lead to stillbirth or other complications. Provided there are no complications, sequelae are rare; after healing, the scabs may leave pale marks before becoming darker scars. Prior to the 2022 outbreak, the risk of death in those infected was estimated from 0% to 11%. With other historic case fatality rates being reported as 6% in Nigeria and 10-15% in the Democratic Republic of Congo and the Central African Republic , with a higher death rate in the more virulent Clade 1 variant that is endemic to central Africa. However, in the 2022 global outbreak 112 deaths were reported in 87,000 cases, with other sources reporting a risk of death as high as 0.025%. Most reported deaths in this outbreak were among those who were immunocompromised either due to medication or poorly controlled HIV infection. It is thought that small mammals provide a reservoir for the virus in endemic areas. Spread among animals occurs via the fecal–oral route and through the nose, through wounds and eating infected meat. The disease has also been reported in a wide range of other animals including monkeys, anteaters, hedgehogs, prairie dogs, squirrels, and shrews. Signs and symptoms in animals are not well researched and further studies are in progress. There have been instances of animal infection outside of endemic Africa; during the 2003 US outbreak, prairie dogs ( Cynomys ludovicianus ) became infected and presented with fever, cough, sore eyes , poor feeding and rash. There has also been an instance of a domestic dog ( Canis familiaris ) which became infected displaying lesions and ulceration. Complications include secondary infections , pneumonia , sepsis , encephalitis , and loss of vision following corneal infection. Persons with weakened immune systems, whether due to medication, medical conditions, or HIV, are more likely to develop severe disease. If infection occurs during pregnancy, this may lead to stillbirth or other complications. Provided there are no complications, sequelae are rare; after healing, the scabs may leave pale marks before becoming darker scars. Prior to the 2022 outbreak, the risk of death in those infected was estimated from 0% to 11%. With other historic case fatality rates being reported as 6% in Nigeria and 10-15% in the Democratic Republic of Congo and the Central African Republic , with a higher death rate in the more virulent Clade 1 variant that is endemic to central Africa. However, in the 2022 global outbreak 112 deaths were reported in 87,000 cases, with other sources reporting a risk of death as high as 0.025%. Most reported deaths in this outbreak were among those who were immunocompromised either due to medication or poorly controlled HIV infection. It is thought that small mammals provide a reservoir for the virus in endemic areas. Spread among animals occurs via the fecal–oral route and through the nose, through wounds and eating infected meat. The disease has also been reported in a wide range of other animals including monkeys, anteaters, hedgehogs, prairie dogs, squirrels, and shrews. Signs and symptoms in animals are not well researched and further studies are in progress. There have been instances of animal infection outside of endemic Africa; during the 2003 US outbreak, prairie dogs ( Cynomys ludovicianus ) became infected and presented with fever, cough, sore eyes , poor feeding and rash. There has also been an instance of a domestic dog ( Canis familiaris ) which became infected displaying lesions and ulceration. Mpox in both humans and animals is caused by infection with the monkeypox virus – a double-stranded DNA virus in the genus Orthopoxvirus , family Poxviridae , making it closely related to the smallpox , cowpox , and vaccinia viruses. The two subtypes of virus are Clade I and Clade II. Clade II is further divided into subclades: Clade IIa and Clade IIb. Cases identified as part of the 2022-2023 global outbreak are caused by Clade IIb. Clade I is largely limited to the DRC and is estimated to cause more severe disease and higher mortality than Clades IIa and IIb. The virus is considered to be endemic in tropical rainforest regions of Central and West Africa. In addition to monkeys, the virus has been identified in Gambian pouched rats ( Cricetomys gambianus ), dormice ( Graphiurus spp.) and African squirrels ( Heliosciurus , and Funisciurus ). The use of these animals as food may be an important source of transmission to humans. Mpox can be transmitted from one person to another through contact with infectious lesion material or fluid on the skin, in the mouth or on the genitals; this includes touching, close contact and during sex. It may also spread by means of respiratory droplets from talking, coughing or sneezing. During the 2022–2023 outbreak, transmission between people was almost exclusively via sexual contact. There is a lower risk of infection from fomites (objects which can become infectious after being touched by an infected person) such as clothing or bedding, but precautions should be taken. The virus then enters the body through broken skin, or mucosal surfaces such as the mouth, respiratory tract, or genitals. The natural reservoir of monkeypox virus is thought to be small mammals in tropical Africa. The virus can be transmitted from animal to human from bites or scratches, or during activities such as hunting, skinning, or cooking infected animals . Clinical differential diagnosis must consider other rash illnesses, such as chickenpox, measles, bacterial skin infections, scabies , syphilis and medication-associated allergies. Diagnosis can be verified by testing for the virus. Polymerase chain reaction (PCR) testing of samples from skin lesions is the preferred laboratory test. The MVA-BN vaccine, originally developed for smallpox, has been approved for use by persons who are either considered at high risk of exposure to mpox, or who may have recently been exposed to it. The United States Centers for Disease Control and Prevention (CDC) recommends that persons investigating mpox outbreaks, those caring for infected individuals or animals, and those exposed by close or intimate contact with infected individuals or animals should receive a vaccination. Historically, smallpox vaccine had been reported to reduce the risk of mpox among previously vaccinated persons in Africa. The decrease in immunity to poxviruses in exposed populations is a factor in the increasing prevalence of human mpox. It is attributed to waning cross-protective immunity among those vaccinated before 1980, when mass smallpox vaccinations were discontinued, and to the gradually increasing proportion of unvaccinated individuals. The CDC has made detailed recommendations in addition to the standard precautions for infection control. These include that healthcare providers don a gown, mask, goggles, and a disposable filtering respirator (such as an N95 ), and that an infected person should be isolated a private room to keep others from possible contact. Those living in countries where mpox is endemic should avoid contact with sick mammals such as rodents, marsupials, non-human primates (dead or alive) that could harbour monkeypox virus and should refrain from eating or handling wild game ( bush meat ). During the 2022–2023 outbreak, several public health authorities launched public awareness campaigns in order to reduce spread of the disease. Most cases of mpox present with mild symptoms and there is complete recovery within 2 to 4 weeks. There is no specific treatment for the disease, although antivirals such as tecovirimat have been approved for the treatment of severe mpox. A 2023 Cochrane review found no completed randomised controlled trials studying therapeutics for the treatment of Mpox. The review identified non-randomised controlled trials which evaluated the safety of therapeutics for Mpox, finding no significant risks from tecovirimat and low certainty evidence that suggests brincidofovir may cause mild liver injury. Pain is common and may be severe; supportive care such as pain or fever control may be administered. Patients with mild disease should isolate at home, stay hydrated, eat well, and take steps to maintain their mental health. Patients who are at high risk from the disease include children, pregnant women, the elderly and those who are immunocompromised . For these patients, or those who have severe disease, hospital admission and careful monitoring of symptoms is recommended, Symptomatic treatment is recommended for complications such as proctitis , and pruritis . Mpox was first identified as a distinct illness in 1958 among laboratory monkeys in Copenhagen , Denmark. The first documented cases in humans were in 1970, in six unvaccinated children during the smallpox eradication efforts; the first being a 9-month-old boy in the Democratic Republic of the Congo (DRC). From 1981 to 1986, over 300 cases of human mpox were reported in the DRC, the majority being due to contact with animals. The virus has been detected In Gambian pouched rats , dormice and African squirrels, which are often used as food. Many more mpox cases have been reported in Central and West Africa, and in the Democratic Republic of the Congo in particular: 2,000 cases per year are known between 2011 and 2014. The collected data is often incomplete and unconfirmed, which hinders realistic estimations of the number of cases of mpox over time. Originally thought to be uncommon in humans, cases increased since the 1980s, possibly as a result of waning immunity since the stopping of routine smallpox vaccination. Historically, the case fatality rate (CFR) of past outbreaks was estimated at between 1% and 10%, with Clade I considered to be more severe than Clade II. However the CFR of the 2022–2023 global outbreak (caused by Clade IIb) has been very low - estimated at 0.16%, with the majority of deaths in individuals who were already immunocompromised . The huge difference between these estimates is attributed to: - The natural reservoir of monkeypox virus has not been conclusively determined, although small rodents are the most likely candidate. Without a major vaccination campaign, mpox outbreaks in humans will continue indefinitely in the endemic areas, with an ongoing risk that disease outbreaks will spread to non-endemic areas. Other evidence—that the virus is evolving to be more transmissible among humans, that it can infect a wide range of host species, and that human-to-animal transmission can occur—led to concerns that mpox may either become established in new natural reservoirs outside of Africa, or cause future global epidemics. Following the 2022–2023 outbreak, mpox (clade IIb) remains present in the human population outside Africa at very low levels. In November 2023, the WHO reported increasing numbers of cases of mpox (clade I) in the Democratic Republic of the Congo, with 12,569 cases year-to-date and 651 fatalities; there was also the first evidence of sexual transmission of clade I. Mpox was first identified as a distinct illness in 1958 among laboratory monkeys in Copenhagen , Denmark. The first documented cases in humans were in 1970, in six unvaccinated children during the smallpox eradication efforts; the first being a 9-month-old boy in the Democratic Republic of the Congo (DRC). From 1981 to 1986, over 300 cases of human mpox were reported in the DRC, the majority being due to contact with animals. The virus has been detected In Gambian pouched rats , dormice and African squirrels, which are often used as food. Many more mpox cases have been reported in Central and West Africa, and in the Democratic Republic of the Congo in particular: 2,000 cases per year are known between 2011 and 2014. The collected data is often incomplete and unconfirmed, which hinders realistic estimations of the number of cases of mpox over time. Originally thought to be uncommon in humans, cases increased since the 1980s, possibly as a result of waning immunity since the stopping of routine smallpox vaccination. Historically, the case fatality rate (CFR) of past outbreaks was estimated at between 1% and 10%, with Clade I considered to be more severe than Clade II. However the CFR of the 2022–2023 global outbreak (caused by Clade IIb) has been very low - estimated at 0.16%, with the majority of deaths in individuals who were already immunocompromised . The huge difference between these estimates is attributed to: -The natural reservoir of monkeypox virus has not been conclusively determined, although small rodents are the most likely candidate. Without a major vaccination campaign, mpox outbreaks in humans will continue indefinitely in the endemic areas, with an ongoing risk that disease outbreaks will spread to non-endemic areas. Other evidence—that the virus is evolving to be more transmissible among humans, that it can infect a wide range of host species, and that human-to-animal transmission can occur—led to concerns that mpox may either become established in new natural reservoirs outside of Africa, or cause future global epidemics. Following the 2022–2023 outbreak, mpox (clade IIb) remains present in the human population outside Africa at very low levels. In November 2023, the WHO reported increasing numbers of cases of mpox (clade I) in the Democratic Republic of the Congo, with 12,569 cases year-to-date and 651 fatalities; there was also the first evidence of sexual transmission of clade I. This section is an incomplete list of disease outbreaks which have been reported, including significant outbreaks in the endemic countries in tropical Africa (Benin, Cameroon, the Central African Republic, the Democratic Republic of the Congo, Gabon, Ghana, Ivory Coast, Liberia, Nigeria, the Republic of the Congo, Sierra Leone, and South Sudan). Outbreaks of mpox are frequent in areas where the disease is endemic - these areas often have poor healthcare infrastructure and outbreaks are rarely documented. In May 2003, a young child became ill with fever and rash after being bitten by a prairie dog purchased at a local swap meet near Milwaukee , Wisconsin . In total, 71 cases of mpox were reported through 20 June 2003. All cases were traced to Gambian pouched rats imported from Accra , Ghana , in April 2003 by a Texas exotic animal distributor. No deaths resulted. Electron microscopy and serologic studies were used to confirm that the disease was human mpox. Everyone affected reported direct or close contact with prairie dogs, later found to be infected with the monkeypox virus. In July 2021, in the US, an American returning from a trip in Nigeria was diagnosed with mpox. Subsequent testing identified the virus as belonging to clade II. The patient was hospitalized and treated with tecovirimat and was discharged after 32 days. During 2022, an outbreak of Clade I mpox was reported in refugee camps in Sudan. In September 2017, monkeypox virus was reported in Nigeria. The subsequent outbreak was, at that time, the largest ever outbreak of clade II of the virus, with 118 confirmed cases. Unlike previous outbreaks of this clade, infection was predominantly among young male adults and human-to-human transmission appears to have readily occurred. Seven deaths (5 male, 2 female, case fatality rate of 6%) were reported, including a baby and four HIV/AIDS patients. Additionally, a pregnant woman in her second trimester had a spontaneous miscarriage attributed to monkeypox virus infection. In May 2022, the Nigerian government released a report stating that between 2017 and 2022, 558 cases were confirmed across 32 states and the Federal Capital Territory. There were 8 deaths reported, making for a 1.4% Case Fatality Ratio . In 2022, NCDC implemented a National Technical Working Group for reporting and monitoring infections, strengthening response capacity. In September 2018, the United Kingdom's first case of mpox was recorded. The person, a Nigerian national, is believed to have contracted mpox in Nigeria before travelling to the United Kingdom. A second case was confirmed in the town of Blackpool , with a further case that of a medical worker who cared for the case from Blackpool. In December 2019, mpox was diagnosed in a person in South West England who had travelled to the UK from Nigeria. In May 2021, in the UK, three cases of mpox from a single household were identified by Public Health Wales . The index case had travelled from Nigeria . In May 2019, a 38-year-old man who travelled from Nigeria was hospitalised in an isolation ward at the National Centre for Infectious Diseases in Singapore, after being confirmed as the country's first case of mpox. As a result, 22 people were quarantined. The case may have been linked to a simultaneous outbreak in Nigeria. An outbreak of mpox caused by Clade IIb of the virus was first identified in May 2022. The first case was detected in London, United Kingdom, on 6 May in a patient with a recent travel history from Nigeria (where the disease is endemic ). Subsequent cases were reported from an increasing number of countries and regions. In July 2022, the World Health Organization (WHO) declared the outbreak a public health emergency of international concern (PHEIC); in May 2023, the PHEIC was terminated due to steady progress in controlling the spread of the disease. As of January 2024, Clade IIb mpox cases outside of endemic regions in Africa continue to be reported at a low level. During 2023, a Clade I outbreak of mpox disease in the Democratic Republic of Congo (DRC) resulted in 14,626 suspected cases being reported, with 654 associated deaths, making for a case-fatality rate (CFR) of 4.5%. The outbreak continued into 2024 with an additional 3,576 suspected mpox cases and 265 deaths being reported in the DRC through the first 9 weeks of the year, making for an estimated CFR of 7.4%. The outbreak appears to be of a primarily sexually transmitted nature and cases are occurring in areas without a history of mpox, such as South Kivu and Kinshasa. The outbreak seems to consist of two separate sub-variants of clade I, with one of the sub-variants having a novel mutation making detection with standard assays unreliable. The outbreak spread to the neighbouring country of the Republic of Congo , with 43 mpox cases being reported in March 2024. In May 2003, a young child became ill with fever and rash after being bitten by a prairie dog purchased at a local swap meet near Milwaukee , Wisconsin . In total, 71 cases of mpox were reported through 20 June 2003. All cases were traced to Gambian pouched rats imported from Accra , Ghana , in April 2003 by a Texas exotic animal distributor. No deaths resulted. Electron microscopy and serologic studies were used to confirm that the disease was human mpox. Everyone affected reported direct or close contact with prairie dogs, later found to be infected with the monkeypox virus. In July 2021, in the US, an American returning from a trip in Nigeria was diagnosed with mpox. Subsequent testing identified the virus as belonging to clade II. The patient was hospitalized and treated with tecovirimat and was discharged after 32 days. During 2022, an outbreak of Clade I mpox was reported in refugee camps in Sudan. In September 2017, monkeypox virus was reported in Nigeria. The subsequent outbreak was, at that time, the largest ever outbreak of clade II of the virus, with 118 confirmed cases. Unlike previous outbreaks of this clade, infection was predominantly among young male adults and human-to-human transmission appears to have readily occurred. Seven deaths (5 male, 2 female, case fatality rate of 6%) were reported, including a baby and four HIV/AIDS patients. Additionally, a pregnant woman in her second trimester had a spontaneous miscarriage attributed to monkeypox virus infection. In May 2022, the Nigerian government released a report stating that between 2017 and 2022, 558 cases were confirmed across 32 states and the Federal Capital Territory. There were 8 deaths reported, making for a 1.4% Case Fatality Ratio . In 2022, NCDC implemented a National Technical Working Group for reporting and monitoring infections, strengthening response capacity. In September 2018, the United Kingdom's first case of mpox was recorded. The person, a Nigerian national, is believed to have contracted mpox in Nigeria before travelling to the United Kingdom. A second case was confirmed in the town of Blackpool , with a further case that of a medical worker who cared for the case from Blackpool. In December 2019, mpox was diagnosed in a person in South West England who had travelled to the UK from Nigeria. In May 2021, in the UK, three cases of mpox from a single household were identified by Public Health Wales . The index case had travelled from Nigeria .In May 2019, a 38-year-old man who travelled from Nigeria was hospitalised in an isolation ward at the National Centre for Infectious Diseases in Singapore, after being confirmed as the country's first case of mpox. As a result, 22 people were quarantined. The case may have been linked to a simultaneous outbreak in Nigeria. An outbreak of mpox caused by Clade IIb of the virus was first identified in May 2022. The first case was detected in London, United Kingdom, on 6 May in a patient with a recent travel history from Nigeria (where the disease is endemic ). Subsequent cases were reported from an increasing number of countries and regions. In July 2022, the World Health Organization (WHO) declared the outbreak a public health emergency of international concern (PHEIC); in May 2023, the PHEIC was terminated due to steady progress in controlling the spread of the disease. As of January 2024, Clade IIb mpox cases outside of endemic regions in Africa continue to be reported at a low level. During 2023, a Clade I outbreak of mpox disease in the Democratic Republic of Congo (DRC) resulted in 14,626 suspected cases being reported, with 654 associated deaths, making for a case-fatality rate (CFR) of 4.5%. The outbreak continued into 2024 with an additional 3,576 suspected mpox cases and 265 deaths being reported in the DRC through the first 9 weeks of the year, making for an estimated CFR of 7.4%. The outbreak appears to be of a primarily sexually transmitted nature and cases are occurring in areas without a history of mpox, such as South Kivu and Kinshasa. The outbreak seems to consist of two separate sub-variants of clade I, with one of the sub-variants having a novel mutation making detection with standard assays unreliable. The outbreak spread to the neighbouring country of the Republic of Congo , with 43 mpox cases being reported in March 2024.
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List of diseases (L)
This is a list of diseases starting with the letter "L".
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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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List of notifiable diseases
The following is a list of notifiable diseases arranged by country.
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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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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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https://api.wikimedia.org/core/v1/wikipedia/en/page/Irrua_Specialist_Teaching_Hospital/html
Irrua Specialist Teaching Hospital
Irrua Specialist Teaching Hospital is a federal government of Nigeria teaching hospital located in Irrua, Edo State , Nigeria . The current Chief Medical Director is Professor Reuben A. Eifediyi. The purpose of Irrua specialist Teaching Hospital (ISTH) is to become a Centre of Excellence in Teaching, Research and Service to various health problems facing the rural and suburban/small urban town communities. Their aim is to manage and control viral hemorrhagic fevers, with special reference to Lassa Fever . Irrua specialist teaching hospital is also established to provide specialized, affordable, accessible and qualitative promotive, preventive and curative health care services for patients.Irrua Specialist Teaching Hospital was established by decree 92 of 1993 (Appendix I). [ citation needed ] The hospital was formerly known as Otibhor Okae Teaching Hospital. The current Chief Medical Director is Professor Reuben.A Eifediyi.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Oyewale_Tomori/html
Oyewale Tomori
Oyewale Tomori (born 3 February 1946, Osun State , Nigeria ) is a Nigerian professor of virology , educational administrator , and former vice chancellor of Redeemer's University . In 2024, he became the chair of West Africa National Academy of Scientists. Tomori was born in Ilesa , Osun State, Nigeria on 3 February 1946. He received a Doctor of Veterinary Medicine (DVM) from Ahmadu Bello University , Zaria as well as a Doctorate degree , Ph.D in virology from the University of Ibadan , Oyo State , Nigeria where he was appointed professor of virology in 1981, the same year he received the United States Department of Health and Human Services Public Health Service Certificate for contributions to Lassa Fever Research. Three years (1984) after his appointment as a professor of virology, he was appointed the head of the Department of Virology. At the University of Ibadan Tomori's research interest focuses on viral infections including Ebola hemorrhagic fever , yellow fever , Lassa fever . He served as the Regional Virologist for the World Health Organization Africa Region (1994-2004) before he was appointed as the pioneer vice chancellor of Redeemer's University , Ogun State, Nigeria , a tenure that ended in 2011. He is a recipient of several awards and fellow of many international academic organizations. Among others are;
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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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Lassa fever
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Sindbis virus
Sindbis virus ( SINV ) is a member of the Togaviridae family, in the Alphavirus genus. The virus was first isolated in 1952 in Cairo , Egypt . The virus is transmitted by mosquitoes ( Culex and Culiseta ). SINV is linked to Pogosta disease ( Finland ), Ockelbo disease ( Sweden ) and Karelian fever ( Russia ) . In humans, the symptoms include arthralgia , rash and malaise . Sindbis virus is widely and continuously found in insects and vertebrates in Eurasia, Africa, and Oceania. Clinical infection and disease in humans however has almost only been reported from Northern Europe (Finland, Sweden, Russian Karelia), where SINV is endemic and where large outbreaks occur intermittently. Cases are occasionally reported in Australia, China, and South Africa. SINV is an arbovirus , it is ar thropod - bo rne, and it is maintained in nature by transmission between vertebrate (bird) hosts and invertebrate (mosquito) vectors. Humans are infected with Sindbis virus when bitten by an infected mosquito.Sindbis viruses are enveloped particles with an icosahedral capsid , with a positive single stranded RNA genome, with an approximate size of 11.7 kb. The RNA has a 5' -cap and 3'-polyadenylated tail, and therefore serves directly as messenger RNA ( mRNA ) in a host cell. The genome encodes four non-structural proteins, the capsid, and two envelope proteins. This is characteristic of all Togaviruses . Replication is cytoplasmic and rapid. The genomic RNA is partially translated at the 5' end to produce the non-structural proteins which are then involved in genome replication and the production of new genomic RNA and a shorter sub-genomic RNA strand. This sub-genomic strand is translated into the structural proteins. The viruses assemble at the host cell surfaces and acquire their envelope through budding . A non-coding RNA element has been found to be essential for Sindbis virus genome replication. Recombination has been demonstrated between RNAs of Sindbis virus. The mechanism of recombination appears to be template switching (copy choice) during RNA replication. Sindbis viruses are enveloped particles with an icosahedral capsid , with a positive single stranded RNA genome, with an approximate size of 11.7 kb. The RNA has a 5' -cap and 3'-polyadenylated tail, and therefore serves directly as messenger RNA ( mRNA ) in a host cell. The genome encodes four non-structural proteins, the capsid, and two envelope proteins. This is characteristic of all Togaviruses . Replication is cytoplasmic and rapid. The genomic RNA is partially translated at the 5' end to produce the non-structural proteins which are then involved in genome replication and the production of new genomic RNA and a shorter sub-genomic RNA strand. This sub-genomic strand is translated into the structural proteins. The viruses assemble at the host cell surfaces and acquire their envelope through budding . A non-coding RNA element has been found to be essential for Sindbis virus genome replication. Recombination has been demonstrated between RNAs of Sindbis virus. The mechanism of recombination appears to be template switching (copy choice) during RNA replication.
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Lassa 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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https://api.wikimedia.org/core/v1/wikipedia/en/page/The_Americans_season_4/html
The Americans season 4
The fourth season of the American television drama series The Americans , consisting of 13 episodes, premiered on FX on March 16, 2016, and concluded on June 8, 2016. The events of the fourth season begin immediately after the events of the last episode of the third season in March 1983 and end on the night of Super Bowl XVIII , January 22, 1984, which Paige and Matthew are watching at Stan's house in the finale. The series was renewed for a 13-episode fourth season on March 31, 2015. In April 2015, FX announced Frank Langella would continue his recurring role on the series. The season began principal photography on October 13, 2015. Broadway veteran Ruthie Ann Miles was cast as a new acquaintance of one of Elizabeth's guises. Writing for the season had been completed by January 28, 2016; and the final day of filming was March 9, 2016. The fourth season received widespread acclaim from critics. On Rotten Tomatoes , it received a 99 percent approval rating with an average score of 9.2 out of 10 based on 45 reviews, with a critics consensus of: "With its fourth season, The Americans continues to deliver top-tier spy drama while sending its characters in directions that threaten to destroy their freedoms – and their lives." On Metacritic , the season has a score of 95 out of 100 based on 28 reviews, indicating "universal acclaim". Vikram Murthi of The A.V. Club gave it a perfect "A" grade and wrote, "If the fourth season reminds viewers of anything, it's that The Americans has a masterful control of tone, doling out horror and slow-burn dread like very few of its contemporaries." Ben Travers of Indiewire also gave it an "A" grade and wrote that the season "is on the equally stellar level of its predecessors". Brian Tallerico of RogerEbert.com praised the series and wrote, "It is that depth of character and nuance in the writing that elevates The Americans , along with its willingness to offer stunning narrative developments. [...] I'm now convinced that when we close the final chapter of this televised novel we may finally appreciate one of the best shows we've ever seen." Maureen Ryan of Variety reviewed the show, praising it for its refusal to go in "cartoonish or preposterous directions" and thereby avoiding becoming one of a "cacophony of shows doing superficially outrageous things for attention". Ryan wrote that it "grows louder by the day" and pointed out that Elizabeth and Philip are now "even more untenable, and the show has never been one to drag out developments past their potency". Rob Sheffield of Rolling Stone said that "the acting is impeccable" and that it "keeps getting more intense as it goes along, hitting harder than any drama on television right now". For the 32nd TCA Awards , The Americans won for Outstanding Achievement in Drama, was nominated for Program of the Year and Keri Russell was nominated for Individual Achievement in Drama. For the 68th Primetime Emmy Awards , the series received five nominations, for Outstanding Drama Series , Matthew Rhys for Outstanding Lead Actor in a Drama Series , Keri Russell for Outstanding Lead Actress in a Drama Series , and Joel Fields and Joe Weisberg for Outstanding Writing for a Drama Series for the season finale "Persona Non Grata", while Margo Martindale won for Outstanding Guest Actress in a Drama Series . The prior omissions that the show has received at the Emmys was considered to be snubbed by the Emmys in the drama and acting categories by critics. For both the 7th Critics' Choice Television Awards and 74th Golden Globe Awards , Matthew Rhys and Keri Russell were nominated for Best Actor and Best Actress in a Drama Series, respectively. For the 69th Writers Guild of America Awards , the series won the award for Best Drama Series . The fourth season received widespread acclaim from critics. On Rotten Tomatoes , it received a 99 percent approval rating with an average score of 9.2 out of 10 based on 45 reviews, with a critics consensus of: "With its fourth season, The Americans continues to deliver top-tier spy drama while sending its characters in directions that threaten to destroy their freedoms – and their lives." On Metacritic , the season has a score of 95 out of 100 based on 28 reviews, indicating "universal acclaim". Vikram Murthi of The A.V. Club gave it a perfect "A" grade and wrote, "If the fourth season reminds viewers of anything, it's that The Americans has a masterful control of tone, doling out horror and slow-burn dread like very few of its contemporaries." Ben Travers of Indiewire also gave it an "A" grade and wrote that the season "is on the equally stellar level of its predecessors". Brian Tallerico of RogerEbert.com praised the series and wrote, "It is that depth of character and nuance in the writing that elevates The Americans , along with its willingness to offer stunning narrative developments. [...] I'm now convinced that when we close the final chapter of this televised novel we may finally appreciate one of the best shows we've ever seen." Maureen Ryan of Variety reviewed the show, praising it for its refusal to go in "cartoonish or preposterous directions" and thereby avoiding becoming one of a "cacophony of shows doing superficially outrageous things for attention". Ryan wrote that it "grows louder by the day" and pointed out that Elizabeth and Philip are now "even more untenable, and the show has never been one to drag out developments past their potency". Rob Sheffield of Rolling Stone said that "the acting is impeccable" and that it "keeps getting more intense as it goes along, hitting harder than any drama on television right now". For the 32nd TCA Awards , The Americans won for Outstanding Achievement in Drama, was nominated for Program of the Year and Keri Russell was nominated for Individual Achievement in Drama. For the 68th Primetime Emmy Awards , the series received five nominations, for Outstanding Drama Series , Matthew Rhys for Outstanding Lead Actor in a Drama Series , Keri Russell for Outstanding Lead Actress in a Drama Series , and Joel Fields and Joe Weisberg for Outstanding Writing for a Drama Series for the season finale "Persona Non Grata", while Margo Martindale won for Outstanding Guest Actress in a Drama Series . The prior omissions that the show has received at the Emmys was considered to be snubbed by the Emmys in the drama and acting categories by critics. For both the 7th Critics' Choice Television Awards and 74th Golden Globe Awards , Matthew Rhys and Keri Russell were nominated for Best Actor and Best Actress in a Drama Series, respectively. For the 69th Writers Guild of America Awards , the series won the award for Best Drama Series .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/National_Microbiology_Laboratory/html
National Microbiology Laboratory
The National Microbiology Laboratory ( NML ) is part of the Public Health Agency of Canada (PHAC), the agency of the Government of Canada that is responsible for public health , health emergency preparedness and response, and infectious and chronic disease control and prevention. NML is located in several sites across the country including the Canadian Science Centre for Human and Animal Health (CSCHAH) in Winnipeg, Manitoba . NML has a second site in Winnipeg, the JC Wilt Infectious Disease Research Centre on Logan Avenue which serves as a hub for HIV research and diagnostics in Canada. The three other primary sites include locations in Guelph , St. Hyacinthe and Lethbridge . [ citation needed ] The CSCHAH is a biosafety level 4 infectious disease laboratory facility, the only one of its kind in Canada. With maximum containment, scientists are able to work with pathogens including Ebola , Marburg and Lassa fever . [ citation needed ] The NML's CSCHAH is also home to the Canadian Food Inspection Agency 's National Centre for Foreign Animal Disease , and thus the scientists at the NML share their premises with animal virologists .The National Microbiology Laboratory was preceded by the Bureau of Microbiology which was originally part of the Laboratory Centre for Disease Control of Health Canada in Ottawa . In the 1980s, Health Canada identified both the need to replace existing laboratory space that was reaching the end of its lifespan and the need for Containment Level 4 space in the country. Around the same time, Agriculture Canada (prior to the Canadian Food Inspection Agency being formed) also identified the need for new laboratory space including high-containment. Numerous benefits were identified for housing both laboratories in one building and Winnipeg was chosen as the site; an announcement to that effect was made in October 1987. [ citation needed ] After some debate, the spot chosen for the site was a city works yard near to the Health Sciences Centre (a major teaching hospital), the University of Manitoba 's medical school, and other life science organizations. Construction of the facility that came to be named the Canadian Science Centre for Human and Animal Health (often referred to locally as "the Virology Lab") began with an official ground-breaking in December 1992. The joint venture design team of Toronto-based Dunlop Architects and Winnipeg-based Smith Carter Architects and Engineers visited 30 laboratories to seek best practices in containment and design. Construction was largely complete by the end of 1997 with the first programs beginning in the spring of 1998 and all laboratories coming on line after that. The official opening took place in June 1999. Following the SARS outbreak in 2003, the Public Health Agency of Canada was formed in 2004 to provide a stronger focus on public health and emergency preparedness in the country. It is a member of the federal Health Portfolio (along with Health Canada, the Canadian Institute of Health Research , and other organizations). By 2018 the NML was beginning to use genomics and advanced computing to study microbes at the genetic level in so-called "dry lab" facilities, as opposed to "wet labs" with Petri dishes and cell cultures . The NML (PHAC) fired Chinese nationals Xiangguo Qiu and her husband Keding Cheng from their jobs as BSL4 infectious disease researchers in January 2021; previously in July 2019 the pair had been dismissed from their positions as unpaid members of the University of Winnipeg for their agency in a mysterious trans-Pacific shipment of BSL4-grade virus materials back to their homeland when the RCMP was called in. Human pathogens are classified into risk groups. The criteria to determine the group includes the level of risk to the health of a person or to public health, as well as the likelihood that the human pathogen will actually cause disease in a human, and whether treatment and preventative measures are available. It can depend on the type of work being done as to which level of containment is needed for pathogens from specific risk groups; as an example, culturing (or growing) a virus or bacterium requires higher containment than some diagnostic tests. [ citation needed ] NML operates Containment Level 2, 3 and 4 laboratories. In human health infectious disease laboratories, the design and construction of the facility, the engineering controls, and the training and techniques of staff are all focused on protecting lab workers, containing the pathogens, and preventing contamination of materials to ensure accurate diagnosis and research. All of these factors vary depending on the level of containment. [ citation needed ] The vast majority (87.7%) of NML's lab space is Containment Level 2 (CL2). This is the same type of laboratory found in doctors' offices, hospitals and universities. In a Level 2 lab, work with infectious materials is done inside a biosafety cabinet (BSC) and appropriate personal protective gear is worn relative to activities (gloves, eye protection, lab coats, gowns, etc.). Risk Group 2 pathogens worked with in Level 2 can cause disease but are not a serious hazard and they are often circulating in the community. Environmental contamination must be minimized by the use of hand washing sinks and decontamination facilities such as autoclaves . Examples include E-coli ; whooping cough ; and seasonal influenza . [ citation needed ] NML also has Containment Level 3 (CL3) laboratories (8.6% of lab space). Risk Group 3 pathogens may be transmitted by the airborne route, often need only a low infectious dose to produce effects, and can cause serious or life-threatening disease. CL3 emphasizes additional primary and secondary barriers to minimize the release of infectious organisms into the immediate laboratory and the environment. Additional features to prevent transmission of CL3 organisms are appropriate respiratory protection, HEPA filtration of exhausted laboratory air, and strictly controlled laboratory access. Examples include tuberculosis ; West Nile virus ; and pandemic H1N1 influenza . [ citation needed ] A small percentage of laboratory space (3.6%) is devoted to Containment Level 4 (CL4) at NML. These agents have the potential for aerosol transmission, often have a low infectious dose and produce very serious and often fatal disease; there is no licensed treatment or vaccine available. This level of containment represents an isolated unit independent of other areas. CL4 emphasizes maximum containment of the infectious agent by completely sealing the facility perimeter with confirmation by negative pressure testing, isolation of the researcher from the pathogen by an enclosed positive pressure suit, and decontamination of air and all other materials. Examples include Ebola, Nipah , Marburg , and 1918 pandemic influenza . [ citation needed ]NML programs are housed in several facilities across the country. Two of these facilities are in proximity to each other in Winnipeg: The Canadian Science Centre for Human and Animal Health on Arlington Street and the J.C. Wilt Infectious Diseases Research Centre on Logan Avenue. The other facilities are located in Guelph, ON; St. Hyacinthe, QC and Lethbridge, AB. NML is divided into five main laboratory divisions which are supported by scientific and administrative services. The primary NML divisions are: Bacterial Pathogens - focussing on bacterial diseases such as tuberculosis and antibiotic resistant organisms. Enteric Diseases - focussing on food and water-borne pathogens including E.coli and Salmonella . Viral Diseases - addressing a range of viral diseases, including hepatitis and other blood-borne pathogens, respiratory viruses and viral exanthemata, such as measles . Zoonotic Diseases and Special Pathogens - dealing with viral, bacterial and rickettsial zoonoses (diseases transmitted to humans from other species), such as West Nile Virus and Lyme disease , along with risk group 4 agents such as Ebola, Marburg and Lassa fever viruses. HIV and Retrovirology - providing laboratory services and scientific expertise relating to HIV and emerging retroviruses . The Science Technology Core and Services Division works with these divisions to provide technological approaches, including genomics , proteomics and bioinformatics . There is also the Public Health Risk Sciences Division , which is a specialized resource that provides scientific knowledge and solutions to better assess public health risks and enable decisions, with specific attention to infectious disease threats transmitted from food, the animals, or the physical environment. These science-based divisions are complemented and supported by numerous other units that ensure their ongoing operations such as the Office of Science Planning, Program Support and Services, Scientific Informatic Services, Science Support and Client Services, Surveillance and References Services, the Facility and Property Management Division, and the Biorisk and Occupational Safety Services Division. NML also funds the National Reference Centre for Parasitology in Montreal and has a Laboratory Liaison Technical Officer in most provincial labs.NML employs scientists (MD, PhD, and DVM), biologists, and laboratory technologists, but it also includes informatics specialists, biosafety experts, specialized operations and maintenance staff, and administrative staff, among others. In total, there are approximately 600 staff members as of 2016. [ citation needed ] The laboratory has collaborated with scientists from the People's Liberation Army from at least 2016 to 2020. NML is renowned [ better source needed ] for its work on a broad spectrum of infectious diseases from seasonal influenza to Ebola and its accomplishments are too many to detail. Some recent examples of the work done by NML include their involvement in the response to the West African Ebola outbreak. For a period of about 18 months, teams from NML travelled to West Africa to aid in the diagnostics during the outbreak. They worked closely with the World Health Organization and Médecins sans frontières to ensure people were properly diagnosed so that they could be properly cared for and isolated from others to stop the spread. Also during this outbreak, a promising vaccine and treatment for Ebola that were developed at NML, in conjunction with collaborators, were fast tracked into clinical trials so that they could get to the people that needed it as soon as possible. [ citation needed ] Another accomplishment was the response to the 2009 H1N1 influenza pandemic. In April 2009, the Mexican national lab approached NML for assistance with identifying a respiratory virus that was causing outbreaks in Mexico . NML was able to quickly identify the new virus and recognize that it matched the virus that was beginning to circulate in the U.S. As the lead laboratory in Canada, NML rapidly developed diagnostic tests and equipped provincial labs to be able to test for the new virus. NML also assisted Mexico by providing additional testing and sent staff to their national laboratory to enable to help them set up their own testing protocols. In the international laboratory sector, NML has developed different types of mobile labs : a lab-truck, a lab-trailer, and a "lab in a suitcase". The lab-truck is generally used for in-country deployments at high-profile events such as the 2010 Olympics , the lab-trailer is used for international large-scale events where there may be a threat of bioterrorism or other deliberate acts involving infectious agents, and the lab in a suitcase is frequently used in remote areas of the world with little available infrastructure. An example would be the multiple deployments over the years to combat outbreaks of Ebola in Africa. This model was adopted by many other countries during the 2014-2015 Ebola outbreak in West Africa. NML houses the secretariats for both the Canadian Public Health Laboratory Network (CPHLN) and the Global Health Security Action Group – Laboratory Network (GHSAG-LN). The role of CPHLN is to provide a forum for public health laboratory leaders to share knowledge. The GHSAG-LN network's goals are to coordinate the diagnostic capabilities of all participants and contribute to disease surveillance around the world. The Canadian Network for Public Health Intelligence (CNPHI) is an innovation developed by NML staff. It is a secure web-based system that compiles information from various surveillance systems and issues alerts to users. More than 4,000 public health officials across Canada now subscribe to it. CNPHI tools assist in determining the existence or extent of an outbreak through the recognition of related cases across jurisdictions.From 2000 to 2014, Dr. Frank Plummer was the Scientific Director General of the National Microbiology Laboratory. Under Dr. Plummer's guidance, the NML developed into one of the world's premier institutions in the research, detection, and response to global infectious disease and bio-security threats. Dr. Plummer received his medical degree from the University of Manitoba in 1976. Between 1984 and 2001, Dr. Plummer lived in Nairobi, Kenya where he spearheaded the development of the world renowned "Kenya AIDS Control Program," established by the Universities of Manitoba and Nairobi . This HIV epidemiological work was central to global understanding of the risk factors for HIV transmission and how to prevent its spread. Dr. Plummer was the first to reveal that heterosexual women could also be infected with HIV/AIDS and that a cohort of Nairobi sex workers had a natural immunity to HIV/AIDS . This latter discovery suggested the possibility that a vaccine could eventually be developed. Dr. Plummer stepped down as the NML's Scientific Director General to take the position as senior adviser to the Agency's Chief Public Health Officer in 2014. He remained as a distinguished professor at the University of Manitoba prior to his death in February 2020. In 2015, Dr. Matthew Gilmour became the Scientific Director General of the National Microbiology Laboratory and the Laboratory for Foodborne Zoonoses. Dr. Gilmour spearheaded the partnership that brought these two laboratories together under the National Microbiology Laboratory umbrella. He was previously the Chief, Enteric Diseases and subsequently the Program Director, Bacteriology and Enteric Diseases at the NML. Dr. Gilmour has won a number of scientific awards including Canadian Society of Microbiologists' Canadian Graduate Student Microbiologist of the Year Award; the Public Health Agency of Canada's Most Promising Researcher Merit Award and Dr. Andrés Petrasovits Public Health Merit Award; and Health Canada's Excellence Award in Collaborative Leadership and Award for Excellence in Science. Dr. Gilmour continues to be an Assistant Professor at the University of Manitoba's Department of Medical Microbiology and Infectious Diseases as well as the Secretary Treasurer of the Canadian Association for Clinical Microbiology and Infectious Diseases (CACMID).
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https://api.wikimedia.org/core/v1/wikipedia/en/page/1993_Four_Corners_hantavirus_outbreak/html
1993 Four Corners hantavirus outbreak
The 1993 Four Corners hantavirus outbreak was an outbreak of hantavirus that caused the first known human cases of hantavirus disease in the United States . It occurred within the Four Corners region – the geographic intersection of the U.S. states of Utah , Colorado , New Mexico , and Arizona – of the Southwestern United States in mid-1993. This region is largely occupied by Native American tribal lands, including the Hopi , Ute , Zuni , and Navajo reservations , from which many of the cases were reported. The virus killed 13 people – half of those it infected, for a mortality rate of 50%. The cause of the outbreak was found to be a previously unknown species of hantavirus , which was responsible for a new form of illness known as hantavirus pulmonary syndrome (HPS). The virus is carried by deer mice . Originally referred to as "Four Corners virus", "Muerto Canyon virus", and "Convict Creek virus", it was later named Sin Nombre virus . Transmission to humans was found to have occurred through contact with aerosolized deer mice droppings in enclosed spaces in and around the homes of the victims.In April 1993, a young Navajo woman arrived at the Crownpoint Comprehensive Healthcare Facility emergency room in Crownpoint, New Mexico , complaining of flu -like symptoms and sudden, severe shortness of breath. While at the hospital patient moved to inpatient floor. Doctors found the woman's lungs to be full of fluid, and she died soon after her arrival. An autopsy revealed the woman's lungs to be twice the normal weight for someone her age. The cause of her death could not be immediately determined, and the case was reported to the New Mexico Department of Health. Five days later, her fiancé, a young Navajo man, was en route to her funeral in Gallup when he suddenly became severely short of breath. By the time family brought him by personal vehicle to the Gallup Indian Medical Center emergency room, he had stopped breathing. Emergency room staff performed cardiopulmonary resuscitation . The young man could not be revived by doctors and died. The physicians, recalling the similar symptoms and death of the young woman, reported his death to the New Mexico Department of Health. New Mexico state health officials notified the Centers for Disease Control (CDC). Within a week, a task force had formed in Albuquerque that included Bruce Tempest, chief of medicine at the Indian Medical Center. Tempest quickly discovered that five people, including the young man's fiancée, as well as an Arizona resident, all had experienced the same symptoms and all had died within a six-month period. Tempest learned from the young man's family members that his fiancée had the same symptoms and died on the Navajo Reservation five days earlier. Deaths on the reservations are not reported to the state health department because they are sovereign nations. Tempest had considered plague as the cause because it is endemic to the region, but it had already been ruled out by tests on all of the victims. Within a short time, a dozen more people contracted the mysterious illness, most of them young Navajos in New Mexico. This included two relatives of the young couple who had died within a week of each other. News outlets began reporting on the story of a mystery illness causing deaths among young Navajo, often using the term "Navajo Flu". Hearing a news report, a physician notified health officials to say that the illness had similarities to hantavirus, which he had observed in Korea in the 1950s. The Centers for Disease Control tested for hantavirus even though Asia and Europe were the only documented places hantavirus had been known to occur. No known cases had ever been reported in the United States. In addition, all the cases in Asia and Europe had involved hantaviruses that caused kidney failure, never respiratory failure. The testing revealed a previously unknown hantavirus which was eventually named Sin Nombre virus, Spanish for "No Name" virus. The disease became formally known as hantavirus cardiopulmonary syndrome (HCPS) or simply hantavirus pulmonary syndrome (HPS). Several theories were advanced to explain the emergence of the new virus. These included increased contact between humans and mice due to a "bumper crop" in the deer mouse population. Another theory was that something within the virus had changed, allowing it to jump to humans. A third theory was that nothing had changed, that hantavirus cases had in fact occurred previously but had not been properly diagnosed. This last theory turned out to be the correct one when it was discovered that the first known case had actually occurred in a 38-year-old Utah man in 1959. Like the Korean virus, Sin Nombre virus does not spread person-to-person. Instead, transmission occurs when humans are exposed to air contaminated with aerosolized mouse feces, usually within enclosed spaces. All of the Four Corners victims were found to have significant infestations of deer mice in and around their homes. Doctors reported that all of the Four Corners patients had mild flu-like symptoms such as malaise, headache, cough, and fever, with a sudden onset of pulmonary edema necessitating ventilators before eventually causing death. From April to May 1993, there were 24 reported cases in the region. Twelve of those people died, resulting in a 50% mortality rate. Of the 24 patients, 14 were Native Americans, nine were non-Hispanic whites and one was Hispanic. Navajo leaders reported that similar outbreaks had occurred in 1918, 1933, and 1934. Navajo ethnological stories have identified mice as sources of bad luck and illness since the 19th century. The outbreak was covered in the Forensic Files episode "With Every Breath". [ citation needed ]
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Demographics_of_Nigeria/html
Demographics of Nigeria
Nigeria is the most populous country in Africa and the sixth in the world . It is also one of the most densely populated countries in Africa , with approximately 218.5 million people in an area of 923,768 km 2 (356,669 sq mi) . 54.3% of Nigerians are urban dwellers, with the annual rate of urbanisation being estimated at 3.92%. [lower-alpha 1] Nigeria is home to 371 ethnic groups speaking over 500 languages and the variety of customs and traditions among them gives the country great cultural diversity. The three largest ethnic groups are the Hausa , who make up 25% of the population; the Yoruba , who make up 21%; and the Igbo , who make up 18%. The Ijaw , Efik , Ibibio , Annang , and Ogoni are other Southern populations. Meanwhile, the Tiv , Urhobo-Isoko , Edo and Itsekiri inhabit Nigerian's Midwest. Over 1.2 million people living in Nigeria (0.5% of its total population, or 1 in every 200 people living in Nigeria) are from a continent other than Africa. There are 100,000 people from the United States, 75,000 are from Lebanon , 60,000 are from China and 16,000 are from the United Kingdom. Nigeria has a young population overall, with 42.54% of inhabitants between the ages of 0–14. There is also a very high dependency ratio at 88.2 dependants per 100 non-dependants. The three main religious groups are Muslims (estimated to be 53.5% of the total population), Christians (estimated at 45.9%), and adherents of indigenous religions (estimated at 0.6%). The predominantly Christian Igbo are found in the southeast. Roman Catholicism is the largest Christian denomination in Igboland , but Anglicanism is also strong, as are Pentecostalism and other Evangelical denominations. Persons of different ethnic backgrounds most commonly communicate in English, although knowledge of two or more Nigerian languages is widespread. Hausa , Igbo and Yoruba are the most widely used Nigerian languages. Nigerian Pidgin is used widely as an unofficial medium of communication, especially in the Nigerian cities of Warri , Sapele , Ughelli , Benin and Port Harcourt . Nigeria's population has been increasing rapidly for at least the last 5 decades due to very high birth rates, quadrupling its population during this time. Growth was fastest in the 1980s, after child mortality dropped rapidly. It has slowed slightly since then as both the birth rate and total fertility, rate have declined marginally since a 1978 peak. According to the 2017 revision of the World Population Prospects the total population was 257,541,212 in 2016, compared to only 88,992,220 in 1950. The proportion of children under the age of 15 in 2010 was 44.0%, 53.2% were between 15 and 65 years of age, while 2.7% were 65 years or older. There is a large degree of population momentum , with 3.2 per cent growth leading to the projected population of 546 million by 2100. The federal government has not elected to implement the type of controversial family planning programs that have reduced population growth of other developing nations, a result of low political support for these programs and a cultural preference for large families as well as high levels of social instability. Rising educational levels and health care improvements may enable future parents to plan for smaller families. The former Nigeria's chairman of National Population Commission , Eze Duruiheoma, delivering Nigeria's statement in New York City on sustainable cities , human mobility and international migration in the 51st session of Commission on Population and Development, said that "Nigeria remains the most populous in Africa, the seventh globally with an estimated population of over 198 million. The World Population Prospects predicts that by 2050, Nigeria will become the third most populated country in the world. Over the last 50 years, Nigeria's urban population has grown at an average annual growth rate of more than 6.5% without commensurate increases in social amenities and infrastructure." He also stated that the population "grew substantially from 17.3% in 1967 to 49.4% in 2017." Population by sex and age group (Census 21.III.2006) Population by age group (estimates 1.VII.2016) (Data are projections based on the 2006 Population Census.) Population by age group (estimates 1.VII.2020) (Source: National Population Commission.) Total fertility rate (TFR) (Wanted TFR) and crude birth rate (CBR): Fertility data as of 2013 (DHS Program): Source: Demographic and Health Surveys (DHS) ∗ MICS surveys Contraceptive prevalence , any methods (% of women ages 15–49) ∗ UNICEFs state of the worlds children and child info, United Nations population divisions world contraceptive use, household surveys including demographic and health surveys and multiple indicator cluster surveys. ∗ MICS surveysContraceptive prevalence , any methods (% of women ages 15–49) ∗ UNICEFs state of the worlds children and child info, United Nations population divisions world contraceptive use, household surveys including demographic and health surveys and multiple indicator cluster surveys. The total population in sub-Saharan Africa is projected to increase to almost one billion people, making it the most populated region outside of South-Central Asia. According to the United Nations, the population of Nigeria will reach 375 million by 2050. Nigeria might then be the 3rd most populous country in the world. In 2100, the population of Nigeria may reach 541 million. While the overall population is expected to increase, the growth rate is estimated to decrease from 1.2 per cent per year in 2010 to 0.4 per cent per year in 2050. The birth rate is also projected to decrease from 20.7 to 13.7, while the death rate is projected to increase from 8.5 in 2010 to 9.8 in 2050. By 2050, 69.6% of the population is estimated to be living in urban areas compared to 50.6% in 2010. Registration of vital events in Nigeria is not complete. The Population Department of the United Nations prepared the following estimates ( UN World Population Prospects 2022 ). Life expectancy from 1950 to 2015 ( UN World Population Prospects ): Life expectancy from 1950 to 2015 ( UN World Population Prospects ): The following demographic statistics of Nigeria in 2022 are from the World Population Review. One birth every 4 seconds One death every 13 seconds One net migrant every 9 minutes Net gain of one person every 6 seconds The following demographic statistics are from The World Factbook , unless otherwise indicated. Note 1: on 30 September 2021, the Centers for Disease Control and Prevention issued a Travel Health Notice for a Yellow Fever outbreak in Nigeria; a large, ongoing outbreak of yellow fever in Nigeria began in September 2017; the outbreak is now spread throughout the country with the Nigerian Ministry of Health reporting cases of the disease in multiple states (Bauchi, Benue, Delta, Ebonyi, and Enugu); the CDC recommends travellers going to Nigeria should receive vaccination against yellow fever at least 10 days before travel and should take steps to prevent mosquito bites while there; those never vaccinated against yellow fever should avoid travel to Nigeria during the outbreak Note 2: widespread ongoing transmission of a respiratory illness caused by the novel coronavirus (COVID-19) is occurring throughout Nigeria; as of 6 June 2022, Nigeria has reported a total of 256,148 cases of COVID-19 or 124.3 cumulative cases of COVID-19 per 100,000 population with a total of 3,148 cumulative deaths or a rate of 1.5 cumulative death per 100,000 population; as of 22 May 2022, 12.97% of the population has received at least one dose of COVID-19 vaccine Note 3: on 21 March 2022, the US Centers for Disease Control and Prevention (CDC) issued a Travel Alert for polio in Africa; Nigeria is currently considered a high risk to travellers 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 Definition: age 15 and over can read and write Nigeria is Africa's most populous country. Significant population clusters are scattered throughout the country, with the highest density areas being in the south and southwest.Note 1: on 30 September 2021, the Centers for Disease Control and Prevention issued a Travel Health Notice for a Yellow Fever outbreak in Nigeria; a large, ongoing outbreak of yellow fever in Nigeria began in September 2017; the outbreak is now spread throughout the country with the Nigerian Ministry of Health reporting cases of the disease in multiple states (Bauchi, Benue, Delta, Ebonyi, and Enugu); the CDC recommends travellers going to Nigeria should receive vaccination against yellow fever at least 10 days before travel and should take steps to prevent mosquito bites while there; those never vaccinated against yellow fever should avoid travel to Nigeria during the outbreak Note 2: widespread ongoing transmission of a respiratory illness caused by the novel coronavirus (COVID-19) is occurring throughout Nigeria; as of 6 June 2022, Nigeria has reported a total of 256,148 cases of COVID-19 or 124.3 cumulative cases of COVID-19 per 100,000 population with a total of 3,148 cumulative deaths or a rate of 1.5 cumulative death per 100,000 population; as of 22 May 2022, 12.97% of the population has received at least one dose of COVID-19 vaccine Note 3: on 21 March 2022, the US Centers for Disease Control and Prevention (CDC) issued a Travel Alert for polio in Africa; Nigeria is currently considered a high risk to travellers 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 vaccineDefinition: age 15 and over can read and writeNigeria is Africa's most populous country. Significant population clusters are scattered throughout the country, with the highest density areas being in the south and southwest.Today millions of ethnic Nigerians live abroad, the largest communities can be found in the United Kingdom (500,000–3,000,000) and the United States (600,000–1,000,000 Nigerians), other countries that followed closely are South Africa, Gambia , and Canada respectively. There are also large groups in Ireland, Portugal and many other countries. Inspiration for emigration is based heavily on socio-economical issues such as warfare, insecurity, economical instability and civil unrest. Between 1400 and 1900, of 1.4 million of 2 million emigrants were slaves sent to the Americas with the other 600,000 being sent to other destinations via the trans-Saharan, Red Sea and Indian Ocean routes. This is due to the fact that the land now known as Nigeria was a central point for 4 slave trades during the 19th century. Though bondage represented a great deal, an estimated 30,000 Nigerian inhabitants would relocate to Kano City and Gambia to take advantage of financial opportunities afforded by fertile land and available natural resources. What's more, the presence of gold mines and rail lines along the Gold Coast, present-day Ghana, attracted an estimated 6,500 Nigerian citizens to attain financial gain and opportunity. The population of Nigerians in Ghana rose to roughly 149,000 before the 1969 alien expulsion order would displace nearly the entire population to surrounding countries. Nigeria is nearly equally divided between Islam and Christianity. The majority of Nigerian Muslims are Sunni and mostly live in the northern, central and south-western states of the country, while Christians dominate in some central states (especially Plateau and Benue states), and the south-east and south-south regions. Other religions practised in Nigeria include African Traditional Religion , Hinduism , Bahá'í Faith , Judaism, The Grail Movement , and the Reformed Ògbóni Fraternity, one of the traditional socio-religious institutions of the Yorùbá people and their Òrìṣà religion known as Ẹ̀sìn Òrìṣà Ìbílẹ̀ in the Yorùbá language . According to a 2009 Pew survey, 50.4% of Nigeria's population were Muslims . A later Pew study in 2011 calculated that Christians now formed 50.8% of the population. Adherents of other religions made up 1% of the population. The shift of population balance between Muslims and Christians is a result of northern and southern Nigeria being in different stages of demographic transition. The Muslim-dominated north is in an earlier stage of the demographic transition with much higher fertility rates than the south, whose split Christian/Muslim population is further along in the transition, and whose fertility rates are declining. Decreasing fertility can be linked to more access to education, use of contraceptives, and differing beliefs regarding family planning. The 1999 introduction of Sharia law in twelve northern Nigerian states led to massive violence and unrest and caused an ethnic and religious rift between Sharia and Non-Sharia states, a divide that has deepened with time. Nigeria is home to a substantial network of organised crime , active especially in drug trafficking. Nigerian criminal groups are heavily involved in drug trafficking, shipping heroin from Asian countries to Europe and America; and cocaine from South America to Europe and South Africa. The various Nigerian confraternities or "campus cults" are active in both organised crime and in political violence as well as providing a network of corruption within Nigeria. As confraternities have extensive connections with political and military figures, they offer excellent alumni networking opportunities. The Supreme Vikings Confraternity, for example, boasts that twelve members of the Rivers State House of Assembly are cult members. On lower levels of society, there are the " area boys ", these are organised gangs mostly active in Lagos who specialise in mugging and small-scale drug dealing. According to official statistics, gang violence in Lagos resulted in 273 civilians and 84 policemen killed in the period of August 2000 to May 2001. "The result of factors such as endemic local corruption, which facilitates illicit trafficking ; the Nigerian Civil War , which contributed to a proliferation of firearms; the oil boom of the 1970s, which led to the embezzlement of public funds; and the economic crisis of the 1980s, which was accompanied by a rise in robberies. The expansion of the Nigerian diaspora and organized crime went hand in hand. Global migration boosted prostitution, drug trafficking and fraud, the three main activities of Nigerian syndicates. The smuggling of Nigerian sex workers became a whole industry that now extends from Switzerland to France and Italy (where black prostitutes are called "fireflies"), and has even reached the Prudish Kingdom of Saudi Arabia , from which 1,000 women are said to be deported every month by the authorities." The high crime rate among Nigerian migrants also leads to stereotyping Nigerians as criminals; thus, in Cameroon, Nigerian migrants are perceived collectively by the inhabitants of Cameroon as likely to be oil smugglers or dealers in stolen cars. In the Netherlands , the debate on Nigerian crime reached an intensity described as a " moral panic " by one scholar. In Switzerland , the crime rate of Nigerian young males was reported as 620% that of Swiss males in same age group (2009 data), the second highest crime rate of any nationality, just below that of Angolan nationals (at 630%). Nigeria is also pervaded by political corruption . It is ranked 136 out of 168 countries in Transparency International 's 2015 Corruption Perceptions Index .
2,694
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Brazilian_hemorrhagic_fever/html
Brazilian hemorrhagic fever
Brazilian hemorrhagic fever ( BzHF ) is an infectious disease caused by Brazilian mammarenavirus , an arenavirus . Brazilian mammarenavirus is one of the arenaviruses from South America to cause hemorrhagic fever . It shares a common progenitor with Argentinian mammarenavirus , Machupo mammarenavirus , Tacaribe mammarenavirus , and Guanarito mammarenavirus . It is an enveloped RNA virus and is highly infectious and lethal. Very little is known about this disease, but it is thought to be transmitted by the excreta of rodents . This virus has also been implicated as a means for bioterrorism , as it can be spread through aerosols . As of 2019, there had only been four documented infections of Brazilian mammarenavirus : two occurred naturally, and the other two cases occurred in the clinical setting. The first naturally occurring case was in 1990, when a female agricultural engineer who was staying in the neighborhood of Jardim Sabiá in the municipality of Cotia , a suburb of São Paulo , Brazil contracted the disease (The virus is also known as "Sabiá Virus"). She presented with hemorrhagic fever and died. Her autopsy showed liver necrosis . A virologist who was studying the woman's disease contracted the virus but survived. Ribavirin was not given in these first two cases. Four years later, in 1994, a researcher was exposed to the virus in a level 3 biohazard facility at Yale University when a centrifuge bottle cracked, leaked, and released aerosolized virus particles. He was successfully treated with ribavirin . A fifth case, also naturally acquired in upstate São Paulo, was reported in January 2020. The patient died 12 days after the onset of symptoms. Ribavirin is thought to be effective in treating the illness, similar to other arenaviruses. Compared to the patients who did not receive ribavirin, the patient who was treated with it had a shorter and less severe clinical course. Symptomatic control such as fluids to address dehydration and bleeding may also be required. Brazilian mammarenavirus is a biosafety Level 4 pathogen.
336
Wiki
Lassa fever
https://api.wikimedia.org/core/v1/wikipedia/en/page/Audrey_Hardy/html
Audrey Hardy
1964–2007 2009 2013 2015 Audrey Hardy is a fictional character on the ABC soap opera , General Hospital . She has been portrayed by Rachel Ames on a contract basis from 1964 to 2002, and on a recurring basis from 2002 to 2007, making guest appearances in 2009, 2013, and 2015.Rachel Ames originated the role of Audrey in 1964 in what was originally a thirteen-week stint with an option for an additional thirteen weeks. The character debuted in the episode that originally aired on February 23, 1964. The character's popularity prompted the series to keep the character on canvas. Ames took an extended leave in 1970 when she had to be put on bedrest during her pregnancy. Maura McGiveney played Audrey temporarily while Ames was gone. Ames also crossed over to General Hospital' s spinoff series Port Charles as Audrey in 1997. In 2002, Ames was dropped to recurring status, and ultimately retired from the series in October 2007. Ames briefly reprised the role for a couple of episodes in October 2009 and reprised the role once again in April 2013 for the series' 50th anniversary. Ames once again reprised her role as Audrey on October 30, 2015. Audrey March arrives at General Hospital in 1964 to visit her sister, Lucille March ( Lucille Wall ). She is a registered nurse, who had forsaken the profession for that of an airline stewardess. After noticing Dr. Steve Hardy ( John Beradino ), the Chief of Internal Medicine at General Hospital, Audrey stays in town and becomes a private nurse. Eventually, Steve and Audrey get engaged, but Audrey breaks it off. She accepts a proposal from one of her clients, Randy Washborn. Audrey is diagnosed with lymphoma , and when Randy deserts her she gets back together with Steve. They marry in 1965 after she is recovered. Audrey later works on a book with Dr. Phil Brewer , but the experience ends badly when Phil tries to seduce her. Audrey becomes concerned when she does not conceive, and believing Steve is sterile, Audrey has herself artificially inseminated without Steve's knowledge and becomes pregnant. Audrey is in a car accident and miscarries; she is devastated and separates from Steve. She goes to Vietnam to help war orphans in March 1968. When Audrey returns from Vietnam in January 1969, she continues to push Steve away and after their divorce is final, she marries Tom Baldwin in an effort to prove that she is over Steve. Audrey cannot bring herself to sleep with Tom, and he ends up raping her. After becoming pregnant with Tom's child, Audrey files for divorce and leaves town, determined to protect her unborn child from her violent husband. She returns in 1971, and tells Lucille her son had died at birth. Audrey reconnects with Steve. It is revealed she is lying about her son, whom she named Steve and is in hiding. She plans to remarry Steve, and then convince him to adopt a baby which would be her son. However, Mrs. Peggy Nelson, the woman taking care of the baby, realizes the plan and blackmails Audrey. Peggy Nelson is murdered and Audrey is accused of the crime. Thanks to Steve, Audrey is acquitted. Tom reclaims baby Steve, who is renamed Tommy, forcing Audrey to resume their marriage. Tom kidnaps baby Tommy and flees to Mexico. Tom is later presumed dead and Tommy is returned to Audrey. During the kidnapping ordeal, Tommy had become ill with a heart ailment. Jim Hobart performs surgery and Tommy recovers. Audrey feels gratitude towards Jim and marries him after he injuries his hands and fears he cannot operate again. Audrey faces heartache as she still loves Steve and Jim turns to alcohol to deal with his injury. In 1976, Jim leaves Audrey for a younger woman. Audrey attempts suicide and Steve saves her. Steve proposes to Audrey and she accepts. Steve falls down a flight of stairs and Audrey helps him recuperate. They remarry, and Tom Baldwin returns alive, invalidating their marriage. Tom tries to reclaim Audrey and his son, but eventually gives up and leaves town. Steve and Audrey marry again in 1977 and Steve officially adopts Tommy, renamed Tom Hardy Meanwhile, Audrey had become head of student nurses at General Hospital, and as a result becomes a mentor to nurses such as Bobbie Spencer . Steve and Audrey become involved in various dramas involving the children of Steve's old friend Lars Webber, Terri, Rick and Jeff . Jeff ends up shooting himself, and when he is in the hospital, Terri tells Steve about a letter her mother, Helene, had told her about on her deathbed. Steve finds the letter and learns Jeff is actually his biological son (Steve had relationship with Helene during a time when she was separated from Lars). Steve tells Audrey and they agree to keep the truth a secret. In the winter of 1979, Port Charles is hit by an epidemic of Lassa Fever. General Hospital is placed under quarantine, and when Steve begins to fall victim to the disease, Audrey tells Jeff the truth. Steve recovers and both Rick and Jeff are angry at Steve and Audrey. It takes months for everyone to reconcile. Steve and Audrey are happy to learn that Jeff's son Steven Lars Webber is still alive. Jeff soon leaves town with his son to make a fresh start. Some years later, Tom leaves to attend college and returns in 1987. When Tom marries an African-American doctor, Simone Ravelle, Audrey fears her son's interracial marriage would not be accepted. In time, Audrey and Simone grow close. Simone confides in Audrey when she gets pregnant during an affair with Harrison and does not know who the father is. However, Audrey is relieved when Tom is confirmed to be the little Tommy 's father. In 1993, Audrey organizes a surprise party for Steve's 30th anniversary at General Hospital. Audrey is attacked by psychopath Ryan Chamberlain, who mistakes her for his abusive mother. Audrey quickly recovers and testifies against Ryan at his trial, causing him to be committed to a mental institution. When Tom and Simone divorce in 1995, Audrey disapproves of Simone's relationship with Justus Ward . The following year, Audrey is devastated when her beloved Steve dies of a heart attack. Audrey is comforted by Gail Baldwin , Monica Quartermaine , and Kevin Collins during this difficult time. Steve's death causes strain between Audrey and Tom, who believes the Cassadine family is responsible for bankrupting the hospital and causing stress that caused Steve's heart attack. Tom joins forces with Luke Spencer to bring the Cassadines down, but Audrey refuses to believe they are responsible. Tom eventually leaves town. In 1997, Audrey is attacked during a hostage crisis at General Hospital. Jeff's daughter, Sarah Webber , comes to help Audrey recover and moves in with her. Her younger sister Elizabeth Webber quickly follows and moves in as well. Elizabeth is raped on Valentine's Day in 1998, and Audrey tries to help her by telling her to move on. Sarah confronts Audrey about her attitude and Audrey reveals her own rape to Sarah and later Elizabeth. Elizabeth and Audrey become closer and go to therapy with Gail Baldwin to help each other. Audrey is upset when Elizabeth runs away with Lucky Spencer , but eventually accepts their relationship. Audrey consoles Elizabeth through Lucky's supposed death. Audrey stays extremely close with Elizabeth throughout the years and supports her through Lucky's return and brainwashing, Elizabeth's turbulent marriage to Ric Lansing , and her one-night stand with Zander Smith that results in Audrey's first great-grandchild Cameron . On the 10,000th episode that aired on April 17, 2002, the staff throws a surprise party for Audrey honoring her 10,000th shift as a nurse. Afterwards Audrey is seen sparingly, and officially retires from the Hospital in 2005. She returns for the wedding of Elizabeth and Lucky that October. When Elizabeth and Lucky separate in 2006, Elizabeth moves in with Audrey until they reconcile. In October 2009, Audrey is seen at Lucky and Elizabeth's engagement party. Audrey is referenced in off-screen activities as continuing to live in Port Charles, frequently interacting with her grandchildren and great-grandchildren and enjoying her life as a retiree . In April 2013, Audrey makes an on-screen appearance on what would have been Steve's 50th anniversary at General Hospital. Audrey talks with Elizabeth and they discuss Tom being in Africa, Elizabeth's parents being in Asia, and Tommy getting his medical degree. Audrey makes an appearance when she writes to her granddaughter, Elizabeth, for her upcoming wedding to Jake Doe/Jason Morgan . Audrey March arrives at General Hospital in 1964 to visit her sister, Lucille March ( Lucille Wall ). She is a registered nurse, who had forsaken the profession for that of an airline stewardess. After noticing Dr. Steve Hardy ( John Beradino ), the Chief of Internal Medicine at General Hospital, Audrey stays in town and becomes a private nurse. Eventually, Steve and Audrey get engaged, but Audrey breaks it off. She accepts a proposal from one of her clients, Randy Washborn. Audrey is diagnosed with lymphoma , and when Randy deserts her she gets back together with Steve. They marry in 1965 after she is recovered. Audrey later works on a book with Dr. Phil Brewer , but the experience ends badly when Phil tries to seduce her. Audrey becomes concerned when she does not conceive, and believing Steve is sterile, Audrey has herself artificially inseminated without Steve's knowledge and becomes pregnant. Audrey is in a car accident and miscarries; she is devastated and separates from Steve. She goes to Vietnam to help war orphans in March 1968. When Audrey returns from Vietnam in January 1969, she continues to push Steve away and after their divorce is final, she marries Tom Baldwin in an effort to prove that she is over Steve. Audrey cannot bring herself to sleep with Tom, and he ends up raping her. After becoming pregnant with Tom's child, Audrey files for divorce and leaves town, determined to protect her unborn child from her violent husband. She returns in 1971, and tells Lucille her son had died at birth. Audrey reconnects with Steve. It is revealed she is lying about her son, whom she named Steve and is in hiding. She plans to remarry Steve, and then convince him to adopt a baby which would be her son. However, Mrs. Peggy Nelson, the woman taking care of the baby, realizes the plan and blackmails Audrey. Peggy Nelson is murdered and Audrey is accused of the crime. Thanks to Steve, Audrey is acquitted. Tom reclaims baby Steve, who is renamed Tommy, forcing Audrey to resume their marriage. Tom kidnaps baby Tommy and flees to Mexico. Tom is later presumed dead and Tommy is returned to Audrey. During the kidnapping ordeal, Tommy had become ill with a heart ailment. Jim Hobart performs surgery and Tommy recovers. Audrey feels gratitude towards Jim and marries him after he injuries his hands and fears he cannot operate again. Audrey faces heartache as she still loves Steve and Jim turns to alcohol to deal with his injury. In 1976, Jim leaves Audrey for a younger woman. Audrey attempts suicide and Steve saves her. Steve proposes to Audrey and she accepts. Steve falls down a flight of stairs and Audrey helps him recuperate. They remarry, and Tom Baldwin returns alive, invalidating their marriage. Tom tries to reclaim Audrey and his son, but eventually gives up and leaves town. Steve and Audrey marry again in 1977 and Steve officially adopts Tommy, renamed Tom Hardy Meanwhile, Audrey had become head of student nurses at General Hospital, and as a result becomes a mentor to nurses such as Bobbie Spencer . Steve and Audrey become involved in various dramas involving the children of Steve's old friend Lars Webber, Terri, Rick and Jeff . Jeff ends up shooting himself, and when he is in the hospital, Terri tells Steve about a letter her mother, Helene, had told her about on her deathbed. Steve finds the letter and learns Jeff is actually his biological son (Steve had relationship with Helene during a time when she was separated from Lars). Steve tells Audrey and they agree to keep the truth a secret. In the winter of 1979, Port Charles is hit by an epidemic of Lassa Fever. General Hospital is placed under quarantine, and when Steve begins to fall victim to the disease, Audrey tells Jeff the truth. Steve recovers and both Rick and Jeff are angry at Steve and Audrey. It takes months for everyone to reconcile. Steve and Audrey are happy to learn that Jeff's son Steven Lars Webber is still alive. Jeff soon leaves town with his son to make a fresh start. Some years later, Tom leaves to attend college and returns in 1987. When Tom marries an African-American doctor, Simone Ravelle, Audrey fears her son's interracial marriage would not be accepted. In time, Audrey and Simone grow close. Simone confides in Audrey when she gets pregnant during an affair with Harrison and does not know who the father is. However, Audrey is relieved when Tom is confirmed to be the little Tommy 's father.In 1993, Audrey organizes a surprise party for Steve's 30th anniversary at General Hospital. Audrey is attacked by psychopath Ryan Chamberlain, who mistakes her for his abusive mother. Audrey quickly recovers and testifies against Ryan at his trial, causing him to be committed to a mental institution. When Tom and Simone divorce in 1995, Audrey disapproves of Simone's relationship with Justus Ward . The following year, Audrey is devastated when her beloved Steve dies of a heart attack. Audrey is comforted by Gail Baldwin , Monica Quartermaine , and Kevin Collins during this difficult time. Steve's death causes strain between Audrey and Tom, who believes the Cassadine family is responsible for bankrupting the hospital and causing stress that caused Steve's heart attack. Tom joins forces with Luke Spencer to bring the Cassadines down, but Audrey refuses to believe they are responsible. Tom eventually leaves town. In 1997, Audrey is attacked during a hostage crisis at General Hospital. Jeff's daughter, Sarah Webber , comes to help Audrey recover and moves in with her. Her younger sister Elizabeth Webber quickly follows and moves in as well. Elizabeth is raped on Valentine's Day in 1998, and Audrey tries to help her by telling her to move on. Sarah confronts Audrey about her attitude and Audrey reveals her own rape to Sarah and later Elizabeth. Elizabeth and Audrey become closer and go to therapy with Gail Baldwin to help each other. Audrey is upset when Elizabeth runs away with Lucky Spencer , but eventually accepts their relationship. Audrey consoles Elizabeth through Lucky's supposed death.Audrey stays extremely close with Elizabeth throughout the years and supports her through Lucky's return and brainwashing, Elizabeth's turbulent marriage to Ric Lansing , and her one-night stand with Zander Smith that results in Audrey's first great-grandchild Cameron . On the 10,000th episode that aired on April 17, 2002, the staff throws a surprise party for Audrey honoring her 10,000th shift as a nurse. Afterwards Audrey is seen sparingly, and officially retires from the Hospital in 2005. She returns for the wedding of Elizabeth and Lucky that October. When Elizabeth and Lucky separate in 2006, Elizabeth moves in with Audrey until they reconcile. In October 2009, Audrey is seen at Lucky and Elizabeth's engagement party. Audrey is referenced in off-screen activities as continuing to live in Port Charles, frequently interacting with her grandchildren and great-grandchildren and enjoying her life as a retiree . In April 2013, Audrey makes an on-screen appearance on what would have been Steve's 50th anniversary at General Hospital. Audrey talks with Elizabeth and they discuss Tom being in Africa, Elizabeth's parents being in Asia, and Tommy getting his medical degree. Audrey makes an appearance when she writes to her granddaughter, Elizabeth, for her upcoming wedding to Jake Doe/Jason Morgan . In the pre- Gloria Monty years of GH , Audrey was one of the leading characters of the show, and a 1971 storyline in which she was accused of murder sent General Hospital to the number one spot in the daytime ratings for the first time.
2,710
Wiki
Marburg
https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg/html
Marburg
Marburg ( German pronunciation: [ ˈmaːɐ̯bʊʁk ] or [ ˈmaʁbʊʁk ] ⓘ ) is a university town in the German federal state ( Bundesland ) of Hesse , capital of the Marburg-Biedenkopf district ( Landkreis ). The town area spreads along the valley of the river Lahn and has a population of approximately 76,000. Having been awarded town privileges in 1222, Marburg served as capital of the landgraviate of Hessen-Marburg during periods of the fifteenth to seventeenth centuries. The University of Marburg was founded in 1527 and dominates the public life in the town to this day. Marburg is a historic centre of the pharmaceutical industry in Germany, and there is a plant in the town (by BioNTech ) to produce vaccines to tackle Covid-19 . Like many settlements, Marburg developed at the crossroads of two important early medieval highways: the trade route linking Cologne and Prague and the trade route from the North Sea to the Alps and on to Italy , the former crossing the river Lahn here. A first mention of the settlement dates from 822 in the Reinhardsbrunner Chronik . The settlement was protected and customs were raised by a small castle built during the ninth or tenth century by the Giso. Marburg has been a town since 1140, as proven by coins. From the Gisos, it fell around that time to the Landgraves of Thuringia , residing on the Wartburg above Eisenach . In 1228, the widowed princess-landgravine of Thuringia, Elizabeth of Hungary , chose Marburg as her dowager seat, as she did not get along well with her brother-in-law, the new landgrave. The countess dedicated her life to the sick and would become after her early death in 1231, aged 24, one of the most prominent female saints of the era. She was canonized in 1235. In 1264, St Elizabeth's daughter Sophie of Brabant , succeeded in winning the Landgraviate of Hessen , hitherto connected to Thuringia , for her son Henry . Marburg (alongside Kassel ) was one of the capitals of Hessen from that time until about 1540. Following the first division of the landgraviate, it was the capital of Hessen-Marburg from 1485 to 1500 and again between 1567 and 1605. Hessen was one of the more powerful second-tier principalities in Germany. Its "old enemy" was the Archbishopric of Mainz , the seat of one of the prince-electors , who competed with Hessen in many wars and conflicts for coveted territory, stretching over several centuries. After 1605, Marburg became just another provincial town, known mostly for the University of Marburg . It became a virtual backwater for two centuries after the Thirty Years' War (1618–48), when it was fought over by Hessen-Darmstadt and Hesse-Kassel . The Hessian territory around Marburg lost more than two-thirds of its population, which was more than in any later wars (including World War I and World War II ) combined. Marburg is the seat of the oldest existing Protestant -founded university in the world, the University of Marburg (Philipps-Universität-Marburg), founded in 1527. It is one of the smaller "university towns" in Germany. These include Greifswald , Erlangen , Jena , and Tübingen , as well as the city of Gießen , which is located 30 km south of Marburg. In 1529, Philipp I of Hesse arranged the Marburg Colloquy , to propitiate Martin Luther and Huldrych Zwingli . Owing to its neglect during the entire 18th century, Marburg – like Rye or Chartres – survived as a relatively intact Gothic town, simply because there was no money spent on any new architecture or expansion. When Romanticism became the dominant cultural and artistic paradigm in Germany, Marburg became a centre of activities once again, and many of the leaders of the movement lived, taught, or studied in Marburg. They formed a circle of friends that was of great importance, especially in literature , philology , folklore , and law . The group included Friedrich Carl von Savigny , the most important jurist of his day and father of the Roman Law adaptation in Germany, as well as the poets, writers, and social activists Achim von Arnim , Clemens Brentano , and especially Bettina von Arnim , Clemens Brentano's sister, who became Achim von Arnim's wife. Most famous internationally, however, were the Brothers Grimm , who collected many of their fairy tales here. The best-known illustrations for the fairy tale editions are by the painter Otto Ubbelohde , who also lived in and near Marburg. The original building inspiring his drawing Rapunzel 's Tower stands in Amönau near Marburg. Across the Lahn hills, in the area called Schwalm, the costumes of little girls included a red hood. In the Austro-Prussian War of 1866, the Prince-elector of Hessen had backed Austria . Prussia won and took the opportunity to invade and annex the Electorate of Hessen (as well as Hanover , the city of Frankfurt , and other territories) north of the Main River. However, the pro-Austrian Hesse-Darmstadt remained independent. For Marburg, this turn of events was very positive, because Prussia decided to make Marburg its main administrative centre in this part of the new province Hessen-Nassau and to turn the University of Marburg into the regional academic centre. Thus, Marburg's rise as an administrative and university city began. As the Prussian university system was one of the best in the world at the time, Marburg attracted many respected scholars. However, there was hardly any industry to speak of, so students, professors, and civil servants – who generally had enough but not much money and paid very little in taxes – dominated the town. Franz von Papen , vice-chancellor of Germany in 1934, delivered an anti-Nazi speech at the University of Marburg on 17 June. [ citation needed ] From 1942 to 1945, the whole city of Marburg was turned into a hospital, with schools and government buildings turned into wards to augment the existing hospitals. By the spring of 1945, there were over 20,000 patients – mostly wounded German soldiers. As a result of its designation as a hospital city, and because of a lack of important industrial sites, there was not much damage from bombings except along the railroad tracks. [ citation needed ] In May 1945, the Monuments men officer Walker Hancock set up the first so-called Central Collecting Point in the Marburg State Archives. But since the capacity of the archive building was not sufficient to store the many objects and since other collecting points, for example in Munich , had been set up in the American occupation zone in the meantime, the Marburg facility was closed after more than a year in favor of the Wiesbaden Collecting Point. With the relocation of the sarcophagus of Field Marshal and President Paul von Hindenburg (1847-1934) to the Elisabethkirche in August 1946 the project ended. [ citation needed ] Post-war developments included a population growth first due to war refugees, then to increasing significance of the pharmaceutical industry based in Marburg, and an increase in staff and students for the university. The historic town was in danger of thorough decay, but was renovated from 1972. The university now has about 21 000 students (2023). Like many settlements, Marburg developed at the crossroads of two important early medieval highways: the trade route linking Cologne and Prague and the trade route from the North Sea to the Alps and on to Italy , the former crossing the river Lahn here. A first mention of the settlement dates from 822 in the Reinhardsbrunner Chronik . The settlement was protected and customs were raised by a small castle built during the ninth or tenth century by the Giso. Marburg has been a town since 1140, as proven by coins. From the Gisos, it fell around that time to the Landgraves of Thuringia , residing on the Wartburg above Eisenach .In 1228, the widowed princess-landgravine of Thuringia, Elizabeth of Hungary , chose Marburg as her dowager seat, as she did not get along well with her brother-in-law, the new landgrave. The countess dedicated her life to the sick and would become after her early death in 1231, aged 24, one of the most prominent female saints of the era. She was canonized in 1235. In 1264, St Elizabeth's daughter Sophie of Brabant , succeeded in winning the Landgraviate of Hessen , hitherto connected to Thuringia , for her son Henry . Marburg (alongside Kassel ) was one of the capitals of Hessen from that time until about 1540. Following the first division of the landgraviate, it was the capital of Hessen-Marburg from 1485 to 1500 and again between 1567 and 1605. Hessen was one of the more powerful second-tier principalities in Germany. Its "old enemy" was the Archbishopric of Mainz , the seat of one of the prince-electors , who competed with Hessen in many wars and conflicts for coveted territory, stretching over several centuries. After 1605, Marburg became just another provincial town, known mostly for the University of Marburg . It became a virtual backwater for two centuries after the Thirty Years' War (1618–48), when it was fought over by Hessen-Darmstadt and Hesse-Kassel . The Hessian territory around Marburg lost more than two-thirds of its population, which was more than in any later wars (including World War I and World War II ) combined.Marburg is the seat of the oldest existing Protestant -founded university in the world, the University of Marburg (Philipps-Universität-Marburg), founded in 1527. It is one of the smaller "university towns" in Germany. These include Greifswald , Erlangen , Jena , and Tübingen , as well as the city of Gießen , which is located 30 km south of Marburg. In 1529, Philipp I of Hesse arranged the Marburg Colloquy , to propitiate Martin Luther and Huldrych Zwingli .Owing to its neglect during the entire 18th century, Marburg – like Rye or Chartres – survived as a relatively intact Gothic town, simply because there was no money spent on any new architecture or expansion. When Romanticism became the dominant cultural and artistic paradigm in Germany, Marburg became a centre of activities once again, and many of the leaders of the movement lived, taught, or studied in Marburg. They formed a circle of friends that was of great importance, especially in literature , philology , folklore , and law . The group included Friedrich Carl von Savigny , the most important jurist of his day and father of the Roman Law adaptation in Germany, as well as the poets, writers, and social activists Achim von Arnim , Clemens Brentano , and especially Bettina von Arnim , Clemens Brentano's sister, who became Achim von Arnim's wife. Most famous internationally, however, were the Brothers Grimm , who collected many of their fairy tales here. The best-known illustrations for the fairy tale editions are by the painter Otto Ubbelohde , who also lived in and near Marburg. The original building inspiring his drawing Rapunzel 's Tower stands in Amönau near Marburg. Across the Lahn hills, in the area called Schwalm, the costumes of little girls included a red hood.In the Austro-Prussian War of 1866, the Prince-elector of Hessen had backed Austria . Prussia won and took the opportunity to invade and annex the Electorate of Hessen (as well as Hanover , the city of Frankfurt , and other territories) north of the Main River. However, the pro-Austrian Hesse-Darmstadt remained independent. For Marburg, this turn of events was very positive, because Prussia decided to make Marburg its main administrative centre in this part of the new province Hessen-Nassau and to turn the University of Marburg into the regional academic centre. Thus, Marburg's rise as an administrative and university city began. As the Prussian university system was one of the best in the world at the time, Marburg attracted many respected scholars. However, there was hardly any industry to speak of, so students, professors, and civil servants – who generally had enough but not much money and paid very little in taxes – dominated the town.Franz von Papen , vice-chancellor of Germany in 1934, delivered an anti-Nazi speech at the University of Marburg on 17 June. [ citation needed ] From 1942 to 1945, the whole city of Marburg was turned into a hospital, with schools and government buildings turned into wards to augment the existing hospitals. By the spring of 1945, there were over 20,000 patients – mostly wounded German soldiers. As a result of its designation as a hospital city, and because of a lack of important industrial sites, there was not much damage from bombings except along the railroad tracks. [ citation needed ] In May 1945, the Monuments men officer Walker Hancock set up the first so-called Central Collecting Point in the Marburg State Archives. But since the capacity of the archive building was not sufficient to store the many objects and since other collecting points, for example in Munich , had been set up in the American occupation zone in the meantime, the Marburg facility was closed after more than a year in favor of the Wiesbaden Collecting Point. With the relocation of the sarcophagus of Field Marshal and President Paul von Hindenburg (1847-1934) to the Elisabethkirche in August 1946 the project ended. [ citation needed ]Post-war developments included a population growth first due to war refugees, then to increasing significance of the pharmaceutical industry based in Marburg, and an increase in staff and students for the university. The historic town was in danger of thorough decay, but was renovated from 1972. The university now has about 21 000 students (2023). Marburg lies on the river Lahn , 25 km north of Gießen . The federal road Bundesstraße 3 connects it with Gießen and Kassel . It is served by Marburg (Lahn) station (long-distance and local trains) and Marburg Süd station (local trains). The city is divided into the following 25 boroughs ( Ortsbezirke ): As a larger mid-sized city, Marburg, like six other such cities in Hessen, has a special status as compared to the other municipalities in the district. This means that the city takes on tasks more usually performed by the district so that in many ways it is comparable to an urban district ( kreisfreie Stadt ). Before 1974, the city was a district-free city. The mayor of Marburg , Thomas Spies, in office since December 2015, and his predecessor Egon Vaupel (directly elected in January 2005), are members of the Social Democratic Party of Germany . His deputy, the head of the building and youth departments, Nadine Bernshausen, is from Alliance '90/The Greens . Following the city parlament elections of March 2021, the majority in the 59-seat city parliament is held by a coalition of Green party (15 seats), SPD (14 seats) and Klimaliste (4 seats) members. Also represented are the factions of the Christian Democratic Union (13 seats), The Left (7 seats), the Free Democratic Party (2 seats), a CDU splinter group MBL ( Marburger Bürgerliste – 2 seats), the BfM ( Bürger für Marburg – 2 seats), Alternative für Deutschland (1 seat), and the Pirate Party (1 seat). Among the left wing groups are ATTAC , the Worldshop movement, an autonomist - anarchist scene, and a few groups engaged in ecological or human-rights concerns. The city of Marburg, similar to the cities of Heidelberg , Tübingen and Göttingen , has a rich history of student fraternities or Verbindungen of various sorts, including Corps, Landsmannschaften, Burschenschaften, Turnierschaften, etc.Marburg is twinned with: Marburg's coat of arms shows a Hessian landgrave riding a white horse with a flag and a shield on a red background. The shield shows the red-and-white-striped Hessian lion, also to be seen on Hessen's state arms, and the flag shows a stylized M, blue on gold (or yellow). The arms are also the source of the city flag's colors. The flag has three horizontal stripes colored, from top to bottom, red (from the background), white (from the horse) and blue (from the shield). The coat of arms, which was designed in the late nineteenth century, is based on a landgrave seal on a municipal document. It is an example of a very prevalent practice of replacing forgotten coats of arms, or ones deemed not to be representative enough, with motifs taken from seals.The city's name is connected to a filovirus , the Marburg virus , because this disease , a viral hemorrhagic fever resembling ebola , was first recognized and described during an outbreak in the city. In 1967, workers were accidentally exposed to infected green monkey tissue at the city's former industrial plant, the Behring-Werke, then part of Hoechst and today of CSL Behring , founded by Marburg citizen and first Nobel Prize in Medicine winner, Emil Adolf von Behring . During the outbreak, 31 people became infected and seven of them died. The virus is named after the city following the custom of naming viruses after the location of their first recorded outbreak.Many homes have solar panels and in 2008 a law was passed to make the installation of solar systems on new buildings or as part of renovation projects mandatory. 20 percent of heating system requirements ought to have been covered by solar energy in new buildings. Anyone who fails to install solar panels would have been fined €1,000. The new law, approved on 20 June 2008, should have taken effect in October 2008, however, this law was stopped by the Regierungspräsidium Giessen in September 2008. Marburg remains a relatively unspoilt, spire-dominated, castle-crowned Gothic or Renaissance city on a hill partly because it was isolated between 1600 and 1850. Architecturally, it is famous both for its castle Marburger Schloss and its medieval churches. The Elisabethkirche , as one of the two or three first purely Gothic churches north of the Alps outside France, is an archetype of Gothic architecture in Germany. Much of the physical attractiveness of Marburg is due to Hanno Drechsler who was Lord Mayor between 1970 and 1992. He promoted urban renewal, the restoration of the Oberstadt (uptown), and he established one of the first pedestrian zones in Germany. Marburg's Altstadtsanierung (since 1972) has received many awards and prizes. Parks in the town include the Old Botanical Garden , as well as the new Botanical Garden outside the town proper. The Marktplatz is the heart of Marburg's old town. In the center is a fountain dedicated to St Georg, a popular meeting place for the youths. To the south is the old town hall and the path running north leads to the palace overlooking the town. The University of Marburg , founded in 1527, is one of Germany's oldest universities. It is spread over two campuses: Firmanei at the centre of Marburg, and Lahnberge to the east of the town at the Botanischer Garten (Botanical Garden).
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Marburg Files
The Marburg Files , also known as the Windsor Files or Duke of Windsor Files , are a series of top-secret documents discovered in Germany during May 1945 near the Harz Mountains and compiled at Marburg Castle , Hesse . As American troops were traveling through the outskirts of Degenershausen Estate , they found large numbers of abandoned or destroyed German military vehicles scattered along the side roads, with some containing various archives from the Nazi government . First Lieutenant David Silberberg initially discovered documents signed by the foreign minister of Nazi Germany, Joachim von Ribbentrop , and returned to Degenershausen to study further the background of his findings. After being advised of the locations of Meisdorf House and Marburg Castle, he escorted intelligence officers to the sites where a number of additional items were discovered. During this time, American troops arrested a German soldier named Karl von Loesch, an assistant to Hitler's personal translator Paul-Otto Schmidt , as he was retreating from Treffurt , near Eisenach . Schmidt had instructed him to destroy all the top-secret papers which he had placed in archives. Von Loesch destroyed the majority, but privately decided to keep some, and interred them in the grounds near the outskirts of Marburg. He was subsequently, by chance, introduced to Lieutenant Colonel R. C. Thomson, chief of the British documents team, and offered to lead Thomson's team to the location of the buried correspondence in exchange for immunity from prosecution . Around 400 tonnes of material was exhumed by the United States military and transported to Marburg Castle for review. Upon inspection, at least 60 documents appeared to contain correspondence between the Duke of Windsor and the Nazi German high command. American diplomats examined the contents before relaying a mix of original drafts and replicas to the British government. UK Prime Minister Winston Churchill discussed the files with King George VI , who insisted the files be suppressed and never released to the public. The entire collection was sent to the United Kingdom in 1948 and housed at Whaddon Hall , Buckinghamshire . The papers and correspondence discovered are alleged to have further detailed a plot by the Nazis, titled Operation Willi and orchestrated in 1940, to persuade the Duke of Windsor to officially join sides with the Nazis and move him to Germany in a bid to bring the UK to peace negotiations. It proposed convincing the Duke of a fictitious plot by King George VI and Prime Minister Winston Churchill to have him assassinated upon his arrival in The Bahamas , and conspiring with him to stage a kidnapping in the hope of blackmailing the monarchy and the UK into surrender. The papers are also alleged to reveal a plan to reinstate the Duke as king and recognise his wife, Wallis Simpson , as queen, in exchange for Nazi forces being given free movement across Europe . Documents considered the most damning for the British royal family were among his final communications with the Nazis before his departure to the Bahamas, in which it has been alleged the Duke encouraged relentless bombing attacks on the United Kingdom in a bid to force the British government to begin peace negotiations. There is not believed to be any form of evidence that the Duke accepted any terms offered by the Nazis in a bid to co-operate with Operation Willi, with historians stating he was initially more impressed by the encouragement he had from the British government to become Governor of the Bahamas , but some documents are alleged to confirm he sympathised with Nazi ideologies. British, French and American historians initially agreed to work together from 1946 in hope of releasing only documents that they felt were essential to release. A small batch was released in 1954, before the entire volume was forced into publication in 1957 with further files released in 1996 at the Public Record Office in Kew . The release of the files was reported to have caused the Duke considerable annoyance. The Marburg Files are the main subject and focus of the episode " Vergangenheit " ("Past") of the Netflix television series The Crown , which depicts Queen Elizabeth II 's initial review of the documents. The episode's director Philippa Lowthorpe has stated that replicas of genuine files were used during filming. Despite confirming that Queen Elizabeth did condemn the Duke, historian Hugo Vickers has suggested that the episode falsely implies that the Duke was banished from the royal family upon release of the Marburg Files. He remained in contact with his family and public appearances continued.
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Marburg virus disease
Marburg virus disease ( MVD ; formerly Marburg hemorrhagic fever ) is a viral hemorrhagic fever in human and non-human primates caused by either of the two Marburgviruses : Marburg virus (MARV) and Ravn virus (RAVV). Its clinical symptoms are very similar to those of Ebola virus disease (EVD). Egyptian fruit bats are believed to be the normal carrier in nature and Marburg virus RNA has been isolated from them. The most detailed study on the frequency, onset, and duration of MVD clinical signs and symptoms was performed during the 1998–2000 mixed MARV/RAVV disease outbreak. A skin rash , red or purple spots (e.g. petechiae or purpura ), bruises , and hematomas (especially around needle injection sites) are typical hemorrhagic manifestations. However, contrary to popular belief, hemorrhage does not lead to hypovolemia and is not the cause of death (total blood loss is minimal except during labor ). Instead, death occurs due to multiple organ dysfunction syndrome (MODS) due to fluid redistribution, hypotension , disseminated intravascular coagulation , and focal tissue necroses . Clinical phases of Marburg hemorrhagic fever's presentation are described below. Note that phases overlap due to variability between cases.MVD is caused by two viruses; Marburg virus (MARV) and Ravn virus (RAVV) , family Filoviridae. : 458 Marburgviruses are endemic in arid woodlands of equatorial Africa . Most marburgvirus infections were repeatedly associated with people visiting natural caves or working in mines . In 2009, the successful isolation of infectious MARV and RAVV was reported from healthy Egyptian fruit bat caught in caves. This isolation strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses and that visiting bat-infested caves is a risk factor for acquiring marburgvirus infections. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. Another risk factor is contact with nonhuman primates, although only one outbreak of MVD (in 1967) was due to contact with infected monkeys. Contrary to Ebola virus disease (EVD) , which has been associated with heavy rains after long periods of dry weather, triggering factors for spillover of marburgviruses into the human population have not yet been described.MVD is clinically indistinguishable from Ebola virus disease (EVD) , and it can also easily be confused with many other diseases prevalent in Equatorial Africa , such as other viral hemorrhagic fevers , falciparum malaria , typhoid fever , shigellosis , rickettsial diseases such as typhus , cholera , gram-negative sepsis , borreliosis such as relapsing fever or EHEC enteritis . Other infectious diseases that ought to be included in the differential diagnosis include leptospirosis , scrub typhus , plague , Q fever , candidiasis , histoplasmosis , trypanosomiasis , visceral leishmaniasis , hemorrhagic smallpox , measles , and fulminant viral hepatitis . Non-infectious diseases that can be confused with MVD are acute promyelocytic leukemia , hemolytic uremic syndrome , snake envenomation , clotting factor deficiencies/platelet disorders, thrombotic thrombocytopenic purpura , hereditary hemorrhagic telangiectasia , Kawasaki disease , and even warfarin intoxication. The most important indicator that may lead to the suspicion of MVD at clinical examination is the medical history of the patient, in particular the travel and occupational history (which countries and caves were visited?) and the patient's exposure to wildlife (exposure to bats or bat excrements?). MVD can be confirmed by isolation of marburgviruses from or by detection of marburgvirus antigen or genomic or subgenomic RNAs in patient blood or serum samples during the acute phase of MVD. Marburgvirus isolation is usually performed by inoculation of grivet kidney epithelial Vero E6 or MA-104 cell cultures or by inoculation of human adrenal carcinoma SW-13 cells, all of which react to infection with characteristic cytopathic effects . Filovirions can easily be visualized and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot differentiate the various filoviruses alone despite some overall length differences. Immunofluorescence assays are used to confirm marburgvirus presence in cell cultures. During an outbreak, virus isolation and electron microscopy are most often not feasible options. The most common diagnostic methods are therefore RT-PCR in conjunction with antigen-capture ELISA , which can be performed in field or mobile hospitals and laboratories. Indirect immunofluorescence assays (IFAs) are not used for diagnosis of MVD in the field anymore. [ citation needed ] Marburg virus disease (MVD) is the official name listed in the World Health Organization 's International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). In the scientific literature, Marburg hemorrhagic fever (MHF) is often used as an unofficial alternative name for the same disease. Both disease names are derived from the German city Marburg , where MARV was first discovered. Marburg virus disease (MVD) is the official name listed in the World Health Organization 's International Statistical Classification of Diseases and Related Health Problems 10 (ICD-10) for the human disease caused by any of the two marburgviruses Marburg virus (MARV) and Ravn virus (RAVV). In the scientific literature, Marburg hemorrhagic fever (MHF) is often used as an unofficial alternative name for the same disease. Both disease names are derived from the German city Marburg , where MARV was first discovered. The details of the initial transmission of MVD to humans remain incompletely understood. Transmission most likely occurs from Egyptian fruit bats or another natural host, such as non-human primates or through the consumption of bushmeat , but the specific routes and body fluids involved are unknown. Human-to-human transmission of MVD occurs through direct contact with infected bodily fluids such as blood. Transmission events are relatively rare – there have been only 11 recorded outbreaks of MARV between 1975 and 2011, with one event involving both MARV and RAVV. There are currently no Food and Drug Administration -approved vaccines for the prevention of MVD. Many candidate vaccines have been developed and tested in various animal models. Of those, the most promising ones are DNA vaccines or based on Venezuelan equine encephalitis virus replicons , vesicular stomatitis Indiana virus (VSIV) or filovirus-like particles (VLPs) as all of these candidates could protect nonhuman primates from marburgvirus-induced disease. DNA vaccines have entered clinical trials. Marburgviruses are highly infectious , but not very contagious . They do not get transmitted by aerosol during natural MVD outbreaks. Due to the absence of an approved vaccine, prevention of MVD therefore relies predominantly on quarantine of confirmed or high probability cases, proper personal protective equipment , and sterilization and disinfection . [ citation needed ] The natural maintenance hosts of marburgviruses remain to be identified unequivocally. However, the isolation of both MARV and RAVV from bats and the association of several MVD outbreaks with bat-infested mines or caves strongly suggests that bats are involved in Marburg virus transmission to humans. Avoidance of contact with bats and abstaining from visits to caves is highly recommended, but may not be possible for those working in mines or people dependent on bats as a food source. [ citation needed ] Since marburgviruses are not spread via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids , and any possibly contaminated materials and utensils. Patients should be isolated, but still are safe to be visited by family members. Medical staff should be trained in and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified, ideally with the help of local traditional healers . Marburgviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment , laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.The natural maintenance hosts of marburgviruses remain to be identified unequivocally. However, the isolation of both MARV and RAVV from bats and the association of several MVD outbreaks with bat-infested mines or caves strongly suggests that bats are involved in Marburg virus transmission to humans. Avoidance of contact with bats and abstaining from visits to caves is highly recommended, but may not be possible for those working in mines or people dependent on bats as a food source. [ citation needed ]Since marburgviruses are not spread via aerosol, the most straightforward prevention method during MVD outbreaks is to avoid direct (skin-to-skin) contact with patients, their excretions and body fluids , and any possibly contaminated materials and utensils. Patients should be isolated, but still are safe to be visited by family members. Medical staff should be trained in and apply strict barrier nursing techniques (disposable face mask, gloves, goggles, and a gown at all times). Traditional burial rituals, especially those requiring embalming of bodies, should be discouraged or modified, ideally with the help of local traditional healers . Marburgviruses are World Health Organization Risk Group 4 Pathogens, requiring Biosafety Level 4-equivalent containment , laboratory researchers have to be properly trained in BSL-4 practices and wear proper personal protective equipment.There is currently no effective marburgvirus-specific therapy for MVD. Treatment is primarily supportive in nature and includes minimizing invasive procedures, balancing fluids and electrolytes to counter dehydration , administration of anticoagulants early in infection to prevent or control disseminated intravascular coagulation , administration of procoagulants late in infection to control hemorrhaging , maintaining oxygen levels, pain management , and administration of antibiotics or antifungals to treat secondary infections. Although supportive care can improve survival chances, marburg virus disease is fatal in the majority of cases. As of 2023 [ update ] the case fatality rate was assessed to be 61.9%. The WHO identifies marburg virus disease as having pandemic potential. Below is a table of outbreaks concerning MVD from 1967 to 2023: MVD was first documented in 1967, when 31 people became ill in the German towns of Marburg and Frankfurt am Main , and in Belgrade , Yugoslavia . The outbreak involved 25 primary MARV infections and seven deaths, and six nonlethal secondary cases. The outbreak was traced to infected grivets (species Chlorocebus aethiops ) imported from an undisclosed location in Uganda and used in developing poliomyelitis vaccines . The monkeys were received by Behringwerke, a Marburg company founded by the first winner of the Nobel Prize in Medicine , Emil von Behring . The company, which at the time was owned by Hoechst , was originally set up to develop sera against tetanus and diphtheria . Primary infections occurred in Behringwerke laboratory staff while working with grivet tissues or tissue cultures without adequate personal protective equipment . Secondary cases involved two physicians , a nurse , a post-mortem attendant, and the wife of a veterinarian . All secondary cases had direct contact, usually involving blood, with a primary case. Both physicians became infected through accidental skin pricks when drawing blood from patients. In 1975, an Australian tourist became infected with MARV in Rhodesia (today Zimbabwe ). He died in a hospital in Johannesburg , South Africa . His girlfriend and an attending nurse were subsequently infected with MVD, but survived. A case of MARV infection occurred in 1980 in Kenya . A French man, who worked as an electrical engineer in a sugar factory in Nzoia (close to Bungoma ) at the base of Mount Elgon (which contains Kitum Cave ), became infected by unknown means and died on 15 January shortly after admission to Nairobi Hospital. The attending physician contracted MVD, but survived. A popular science account of these cases can be found in Richard Preston 's book The Hot Zone (the French man is referred to under the pseudonym "Charles Monet", whereas the physician is identified under his real name, Shem Musoke). In 1987, a single lethal case of RAVV infection occurred in a 15-year-old Danish boy, who spent his vacation in Kisumu , Kenya . He had visited Kitum Cave on Mount Elgon prior to travelling to Mombasa , where he developed clinical signs of infection. The boy died after transfer to Nairobi Hospital. A popular science account of this case can be found in Richard Preston 's book The Hot Zone (the boy is referred to under the pseudonym "Peter Cardinal"). In 1988, researcher Nikolai Ustinov infected himself lethally with MARV after accidentally pricking himself with a syringe used for inoculation of guinea pigs . The accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor" ) in Koltsovo , USSR (today Russia ). Very little information is publicly available about this MVD case because Ustinov's experiments were classified. A popular science account of this case can be found in Ken Alibek 's book Biohazard . Another laboratory accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor" ) in Koltsovo , USSR , when a scientist contracted MARV by unknown means. A major MVD outbreak occurred among illegal gold miners around Goroumbwa mine in Durba and Watsa , Democratic Republic of Congo from 1998 to 2000, when co-circulating MARV and RAVV caused 154 cases of MVD and 128 deaths. The outbreak ended with the flooding of the mine. In early 2005, the World Health Organization (WHO) began investigating an outbreak of viral hemorrhagic fever in Angola , which was centered in the northeastern Uíge Province but also affected many other provinces. The Angolan government had to ask for international assistance, pointing out that there were only approximately 1,200 doctors in the entire country, with some provinces having as few as two. Health care workers also complained about a shortage of personal protective equipment such as gloves, gowns, and masks. Médecins Sans Frontières (MSF) reported that when their team arrived at the provincial hospital at the center of the outbreak, they found it operating without water and electricity . Contact tracing was complicated by the fact that the country's roads and other infrastructure were devastated after nearly three decades of civil war and the countryside remained littered with land mines . Americo Boa Vida Hospital in the Angolan capital Luanda set up a special isolation ward to treat infected people from the countryside. Unfortunately, because MVD often results in death, some people came to view hospitals and medical workers with suspicion and treated helpers with hostility. For instance, a specially-equipped isolation ward at the provincial hospital in Uíge was reported to be empty during much of the epidemic, even though the facility was at the center of the outbreak. WHO was forced to implement what it described as a "harm reduction strategy", which entailed distributing disinfectants to affected families who refused hospital care. Of the 252 people who contracted MVD during outbreak, 227 died. In 2007, four miners became infected with marburgviruses in Kamwenge District , Uganda . The first case, a 29-year-old man, became symptomatic on July 4, 2007, was admitted to a hospital on July 7, and died on July 13. Contact tracing revealed that the man had had prolonged close contact with two colleagues (a 22-year-old man and a 23-year-old man), who experienced clinical signs of infection before his disease onset. Both men had been admitted to hospitals in June and survived their infections, which were proven to be due to MARV. A fourth, 25-year-old man, developed MVD clinical signs in September and was shown to be infected with RAVV. He also survived the infection. On July 10, 2008, the Netherlands National Institute for Public Health and the Environment reported that a 41-year-old Dutch woman, who had visited Python Cave in Maramagambo Forest during her holiday in Uganda , had MVD due to MARV infection, and had been admitted to a hospital in the Netherlands . The woman died under treatment in the Leiden University Medical Centre in Leiden on July 11. The Ugandan Ministry of Health closed the cave after this case. On January 9 of that year an infectious diseases physician notified the Colorado Department of Public Health and the Environment that a 44-year-old American woman who had returned from Uganda had been hospitalized with a fever of unknown origin . At the time, serologic testing was negative for viral hemorrhagic fever . She was discharged on January 19, 2008. After the death of the Dutch patient and the discovery that the American woman had visited Python Cave, further testing confirmed the patient demonstrated MARV antibodies and RNA . In October 2017 an outbreak of Marburg virus disease was detected in Kween District , Eastern Uganda. All three initial cases (belonging to one family – two brothers and one sister) had died by 3 November. The fourth case – a health care worker – developed symptoms on 4 November and was admitted to a hospital. The first confirmed case traveled to Kenya before the death. A close contact of the second confirmed case traveled to Kampala . It is reported that several hundred people may have been exposed to infection. In August 2021, two months after the re-emergent Ebola epidemic in the Guéckédou prefecture was declared over, a case of the Marburg disease was confirmed by health authorities through laboratory analysis. Other potential case of the disease in a contact awaits official results. This was the first case of the Marburg hemorrhagic fever confirmed to happen in West Africa. The case of Marburg also has been identified in Guéckédou . During the outbreak, a total of one confirmed case, who died ( CFR =100%), and 173 contacts were identified, including 14 high-risk contacts based on exposure. Among them, 172 were followed for a period of 21 days, of which none developed symptoms. One high-risk contact was lost to follow up. Sequencing of an isolate from the Guinean patient showed that this outbreak was caused by the Angola-like Marburg virus. A colony of Egyptian rousettus bats ( reservoir host of Marburg virus ) was found in close proximity (4.5 km) to the village, where the Marburg virus disease outbreak emerged in 2021. Two sampled fruit bats from this colony were PCR-positive on the Marburg virus. In July 2022, preliminary analysis of samples taken from two patients – both deceased – in Ghana indicated the cases were positive for Marburg. However, per standard procedure, the samples were sent to the Pasteur Institute of Dakar for confirmation. On 17 July 2022 the two cases were confirmed by Ghana, which caused the country to declare a Marburg virus disease outbreak. An additional case was identified, bringing the total to three. A disease outbreak was first reported in Equatorial Guinea on 7 February 2023, and on 13 February 2023, it was identified as being Marburg virus disease. It was the first time the disease was detected in the country. Neighbouring Cameroon detected two suspected cases of Marburg virus disease on 13 February 2023, but they were later ruled out. On 25 February, a suspected case of Marburg was reported in the Spanish city of Valencia , however this case was subsequently discounted. As of 4 April 2023, there were 14 confirmed cases and 28 suspected cases, including ten confirmed deaths from the disease in Equatorial Guinea. On 8 June 2023, the World Health Organization declared the outbreak over. In total, 17 laboratory-confirmed cases and 12 deaths were recorded. All the 23 probable cases reportedly died. Four patients recovered from the virus and have been enrolled in a survivors programme to receive psychosocial and other post-recovery support. A Marburg virus disease outbreak in Tanzania was first reported on 21 March 2023 by the Ministry of Health of Tanzania. This was the first time that Tanzania had reported an outbreak of the disease. On 2 June 2023, Tanzania declared the outbreak over. There were 9 total infections, resulting in 6 total deaths. The WHO identifies marburg virus disease as having pandemic potential. Below is a table of outbreaks concerning MVD from 1967 to 2023:MVD was first documented in 1967, when 31 people became ill in the German towns of Marburg and Frankfurt am Main , and in Belgrade , Yugoslavia . The outbreak involved 25 primary MARV infections and seven deaths, and six nonlethal secondary cases. The outbreak was traced to infected grivets (species Chlorocebus aethiops ) imported from an undisclosed location in Uganda and used in developing poliomyelitis vaccines . The monkeys were received by Behringwerke, a Marburg company founded by the first winner of the Nobel Prize in Medicine , Emil von Behring . The company, which at the time was owned by Hoechst , was originally set up to develop sera against tetanus and diphtheria . Primary infections occurred in Behringwerke laboratory staff while working with grivet tissues or tissue cultures without adequate personal protective equipment . Secondary cases involved two physicians , a nurse , a post-mortem attendant, and the wife of a veterinarian . All secondary cases had direct contact, usually involving blood, with a primary case. Both physicians became infected through accidental skin pricks when drawing blood from patients. In 1975, an Australian tourist became infected with MARV in Rhodesia (today Zimbabwe ). He died in a hospital in Johannesburg , South Africa . His girlfriend and an attending nurse were subsequently infected with MVD, but survived. A case of MARV infection occurred in 1980 in Kenya . A French man, who worked as an electrical engineer in a sugar factory in Nzoia (close to Bungoma ) at the base of Mount Elgon (which contains Kitum Cave ), became infected by unknown means and died on 15 January shortly after admission to Nairobi Hospital. The attending physician contracted MVD, but survived. A popular science account of these cases can be found in Richard Preston 's book The Hot Zone (the French man is referred to under the pseudonym "Charles Monet", whereas the physician is identified under his real name, Shem Musoke). In 1987, a single lethal case of RAVV infection occurred in a 15-year-old Danish boy, who spent his vacation in Kisumu , Kenya . He had visited Kitum Cave on Mount Elgon prior to travelling to Mombasa , where he developed clinical signs of infection. The boy died after transfer to Nairobi Hospital. A popular science account of this case can be found in Richard Preston 's book The Hot Zone (the boy is referred to under the pseudonym "Peter Cardinal"). In 1988, researcher Nikolai Ustinov infected himself lethally with MARV after accidentally pricking himself with a syringe used for inoculation of guinea pigs . The accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor" ) in Koltsovo , USSR (today Russia ). Very little information is publicly available about this MVD case because Ustinov's experiments were classified. A popular science account of this case can be found in Ken Alibek 's book Biohazard . Another laboratory accident occurred at the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor" ) in Koltsovo , USSR , when a scientist contracted MARV by unknown means. A major MVD outbreak occurred among illegal gold miners around Goroumbwa mine in Durba and Watsa , Democratic Republic of Congo from 1998 to 2000, when co-circulating MARV and RAVV caused 154 cases of MVD and 128 deaths. The outbreak ended with the flooding of the mine. In early 2005, the World Health Organization (WHO) began investigating an outbreak of viral hemorrhagic fever in Angola , which was centered in the northeastern Uíge Province but also affected many other provinces. The Angolan government had to ask for international assistance, pointing out that there were only approximately 1,200 doctors in the entire country, with some provinces having as few as two. Health care workers also complained about a shortage of personal protective equipment such as gloves, gowns, and masks. Médecins Sans Frontières (MSF) reported that when their team arrived at the provincial hospital at the center of the outbreak, they found it operating without water and electricity . Contact tracing was complicated by the fact that the country's roads and other infrastructure were devastated after nearly three decades of civil war and the countryside remained littered with land mines . Americo Boa Vida Hospital in the Angolan capital Luanda set up a special isolation ward to treat infected people from the countryside. Unfortunately, because MVD often results in death, some people came to view hospitals and medical workers with suspicion and treated helpers with hostility. For instance, a specially-equipped isolation ward at the provincial hospital in Uíge was reported to be empty during much of the epidemic, even though the facility was at the center of the outbreak. WHO was forced to implement what it described as a "harm reduction strategy", which entailed distributing disinfectants to affected families who refused hospital care. Of the 252 people who contracted MVD during outbreak, 227 died. In 2007, four miners became infected with marburgviruses in Kamwenge District , Uganda . The first case, a 29-year-old man, became symptomatic on July 4, 2007, was admitted to a hospital on July 7, and died on July 13. Contact tracing revealed that the man had had prolonged close contact with two colleagues (a 22-year-old man and a 23-year-old man), who experienced clinical signs of infection before his disease onset. Both men had been admitted to hospitals in June and survived their infections, which were proven to be due to MARV. A fourth, 25-year-old man, developed MVD clinical signs in September and was shown to be infected with RAVV. He also survived the infection. On July 10, 2008, the Netherlands National Institute for Public Health and the Environment reported that a 41-year-old Dutch woman, who had visited Python Cave in Maramagambo Forest during her holiday in Uganda , had MVD due to MARV infection, and had been admitted to a hospital in the Netherlands . The woman died under treatment in the Leiden University Medical Centre in Leiden on July 11. The Ugandan Ministry of Health closed the cave after this case. On January 9 of that year an infectious diseases physician notified the Colorado Department of Public Health and the Environment that a 44-year-old American woman who had returned from Uganda had been hospitalized with a fever of unknown origin . At the time, serologic testing was negative for viral hemorrhagic fever . She was discharged on January 19, 2008. After the death of the Dutch patient and the discovery that the American woman had visited Python Cave, further testing confirmed the patient demonstrated MARV antibodies and RNA . In October 2017 an outbreak of Marburg virus disease was detected in Kween District , Eastern Uganda. All three initial cases (belonging to one family – two brothers and one sister) had died by 3 November. The fourth case – a health care worker – developed symptoms on 4 November and was admitted to a hospital. The first confirmed case traveled to Kenya before the death. A close contact of the second confirmed case traveled to Kampala . It is reported that several hundred people may have been exposed to infection. In August 2021, two months after the re-emergent Ebola epidemic in the Guéckédou prefecture was declared over, a case of the Marburg disease was confirmed by health authorities through laboratory analysis. Other potential case of the disease in a contact awaits official results. This was the first case of the Marburg hemorrhagic fever confirmed to happen in West Africa. The case of Marburg also has been identified in Guéckédou . During the outbreak, a total of one confirmed case, who died ( CFR =100%), and 173 contacts were identified, including 14 high-risk contacts based on exposure. Among them, 172 were followed for a period of 21 days, of which none developed symptoms. One high-risk contact was lost to follow up. Sequencing of an isolate from the Guinean patient showed that this outbreak was caused by the Angola-like Marburg virus. A colony of Egyptian rousettus bats ( reservoir host of Marburg virus ) was found in close proximity (4.5 km) to the village, where the Marburg virus disease outbreak emerged in 2021. Two sampled fruit bats from this colony were PCR-positive on the Marburg virus. In July 2022, preliminary analysis of samples taken from two patients – both deceased – in Ghana indicated the cases were positive for Marburg. However, per standard procedure, the samples were sent to the Pasteur Institute of Dakar for confirmation. On 17 July 2022 the two cases were confirmed by Ghana, which caused the country to declare a Marburg virus disease outbreak. An additional case was identified, bringing the total to three. A disease outbreak was first reported in Equatorial Guinea on 7 February 2023, and on 13 February 2023, it was identified as being Marburg virus disease. It was the first time the disease was detected in the country. Neighbouring Cameroon detected two suspected cases of Marburg virus disease on 13 February 2023, but they were later ruled out. On 25 February, a suspected case of Marburg was reported in the Spanish city of Valencia , however this case was subsequently discounted. As of 4 April 2023, there were 14 confirmed cases and 28 suspected cases, including ten confirmed deaths from the disease in Equatorial Guinea. On 8 June 2023, the World Health Organization declared the outbreak over. In total, 17 laboratory-confirmed cases and 12 deaths were recorded. All the 23 probable cases reportedly died. Four patients recovered from the virus and have been enrolled in a survivors programme to receive psychosocial and other post-recovery support. A Marburg virus disease outbreak in Tanzania was first reported on 21 March 2023 by the Ministry of Health of Tanzania. This was the first time that Tanzania had reported an outbreak of the disease. On 2 June 2023, Tanzania declared the outbreak over. There were 9 total infections, resulting in 6 total deaths. Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of MARV has been used successfully in nonhuman primate models as post-exposure prophylaxis. A vaccine candidate has been effective in nonhuman primates. Experimental therapeutic regimens relying on antisense technology have shown promise, with phosphorodiamidate morpholino oligomers (PMOs) targeting the MARV genome New therapies from Sarepta and Tekmira have also been successfully used in humans as well as primates.
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Marburg
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University of Marburg
The Philipps University of Marburg ( German : Philipps-Universität Marburg ) is a public research university located in Marburg , Germany . It was founded in 1527 by Philip I, Landgrave of Hesse , which makes it one of Germany's oldest universities and the oldest still operating Protestant university in the world. It is now a public university of the state of Hesse , without religious affiliation. The University of Marburg has about 23,500 students and 7,500 employees and is located in Marburg , a town of 76,000 inhabitants, with university buildings dotted in or around the town centre. About 14% of the students are international, the highest percentage in Hesse. It offers an International summer university programme and offers student exchanges through the Erasmus programme .In 1609, the University of Marburg established the world's first professorship in chemistry. In 2012 it opened the first German interactive chemistry museum, called Chemicum . Its experimental course programme is aimed at encouraging young people to pursue careers in science. The university was among the first in Germany to offer courses in gender studies. 20 professors were expelled in 1933, among them economist Wilhelm Röpke who emigrated and linguist Hermann Jacobsohn who committed suicide. Since the 1970s, the Department of Social Sciences has been regarded as a leftist stronghold, with Wolfgang Abendroth being a major influence within the field of political science in post-war Germany.20 professors were expelled in 1933, among them economist Wilhelm Röpke who emigrated and linguist Hermann Jacobsohn who committed suicide.Since the 1970s, the Department of Social Sciences has been regarded as a leftist stronghold, with Wolfgang Abendroth being a major influence within the field of political science in post-war Germany.The university is significant for its life-sciences research but is also home to one of the few centers that conduct research on the Middle East, the CNMS (Center for Near and Middle Eastern Studies). The departments of psychology and geography reached Excellence Group status in the Europe-wide CHE Excellence Ranking 2009. Its research is illustrated by its participation in several SFBs ( Sonderforschungsbereiche ). These collaborative research centres are financed by the German Science Foundation DFG . They encourage researchers to cross the boundaries of disciplines, institutes, departments and faculties within the participating university. The current SFB at Philipps-University Marburg are: Alter Botanischer Garten Marburg , the university's old botanical garden Botanischer Garten Marburg , the university's current botanical garden Forschungsinstitut Lichtbildarchiv älterer Originalurkunden bis 1250 (Collection of photographs taken from medieval charters) Bildarchiv Foto Marburg (German national picture archive of arts) Religionskundliche Sammlung (Collection of religious objects) Deutscher Sprachatlas (Linguistic Atlas of Germany) Mineralogisches Museum (Museum of Mineralogy) Museum für Kunst und Kulturgeschichte (Museum of Arts) Museum Anatomicum (Museum of Anatomy and Medical History) As per the QS World University Rankings of 2024, the institution is situated within the 761–770 range globally, and it holds the 40–41 position nationally. According to the THE World University Rankings of 2024, it ranks within the 401–500 bracket globally, while its national standing falls between 37 and 41. In the ARWU World Rankings of 2023, the university is listed in the 401–500 range worldwide, and it takes a national position between 25 and 31. The university is significant for its life-sciences research but is also home to one of the few centers that conduct research on the Middle East, the CNMS (Center for Near and Middle Eastern Studies). The departments of psychology and geography reached Excellence Group status in the Europe-wide CHE Excellence Ranking 2009. Its research is illustrated by its participation in several SFBs ( Sonderforschungsbereiche ). These collaborative research centres are financed by the German Science Foundation DFG . They encourage researchers to cross the boundaries of disciplines, institutes, departments and faculties within the participating university. The current SFB at Philipps-University Marburg are: Alter Botanischer Garten Marburg , the university's old botanical garden Botanischer Garten Marburg , the university's current botanical garden Forschungsinstitut Lichtbildarchiv älterer Originalurkunden bis 1250 (Collection of photographs taken from medieval charters) Bildarchiv Foto Marburg (German national picture archive of arts) Religionskundliche Sammlung (Collection of religious objects) Deutscher Sprachatlas (Linguistic Atlas of Germany) Mineralogisches Museum (Museum of Mineralogy) Museum für Kunst und Kulturgeschichte (Museum of Arts) Museum Anatomicum (Museum of Anatomy and Medical History)As per the QS World University Rankings of 2024, the institution is situated within the 761–770 range globally, and it holds the 40–41 position nationally. According to the THE World University Rankings of 2024, it ranks within the 401–500 bracket globally, while its national standing falls between 37 and 41. In the ARWU World Rankings of 2023, the university is listed in the 401–500 range worldwide, and it takes a national position between 25 and 31. Marburg was always known as a humanities -focused university. It retained that strength, especially in Philosophy and Theology for a long time after World War II . [ citation needed ]Marburg was always known as a humanities -focused university. It retained that strength, especially in Philosophy and Theology for a long time after World War II . [ citation needed ]
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Marburg
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Marburg virus
Marburg virus (MARV) is a hemorrhagic fever virus of the Filoviridae family of viruses and a member of the species Marburg marburgvirus , genus Marburgvirus . It causes Marburg virus disease in primates, a form of viral hemorrhagic fever . The virus is considered to be extremely dangerous. The World Health Organization (WHO) rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment ). In the United States, the National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent . It is also listed as a biological agent for export control by the Australia Group . The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected sex and broken skin. The disease can cause haemorrhage , fever, and other symptoms similar to Ebola , which belongs to the same family of viruses. According to the WHO, there are no approved vaccines or antiviral treatment for Marburg, but early, professional treatment of symptoms like dehydration considerably increases survival chances. In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala , Uganda. Marburg virus was first described in 1967. It was discovered that year during a set of outbreaks of Marburg virus disease in the German cities of Marburg and Frankfurt and the Yugoslav capital Belgrade . Laboratory workers were exposed to tissues of infected grivet monkeys (the African green monkey, Chlorocebus aethiops ) at the Behringwerke , a major industrial plant in Marburg which was then part of Hoechst , and later part of CSL Behring . During the outbreaks, thirty-one people became infected and seven of them died. The virus is one of two members of the species Marburg marburgvirus , which is included in the genus Marburgvirus , family Filoviridae , and order Mononegavirales . The name Marburg virus is derived from Marburg (the city in Hesse , Germany, where the virus was first discovered) and the taxonomic suffix virus . Marburg virus was first introduced under this name in 1967. The virus name was changed to Lake Victoria marburgvirus in 2005, confusingly making the only difference in distinguishing between a Marburg virus organism and its species as a whole italicization, as in Lake Victoria marburgvirus . Still, most scientific articles continued to use the name Marburg virus. Consequently, in 2010, the name Marburg virus was reinstated and the species name changed. Marburg virus was first described in 1967. It was discovered that year during a set of outbreaks of Marburg virus disease in the German cities of Marburg and Frankfurt and the Yugoslav capital Belgrade . Laboratory workers were exposed to tissues of infected grivet monkeys (the African green monkey, Chlorocebus aethiops ) at the Behringwerke , a major industrial plant in Marburg which was then part of Hoechst , and later part of CSL Behring . During the outbreaks, thirty-one people became infected and seven of them died. The virus is one of two members of the species Marburg marburgvirus , which is included in the genus Marburgvirus , family Filoviridae , and order Mononegavirales . The name Marburg virus is derived from Marburg (the city in Hesse , Germany, where the virus was first discovered) and the taxonomic suffix virus . Marburg virus was first introduced under this name in 1967. The virus name was changed to Lake Victoria marburgvirus in 2005, confusingly making the only difference in distinguishing between a Marburg virus organism and its species as a whole italicization, as in Lake Victoria marburgvirus . Still, most scientific articles continued to use the name Marburg virus. Consequently, in 2010, the name Marburg virus was reinstated and the species name changed. Like all mononegaviruses , marburg virions contain non-infectious, linear nonsegmented, single-stranded RNA genomes of negative polarity that possess inverse-complementary 3' and 5' termini, do not possess a 5' cap , are not polyadenylated , and are not covalently linked to a protein . Marburgvirus genomes are approximately 19 kbp long and contain seven genes in the order 3'-UTR - NP - VP35 - VP40 - GP - VP30 - VP24 - L - 5'-UTR . Like all filoviruses , marburgvirions are filamentous particles that may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched. Marburgvirions are generally 80 nm in width , but vary somewhat in length. In general, the median particle length of marburgviruses ranges from 795 to 828 nm (in contrast to ebolavirions , whose median particle length was measured to be 974–1,086 nm), but particles as long as 14,000 nm have been detected in tissue culture. Marburgvirions consist of seven structural proteins. At the center is the helical ribonucleocapsid , which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP 1,2 ) that projects 7 to 10 nm spikes away from its surface. While nearly identical to ebolavirions in structure, marburgvirions are antigenically distinct. Niemann–Pick C1 (NPC1) cholesterol transporter protein appears to be essential for infection with both Ebola and Marburg virus. Two independent studies reported in the same issue of Nature showed that Ebola virus cell entry and replication requires NPC1. When cells from patients lacking NPC1 were exposed to Ebola virus in the laboratory, the cells survived and appeared immune to the virus , further indicating that Ebola relies on NPC1 to enter cells. This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to one of the deadliest known viruses affecting humans. The same studies described similar results with Marburg virus, showing that it also needs NPC1 to enter cells. Furthermore, NPC1 was shown to be critical to filovirus entry because it mediates infection by binding directly to the viral envelope glycoprotein and that the second lysosomal domain of NPC1 mediates this binding. In one of the original studies, a small molecule was shown to inhibit Ebola virus infection by preventing the virus glycoprotein from binding to NPC1. In the other study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse-adapted Ebola virus. The Marburg virus life cycle begins with virion attachment to specific cell-surface receptors , followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol . [ citation needed ] The virus RdRp partially uncoats the nucleocapsid and transcribes the genes into positive-stranded mRNAs , which are then translated into structural and nonstructural proteins . Marburgvirus L binds to a single promoter located at the 3' end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3' end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely to be transcribed. The gene order is therefore a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein , whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-stranded antigenomes that are in turn transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane . Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle. Like all mononegaviruses , marburg virions contain non-infectious, linear nonsegmented, single-stranded RNA genomes of negative polarity that possess inverse-complementary 3' and 5' termini, do not possess a 5' cap , are not polyadenylated , and are not covalently linked to a protein . Marburgvirus genomes are approximately 19 kbp long and contain seven genes in the order 3'-UTR - NP - VP35 - VP40 - GP - VP30 - VP24 - L - 5'-UTR . Like all filoviruses , marburgvirions are filamentous particles that may appear in the shape of a shepherd's crook or in the shape of a "U" or a "6", and they may be coiled, toroid, or branched. Marburgvirions are generally 80 nm in width , but vary somewhat in length. In general, the median particle length of marburgviruses ranges from 795 to 828 nm (in contrast to ebolavirions , whose median particle length was measured to be 974–1,086 nm), but particles as long as 14,000 nm have been detected in tissue culture. Marburgvirions consist of seven structural proteins. At the center is the helical ribonucleocapsid , which consists of the genomic RNA wrapped around a polymer of nucleoproteins (NP). Associated with the ribonucleoprotein is the RNA-dependent RNA polymerase (L) with the polymerase cofactor (VP35) and a transcription activator (VP30). The ribonucleoprotein is embedded in a matrix, formed by the major (VP40) and minor (VP24) matrix proteins. These particles are surrounded by a lipid membrane derived from the host cell membrane. The membrane anchors a glycoprotein (GP 1,2 ) that projects 7 to 10 nm spikes away from its surface. While nearly identical to ebolavirions in structure, marburgvirions are antigenically distinct. Niemann–Pick C1 (NPC1) cholesterol transporter protein appears to be essential for infection with both Ebola and Marburg virus. Two independent studies reported in the same issue of Nature showed that Ebola virus cell entry and replication requires NPC1. When cells from patients lacking NPC1 were exposed to Ebola virus in the laboratory, the cells survived and appeared immune to the virus , further indicating that Ebola relies on NPC1 to enter cells. This might imply that genetic mutations in the NPC1 gene in humans could make some people resistant to one of the deadliest known viruses affecting humans. The same studies described similar results with Marburg virus, showing that it also needs NPC1 to enter cells. Furthermore, NPC1 was shown to be critical to filovirus entry because it mediates infection by binding directly to the viral envelope glycoprotein and that the second lysosomal domain of NPC1 mediates this binding. In one of the original studies, a small molecule was shown to inhibit Ebola virus infection by preventing the virus glycoprotein from binding to NPC1. In the other study, mice that were heterozygous for NPC1 were shown to be protected from lethal challenge with mouse-adapted Ebola virus. The Marburg virus life cycle begins with virion attachment to specific cell-surface receptors , followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol . [ citation needed ] The virus RdRp partially uncoats the nucleocapsid and transcribes the genes into positive-stranded mRNAs , which are then translated into structural and nonstructural proteins . Marburgvirus L binds to a single promoter located at the 3' end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3' end of the genome are transcribed in the greatest abundance, whereas those toward the 5' end are least likely to be transcribed. The gene order is therefore a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein , whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-stranded antigenomes that are in turn transcribed into negative-stranded virus progeny genome copies. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane . Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle. In 2009, the successful isolation of infectious MARV was reported from caught healthy Egyptian fruit bats ( Rousettus aegyptiacus ) . This isolation, together with the isolation of infectious RAVV , strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. In 2012 the first experimental infection study of Rousettus aegyptiacus with MARV provided further insight into the possible involvement of these bats in MARV ecology. Experimentally infected bats developed relatively low viremia lasting at least five days, but remained healthy and did not develop any notable gross pathology. The virus also replicated to high titers in major organs (liver and spleen), and organs that might possibly be involved in virus transmission (lung, intestine, reproductive organs, salivary gland, kidney, bladder, and mammary gland). The relatively long period of viremia noted in this experiment could possibly also facilitate mechanical transmission by blood sucking arthropods in addition to infection of susceptible vertebrate hosts by direct contact with infected blood. The viral strains fall into two clades: Ravn virus and Marburg virus. The Marburg strains can be divided into two: A and B. The A strains were isolated from Uganda (five from 1967), Kenya (1980) and Angola (2004–2005) while the B strains were from the Democratic Republic of the Congo epidemic (1999–2000) and a group of Ugandan isolates isolated in 2007–2009. The mean evolutionary rate of the whole genome was 3.3 × 10 −4 substitutions/site/year (credibility interval 2.0–4.8). The Marburg strains had a mean root time of the most recent common ancestor of 177.9 years ago (95% highest posterior density 87–284) suggesting an origin in the mid 19th century. In contrast, the Ravn strains origin dated back to a mean 33.8 years ago (the early 1980s). The most probable location of the Marburg virus ancestor was Uganda whereas that of the RAVV ancestor was Kenya. [ citation needed ]MARV is one of two Marburg viruses that causes Marburg virus disease (MVD) in humans (in the literature also often referred to as Marburg hemorrhagic fever, MHF). The other one is Ravn virus (RAVV). Both viruses fulfill the criteria for being a member of the species Marburg marburgvirus because their genomes diverge from the prototype Marburg marburgvirus or the Marburg virus variant Musoke (MARV/Mus) by <10% at the nucleotide level. See Ghana Marburg virus outbreak 2022 . See Ghana Marburg virus outbreak 2022 . The first clinical study testing the efficacy of a Marburg virus vaccine was conducted in 2014. The study tested a DNA vaccine and concluded that individuals inoculated with the vaccine exhibited some level of antibodies. However, these vaccines were not expected to provide definitive immunity. Several animal models have shown to be effective in the research of Marburg virus, such as hamsters, mice, and non-human primates (NHPs). Mice are useful in the initial phases of vaccine development as they are ample models for mammalian disease, but their immune systems are still different enough from humans to warrant trials with other mammals. Of these models, the infection in macaques seems to be the most similar to the effects in humans. A variety of other vaccines have been considered. Virus replicon particles (VRPs) were shown to be effective in guinea pigs, but lost efficacy once tested on NHPs. Additionally, an inactivated virus vaccine proved ineffective. DNA vaccines showed some efficacy in NHPs, but all inoculated individuals showed signs of infection. Because Marburg virus and Ebola virus belong to the same family, Filoviridae, some scientists have attempted to create a single-injection vaccine for both viruses. This would both make the vaccine more practical and lower the cost for developing countries. Using a single-injection vaccine has shown to not cause any adverse reactogenicity, which the possible immune response to vaccination, in comparison to two separate vaccinations. As of June 23, 2022, researchers working with the Public Health Agency of Canada conducted a study which showed promising results of a recombinant vesicular stomatitis virus (rVSV) vaccine in guinea pigs, entitled PHV01. According to the study, inoculation with the vaccine approximately one month prior to infection with the virus provided a high level of protection. Even though there is much experimental research on Marburg virus, there is still no prominent vaccine. Human vaccination trials are either ultimately unsuccessful or are missing data specifically regarding Marburg virus. Due to the cost needed to handle Marburg virus at qualified facilities, the relatively few number of fatalities, and lack of commercial interest, the possibility of a vaccine has simply not come to fruition. The Soviet Union had an extensive offensive and defensive biological weapons program that included MARV. At least three Soviet research institutes had MARV research programs during the Cold War : The Virology Center of the Scientific-Research Institute for Microbiology in Zagorsk (today Sergiev Posad ), the Scientific-Production Association "Vektor" (today the State Research Center of Virology and Biotechnology "Vektor" ) in Koltsovo , and the Irkutsk Scientific-Research Anti-Plague Institute of Siberia and the Far East in Irkutsk . As most performed research was highly classified , it remains unclear how successful the MARV program was. However, Soviet defector Ken Alibek claimed that a weapon filled with MARV was tested at the Stepnogorsk Scientific Experimental and Production Base in Stepnogorsk , Kazakh Soviet Socialist Republic (today Kazakhstan ), suggesting that the development of a MARV biological weapon had reached advanced stages. Independent confirmation for this claim is lacking. At least one laboratory accident with MARV, resulting in the death of Koltsovo researcher Nikolai Ustinov, occurred during the Cold War in the Soviet Union and was first described in detail by Alibek. MARV is a select agent under US law.
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Kitum Cave
Kitum Cave is located in Mount Elgon National Park , Kenya . In the 1980s, two European visitors contracted Marburg virus disease there. It is one of five named "elephant caves" of Mount Elgon where animals, including elephants, "mine" the rock for its sodium-rich salts.Kitum Cave is a non-solutional cave developed in pyroclastic (volcanic) rocks (not, as some have presumed, a lava tube ). It extends about 200 metres (700 ft) into the side of Mount Elgon near the Kenyan border with Uganda . The walls are rich in salt , and animals such as elephants have gone deep into the cave for centuries in search of salt. The elephants use their tusks to break off pieces of the cave wall that they then chew and swallow, leaving the walls scratched and furrowed; their actions have likely enlarged the cave over time. Other animals including bushbuck , buffalo and hyenas come to Kitum Cave to consume salt left by the elephants. There is a lot of bat guano deeper in the cave from fruit-eating and insectivorous bats . There is also a deep crevasse into which young elephants have fallen and died.In the 1980s, two visitors to the cave contracted Marburg virus disease . In 1980, a French man died from the disease after visiting the cave, and in 1987 a 15-year-old Danish boy who lived in Kenya also fell ill and died after visiting the cave. Two different but very similar viruses have been catalogued from these infections: the 1980 virus is named after a doctor, Shem Musoke, who survived being infected by the French patient, while the 1987 virus is named Ravn , after the last name of the Danish patient. Based on these cases, an expedition was staged by the United States Army Medical Research Institute of Infectious Disease (USAMRIID) in an attempt to identify the vector species presumably residing in the cave. Despite sampling a wide variety of species (including fruit bats), no Marburg disease-causing viruses were found and the animal vector remained a mystery. These events were dramatized by Richard Preston in the best-selling book The Hot Zone (1994). In September 2007, similar expeditions to active mines in Gabon and Uganda found solid evidence of reservoirs of Marburg disease-causing virus in cave-dwelling Egyptian fruit bats . The Ugandan mines both had colonies of the same species of African fruit bats that colonize Kitum Cave, suggesting that the long-sought vector at Kitum was indeed the bats and their guano . The study was conducted after two mine workers contracted Marburg virus disease in August 2007, both without being bitten by any bats, suggesting that the virus may be propagated through inhalation of powdered guano.
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University Hospital of Giessen and Marburg
The University Hospital of Giessen and Marburg ( Universitätsklinikum Gießen und Marburg GmbH ) (UKGM) is a German university hospital based in Giessen and Marburg . The Giessen site is the teaching hospital of the University of Giessen whereas the Marburg site is the teaching hospital of the University of Marburg . It is the first privatized university hospital in Germany and, due to the merger of the two sites, one of the largest hospitals in Germany. In total it has 2,285 beds, thereof 1,145 in Giessen and 1,140 in Marburg.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg,_South_Africa/html
Marburg, South Africa
Marburg is a settlement in the Ugu District Municipality in the KwaZulu-Natal province of South Africa , situated approximately 112 kilometres south-west of the city of Durban . Marburg was a Norwegian settlement given the name Marburg for a nearby German mission. The Norwegian founders played a significant role in the development of Marburg and Port Shepstone , which it forms part of today. The British colonial government gave the settlers a free voyage to South Africa and also houses and 100 acres of land. Marburg was the only successful Scandinavian settlement in South Africa. Marburg was established in 1882 by Norwegian immigrants and was likely named after Marburg , a city 74 km north of Frankfurt in Germany. The Land and Immigration Board contemplated bringing German settlers to the Marburg area in 1881, but met opposition from the German government. Consequentially, immigration agent Walter Peace suggested promoting settlement in Marburg by Norwegians . On July 20, 1882, the first Norwegians ventured aboard the steamship Lapland for their 39-day voyage from Hull, England to Mzimkulu near Port Shepstone , South Africa . Arriving in Africa on August 28, 1882, the Norwegians were brought ashore the following day. The 246 Norwegians onboard Lapland were first and foremost fishermen, but slowly adjusted to the agrarian lifestyle at their 100-acre agricultural Marburg community. Many of the original 1882 founders later left Marburg, including ten families which left for Australia . However, a number remained in South Africa though not all remained in Marburg. A number joined the Norwegian community in Durban , while others went to Johannesburg and other parts near Alfred County . Emigration to South Africa from Norway in 1876-85 was dominated by emigrants from Romsdal , and more specifically, from Sunnmøre . Marburg's founders were first and foremost from à lesund in Sunnmøre. When Marburg settlers celebrated their 50th anniversary in 1932, there were twenty Norwegian families left in town. 84 original settlers were still alive, and the Norwegian community had produced 208 children, 425 grandchildren, and 130 great-grandchildren. In 1950, the Group Areas Act . racially divided Port Shepstone similar to many other towns and cities in South Africa in which Marburg was classified as the " Indian area" of Port Shepstone. Marburg was one of the four Indian proclaimed townships in the KwaZulu-Natal province and its neighbouring suburb of Merlewood to the west was classified as the " Coloured area" of Port Shepstone.The Land and Immigration Board contemplated bringing German settlers to the Marburg area in 1881, but met opposition from the German government. Consequentially, immigration agent Walter Peace suggested promoting settlement in Marburg by Norwegians . On July 20, 1882, the first Norwegians ventured aboard the steamship Lapland for their 39-day voyage from Hull, England to Mzimkulu near Port Shepstone , South Africa . Arriving in Africa on August 28, 1882, the Norwegians were brought ashore the following day. The 246 Norwegians onboard Lapland were first and foremost fishermen, but slowly adjusted to the agrarian lifestyle at their 100-acre agricultural Marburg community. Many of the original 1882 founders later left Marburg, including ten families which left for Australia . However, a number remained in South Africa though not all remained in Marburg. A number joined the Norwegian community in Durban , while others went to Johannesburg and other parts near Alfred County . Emigration to South Africa from Norway in 1876-85 was dominated by emigrants from Romsdal , and more specifically, from Sunnmøre . Marburg's founders were first and foremost from à lesund in Sunnmøre. When Marburg settlers celebrated their 50th anniversary in 1932, there were twenty Norwegian families left in town. 84 original settlers were still alive, and the Norwegian community had produced 208 children, 425 grandchildren, and 130 great-grandchildren. In 1950, the Group Areas Act . racially divided Port Shepstone similar to many other towns and cities in South Africa in which Marburg was classified as the " Indian area" of Port Shepstone. Marburg was one of the four Indian proclaimed townships in the KwaZulu-Natal province and its neighbouring suburb of Merlewood to the west was classified as the " Coloured area" of Port Shepstone.Marburg lies in a hilly area approximately 3 kilometres (2 mi) west of the Port Shepstone CBD and is bounded by the N2 freeway to the east. Marburg is situated among the suburbs of Merlewood, Grosvenor, Umbango, Protea Park and Albersville.As the largest industrial centre along the KwaZulu-Natal South Coast , Marburg is known for its industrial activity, home to a number of businesses particularly in the automotive and hardware retail sector. Marburg lies at the meeting point of three major routes (N2, R61 and R102) known as the Marburg Interchange, which includes the Oribi Toll Plaza (charging motorists on the N2 and R61 while the R102 is designated as an untolled alternative route). Marburg is also accessed via the Main Harding Road connecting from the Port Shepstone CBD, Izotsha Road from Izotsha and Gamalakhe in the south and Oscar Borcherds Road from Protea Park and the Umzimkhulu Sugar Mill in the north.
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Marburg (disambiguation)
Marburg is a town in Hesse, Germany. Marburg may also refer to: Places People Medicine Other See also
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Otto Marburg
Otto Marburg (May 25, 1874 – June 13, 1948) was an Austrian neurologist known for his contributions to the understanding of multiple sclerosis and for advances in neurooncology . Marburg was born in Römerstadt in Moravia , Austria-Hungary (today Rýmařov , Czech Republic ). He was Jewish . From 1919 to 1938, he was head of the Neurological Institute at the University of Vienna . Following the 1938 Anschluss , Marburg was forced to emigrate to the United States as a refugee . Arriving in New York City , he joined Columbia University 's College of Physicians and Surgeons as a clinical professor of neurology. He was the author of several standard texts about the nervous system, and a subtype of multiple sclerosis ( Marburg multiple sclerosis ) has been named after him. Marburg died of cancer in New York in 1948, at the age of 74. Otto Marburg was not associated with the Marburg virus , which was discovered in 1967 in the German town of Marburg .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Hesse-Marburg/html
Hesse-Marburg
The Landgraviate of Hesse-Marburg ( German : Landgrafschaft Hessen-Marburg ) was a German landgraviate , and independent principality , within the Holy Roman Empire , that existed between 1458 and 1500, and between 1567 and 1604/1650. It consisted of the city of Marburg and the surrounding towns of Gießen , Nidda and Eppstein , approximately what is today called Upper Hesse ( Oberhessen ). The area had been a semi-independent county under the counts Giso or Gisonen since the 11th century, which at their extinction fell to the Landgraves of Thuringia in the 1130s. When the daughter of St. Elizabeth of Hungary , Sophie of Brabant , was able to secure the Western parts of Thuringia for her son Henry the Child in 1265, therefore founding the state of Landgraviate of Hesse , the Marburg area became its core territory. However, Hesse-Marburg, by its name, refers only to the subdivision around Marburg. Basically the old county. This became an independent principality due to inheritance, i.e. by a landgrave splitting his possessions among two or more sons. This was first the case in 1485, but as the landgrave died without issue, and the landgraviate reverted to the greater Hesse. This was again the case in 1567, Philip I, Landgrave of Hesse or Philip the Magnanimous split his large landgraviate into four parts, Hesse-Marburg being one of them. When, in 1604 Louis IV, Landgrave of Hesse-Marburg died without male issue, he bequeathed equal shares of his territory to the landgraviates of Hesse-Kassel (Marburg) and Hesse-Darmstadt ( Gießen, Nidda ), yet under the condition that both territories should remain Lutheran. Hesse-Kassel was Calvinist at that time. As the two lines argued over the details of the division, Maurice, Landgrave of Hesse-Kassel annexed the whole territory and introduced Calvinism . After a long dispute and armed conflict, Maurice — who had enemies at home as well — resigned in 1627 and left his part of the territory to the Landgraviate of Hesse-Darmstadt. However, in the Hessian War of 1645–48, which was a sub-conflict of the Thirty Years' War , the two lines, which were on different sides, again fought over the territory. This war led to the loss of life of up to two-thirds of the civilian population, one of the highest death toll in any German region in history. In the end, the territory was divided as stipulated in Louis IV's will. Hesse-Kassel taking the northern and Hesse-Darmstadt the southern part. All areas of Hesse-Marburg are today located within the German state of Hesse .50°48′36″N 8°46′15″W / 50.81000°N 8.77083°W / 50.81000; -8.77083
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St. Elizabeth's Church, Marburg
St. Elizabeth's Church (Elisabethkirche) in Marburg , Germany , was built by the Order of the Teutonic Knights in honour of Saint Elizabeth of Hungary . Her tomb made the church an important pilgrimage destination during the late Middle Ages .The church is one of the earliest purely Gothic churches in German -speaking areas, and is held to be a model for the architecture of Cologne Cathedral . It is built from sandstone in a cruciform layout. The nave and its flanking aisles have a vaulted ceiling more than 20 m (66 ft) high. The triple choir consists of the Elisabeth choir, the High choir and the Landgrave choir. The crossing is separated from the nave by a stone rood screen . In earlier times, the front part of the church had been reserved for the knights of the Order. The church has two towers with an approximate height of 80 m (263 ft). The northern one is crowned by a star, the southern one by a knight. It served as an inspiration for St. Paul's Church in Strasbourg . The Gothic shrine of St. Elizabeth is the most important treasure of the church, but other pieces of religious art are also exhibited.Construction started in 1235, the year Saint Elizabeth was canonized . The church was consecrated in 1283. However, the towers were not finished until 1340. The church was the property of the Order of the Teutonic Knights; some buildings of the Order still exist near the church, among them the Deutschhausgut , which now houses the mineral collection and the department of geography of the Philipps University of Marburg . Until the 16th century, the Landgraves of Hesse were buried in the church. In the context of the Reformation , Philip I, Landgrave of Hesse had Elizabeth's remains removed, in order to deter pilgrims from the Protestant city of Marburg. Today, relics of Elizabeth can be found in St. Elizabeth Convent in Vienna , and in Košice . The Reliquary of St. Elizabeth is in the Swedish History Museum , Stockholm. Most of the knights and clerics of the Order who were attached to the church converted to Protestantism during the 16th century, and the church was used for Protestant services from that point on. For a short time at the beginning of the 19th century, both Catholic Mass and Protestant communion services were celebrated in separate parts of the church. After World War II , former German president Paul von Hindenburg and his wife were buried in the Elizabeth Church, after the removal of their remains from a salt mine where they were hidden under orders of their son Oskar von Hindenburg to protect them from Soviet Forces, later to be found by the US Army, and finally put to rest in this 13th-century church.In order to start a long-needed renovation of the church and the remodelling of its immediate neighbourhood, the Stiftung Heilige Elisabeth foundation was established in 2004 and supports the City of Marburg and the Protestant Church of Hesse-Kassel and Waldeck in the financing of the repair measures. [ citation needed ] In 2023 it was reported that renovation work was underway on the stained glass in the church.
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Marburgvirus
The genus Marburgvirus is the taxonomic home of Marburg marburgvirus , whose members are the two known marburgviruses, Marburg virus (MARV) and Ravn virus (RAVV) . Both viruses cause Marburg virus disease in humans and nonhuman primates , a form of viral hemorrhagic fever . Both are select agents , World Health Organization Risk Group 4 Pathogens (requiring Biosafety Level 4-equivalent containment ), National Institutes of Health / National Institute of Allergy and Infectious Diseases Category A Priority Pathogens, Centers for Disease Control and Prevention Category A Bioterrorism Agents , and are listed as Biological Agents for Export Control by the Australia Group . The genus Marburgvirus is a virological taxon included in the family Filoviridae , order Mononegavirales . The genus currently includes a single virus species , Marburg marburgvirus . The members of the genus (i.e. the actual physical entities) are called marburgviruses. The name Marburgvirus is derived from the city of Marburg in Hesse , West Germany (where Marburg virus was first discovered), and the taxonomic suffix -virus (which denotes a virus genus). Even though the virus was named after the city of Marburg, Dr. Ana Gligic, lead virologist at a laboratory in Belgrade , was first who managed to isolate the virus. Until 1998, the family Filoviridae contained only one genus, Filovirus . Once it became clear that marburgviruses and ebolaviruses are fundamentally different, this genus was abolished and a genus "Marburg-like viruses" was established for marburgviruses. In 2002, the genus name was changed to Marburgvirus , and in 2010 and 2011 the genus was emended. A virus that fulfills the criteria for being a member of the family Filoviridae is a member of the genus Marburgvirus if its genome has one gene overlap its fourth gene ( GP ) encodes only one protein (GP 1,2 ) and cotranscriptional editing is not necessary for its expression peak infectivity of its virions is association with particles ≈665 nm in length its genome differs from that of Marburg virus by <50% at the nucleotide level its virions show almost no antigenic cross reactivity with ebolavirionsThe species was introduced in 1998 as Marburg virus . Because of easy confusion with its virus member Marburg virus , the species name was changed to Lake Viktoria marburgvirus in 2005. In 2010, it was proposed to change the name to Marburg marburgvirus , and this proposal was accepted in early 2012 by the ICTV. Marburg marburgvirus (also referred to as Lake Victoria marburgvirus ) is a virological taxon (i.e. a man-made concept) included in the genus Marburgvirus , family Filoviridae , order Mononegavirales . The species has two virus members, Marburg virus (MARV) and Ravn virus (RAVV) . The members of the species (i.e. the actual physical entities) are called Marburg marburgviruses. The name Marburg marburgvirus is derived from the city of Marburg in Hesse , West Germany (where Marburg virus was first discovered), and the taxonomic suffix marburgvirus (which denotes a marburgvirus species). A virus that fulfills the criteria for being a member of the genus Marburgvirus is a member of the species Marburg marburgvirus if it has the properties of marburgviruses (because there is currently only marburgvirus species) and if its genome differs from that of Marburg virus (variant Musoke) by <30% at the nucleotide level.
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Marburg Colloquy
The Marburg Colloquy was a meeting at Marburg Castle , Marburg , Hesse , Germany , which attempted to solve a disputation between Martin Luther and Ulrich Zwingli over the Real Presence of Christ in the Eucharist . It took place between 1 October and 4 October 1529. The leading Protestant reformers of the time attended at the behest of Philip I of Hessen . Philip's primary motivation for this conference was political; he wished to unite the Protestant states in political alliance, and to this end, religious harmony was an important consideration. After the Diet of Speyer had confirmed the edict of Worms , Philip I felt the need to reconcile the diverging views of Martin Luther and Ulrich Zwingli in order to develop a unified Protestant theology. Besides Luther and Zwingli, the reformers Stephan Agricola , Johannes Brenz , Martin Bucer , Caspar Hedio , Justus Jonas , Philip Melanchthon , Johannes Oecolampadius , Andreas Osiander , and Bernhard Rothmann participated in the meeting. If Philip wanted the meeting to be a symbol of Protestant unity he was disappointed. Luther and Zwingli fell out over the sacrament of the Eucharist .Philip of Hesse had a political motivation to unify all the leading Protestants because he believed that as a divided entity they were vulnerable to Charles V. As a unified force, they would appear to be more powerful. Religious harmony was vital amongst the Protestants for there to be a unification. Although the two prominent reformers , Luther and Zwingli, found a consensus on fourteen theological points, they could not find agreement on the fifteenth point pertaining to the Eucharist . Timothy George , an author and professor of Church History, summarized the incompatible views, "On this issue, they parted without having reached an agreement. Both Luther and Zwingli agreed that the bread in the Supper was a sign. For Luther, however, that which the bread signified, namely the body of Christ, was present "in, with, and under" the sign itself. For Zwingli, though, sign and thing signified were separated by a distance—the width between heaven and earth." Underlying this disagreement was their theology of Christ. Luther believed that the human body of Christ was ubiquitous (present in all places) and so present in the bread and wine. This was possible because the attributes of God infused Christ's human nature. Luther emphasized the oneness of Christ's person. Zwingli, who emphasized the distinction of the natures, believed that while Christ in his deity was omnipresent, Christ's human body could only be present in one place, that is, at the right hand of the Father. The executive editor for Christianity Today magazine carefully detailed the two views that would forever divide the Lutheran and Reformed view of the Supper: Luther claimed that the body of Christ was not eaten in a gross, material way but rather in some mysterious way, which is beyond human understanding. Yet, Zwingli replied, if the words were taken in their literal sense, the body had to be eaten in the most grossly material way. "For this is the meaning they carry: this bread is that body of mine which is given for you. It was given for us in grossly material form, subject to wounds, blows and death. As such, therefore, it must be the material of the supper." Indeed, to press the literal meaning of the text even farther, it follows that Christ would have again to suffer pain, as his body was broken again—this time by the teeth of communicants. Even more absurdly, Christ's body would have to be swallowed, digested, even eliminated through the bowels! Such thoughts were repulsive to Zwingli. They smacked of cannibalism on the one hand and of the pagan mystery religions on the other. The main issue for Zwingli, however, was not the irrationality or exegetical fallacy of Luther's views. It was rather that Luther put "the chief point of salvation in physically eating the body of Christ," for he connected it with the forgiveness of sins. The same motive that had moved Zwingli so strongly to oppose images, the invocation of saints, and baptismal regeneration was present also in the struggle over the Supper: the fear of idolatry. Salvation was by Christ alone, through faith alone, not through faith and bread. The object of faith was that which is not seen (Heb 11:1) and which therefore cannot be eaten except, again, in a nonliteral, figurative sense. "Credere est edere," said Zwingli: "To believe is to eat." To eat the body and to drink the blood of Christ in the Supper, then, simply meant to have the body and blood of Christ present in the mind. Near the end of the colloquy when it was clear an agreement would not be reached, Philipp asked Luther to draft a list of doctrines all that both sides agreed upon. The Marburg Articles , based on what would become the Articles of Schwabach , had 15 points, and every person at the colloquy could agree on the first 14. The 15th article of the Marburg Articles reads: Fifteenth, regarding the Last Supper of our dear Lord Jesus Christ, we believe and hold that one should practice the use of both species as Christ himself did, and that the sacrament at the altar is a sacrament of the true body and blood of Jesus Christ and the spiritual enjoyment of this very body and blood is proper and necessary for every Christian. Furthermore, that the practice of the sacrament is given and ordered by God the Almighty like the Word, so that our weak conscience might be moved to faith through the Holy Spirit. And although we have not been able to agree at this time, whether the true body and blood of Christ are corporally present in the bread and wine [of communion], each party should display towards the other Christian love, as far as each respective conscience allows, and both should persistently ask God the Almighty for guidance so that through his Spirit he might bring us to a proper understanding. The failure to find agreement resulted in strong emotions on both sides. "When the two sides departed, Zwingli cried out in tears, 'There are no people on earth with whom I would rather be at one than the [Lutheran] Wittenbergers.'" Because of the differences, Luther initially refused to acknowledge Zwingli and his followers as Christians, though following the colloquy the two Reformers showed relatively more mutual respect in their writings. At the later Diet of Augsburg , the Zwinglians and Lutherans again explored the same territory as that covered in the Marburg Colloquy and presented separate statements which showed the differences in opinion.
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Marburg-Biedenkopf
Marburg-Biedenkopf is a Kreis ( district ) in the west of Hesse , Germany . Neighboring districts are Waldeck-Frankenberg , Schwalm-Eder , Vogelsbergkreis , Gießen , Lahn-Dill , Siegen-Wittgenstein .The district was created in 1974 when the districts Marburg, Biedenkopf and the former urban district of Marburg were merged. The district has partnerships with Huntingdonshire in the United Kingdom , the borough of Charlottenburg in Berlin , and the district of Kościerzyna in Poland .The main river in the district is the Lahn .The coat of arms shows the lion of Hesse , as Marburg was the seat of the landgraves of Hesse, and also their tomb is located in a church in Marburg. The coat held by the lion shows the black cross of the Counts of the Teutonic Knights , who had a castle in Marburg as well.
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Marburg speech
The Marburg speech ( German : Marburger Rede ) was an address given by German Vice Chancellor Franz von Papen at the University of Marburg on 17 June 1934. It is said to be the last speech made publicly, and on a high level, in Germany against National Socialism . It was done in favour of the old nationalist-militarist clique that had run Germany in the Kaiser's time, who had helped Hitler to power as a prelude to their return, only to find themselves instead pushed aside by the New Order . Papen, encouraged by President Paul von Hindenburg , spoke out publicly about the excesses of the Nazi regime, whose ascent to power, 17 months earlier when Adolf Hitler became chancellor of Germany , had been greatly assisted by him. In his speech, Papen called for an end to rule by terror and the clamouring for a "second revolution" by the Sturmabteilung (SA – the NSDAP's storm troopers), and the restoration of some measure of civil liberties. He also stated: "The government [must be] mindful of the old maxim 'only weaklings suffer no criticism'". The speech was drafted by one of Papen's close advisors, Edgar Julius Jung , with assistance from Papen's secretary Herbert von Bose and Erich Klausener . It was delivered in an auditorium in the "Alte Universität," one of the main buildings in the university, but there is no plaque or any other form of commemoration of the Papen speech which, while historically labelled as Germany's last public speech against National Socialism, [ citation needed ] does not contain the term "Nazi", which the Nazis considered to be a pejorative.… The events of the past one and one-half years have gripped the whole German people and affected them deeply. It seems almost like a dream that out of the valley of misery, hopelessness, hate, and fragmentation we have found our way back to a German national community. The horrendous tensions in which we have lived since the August days of 1914 have dissolved, and out of this discord, the German soul has emerged once again, before which the glorious and yet so painful history of our people pass in review, from the sagas of the German heroes to the trenches of Verdun, and even to the street fights of our time. An unknown soldier of the World War , who conquered the hearts of his countrymen with contagious energy and unshakable faith, has set this soul free. With his Field Marshal he has placed himself at the head of the nation, in order to turn a new page in the book of German destiny and to restore spiritual unity. We have experienced this unity of spirit in the exhilaration of a thousand rallies, flags, and celebrations of a nation that has rediscovered itself. But now, as the enthusiasm has lessened and tough work on this project has become imperative, it has become clear that a reform process of such historical proportions also produces slag, from which it must be cleaned. … The function of the press should be to inform the government where deficiencies have crept in, where corruption has settled, where serious mistakes are being made, where unsuitable men are in the wrong positions, and where transgressions are committed against the spirit of the German revolution. An anonymous or secret news service, no matter how well organized, can never be a substitute for this responsibility of the press.…If other countries claim that freedom has died in Germany, then the openness of my remarks should instruct them that the German government can afford to allow a discussion of the burning questions of the nation. The only ones who have earned the right to enter this debate, however, are those who have put themselves at the service of National Socialism and its efforts without reservation and have proven their loyalty. … If the liberal revolution of 1789 was the revolution of rationalism against religion, against attachment, so the counter-revolution taking place in the twentieth century can only be conservative, in the sense that it does not have a rationalizing and disintegrating effect, but once again places all of life under the natural law of Creation. That is presumably the reason why the cultural leader of the NSDAP, Alfred Rosenberg , spoke of a conservative revolution . From this there emerge in the field of politics the following clear conclusions: The time of emancipation of the lowest social orders against the higher orders is past. This is not a matter of holding down a social class – that would be reactionary – but of preventing a class from arising, gaining the power of the state, and asserting a claim to totality. Every natural and divine order must thereby be lost; it threatens a permanent revolution … The goal of the German Revolution, if it is to be a valid model for Europe, must therefore be the foundation of a natural social order that puts an end to the never-ending struggle for dominance. True dominance cannot be derived from one social order or class. The principle of popular sovereignty has, however, always culminated in class rule. Therefore, an anti-democratic revolution can only be consummated by breaking with the principle of popular sovereignty and returning to natural and divine rule. … But once a revolution has been completed, the government represents only the people as a whole, and is never the champion of individual groups; otherwise it would have to fail in forming a national community … It is not permissible, therefore, to dismiss the mind ( Geist ) with the catchword "intellectualism." Deficient or primitive intellect are not in themselves justification for war against intellectualism. And if today we sometimes complain about 150 percent National Socialists, then we mean those intellectuals without substance, people who would like to deny the right of existence to scientists of world fame just because they are not Party members … The sentence, "men make history," has frequently been misunderstood as well. The Reich government is therefore right to criticize a false personality cult , which is the least Prussian kind of thing one can imagine. Great men are not made by propaganda , but rather grow through their deeds and are recognized by history. Even Byzantinism cannot delude us about the validity of these laws. Whoever speaks of Prussian tradition, therefore, should first of all think of silent and impersonal service, and last or not at all of reward and recognition. … I have so pointedly described the problems of the German Revolution and my attitude toward it, because talk of a second wave that will complete the revolution seems not to want to end. Whoever toys with such ideas should not conceal the fact that the one who threatens with the guillotine is the one who is most likely to come under the executioner's axe. Nor is it apparent to what this second wave is to lead. Have we gone through an anti- Marxist revolution in order to carry out a Marxist program? … No nation can afford a constant revolt from below if it wants to pass the test of history. The Movement must come to a standstill some day; at some time a stable social structure must emerge, maintained by an impartial judiciary and by an undisputed state authority. Nothing can be achieved through everlasting dynamics. Germany must not go adrift on uncharted seas toward unknown shores, with no one knowing when it will stop. History moves on its own; it is unnecessary to drive it on incessantly. If therefore the German revolution should experience a second wave of new life, then not as a social revolution, but as the creative culmination of work already begun. The statesman is there to create standards; the state and the people are his only concerns. The state is the sole power and the last guarantor of something to which every citizen can lay claim: iron-clad justice. Therefore, the state also cannot endure any dualism in the long term, and the success of the German Revolution and the future of our nation depend on whether a satisfactory solution can be found to the dualism between party and state. The Government is well informed on all the self-interest, lack of character, want of truth, unchivalrous conduct, and arrogance trying to rear its head under cover of the German Revolution. It is also not deceived about the fact that the rich store of confidence bestowed upon it by the German people is threatened. If one wishes a close proximity to and a close connection with the people, one must not underestimate the good sense of the people; one must return their confidence and not constantly want to tell them what to do. The German people know that their situation is serious; they feel the economic distress; they are perfectly aware of the defects of many laws conditioned by the emergency; they have a discerning feeling for violence and injustice; they smile at clumsy attempts to deceive them with false optimism. No organization and no propaganda, no matter how good, will in the long run be able to retain trust. I have therefore viewed the wave of propaganda against the so-called petty critics differently from many others. Confidence and readiness to cooperate cannot be won by incitement, especially of youth, nor by threats against helpless segments of the people, but only by discussion with the people with trust on both sides. The people know that great sacrifices are expected from them. They will bear them and follow the Führer with unwavering loyalty, if they are allowed to have their part in the planning and in the work, if every word of criticism is not taken for ill will, and if despairing patriots are not branded as enemies of the state. …" The speech made Hitler furious, and on Hitler's orders, Propaganda Minister Joseph Goebbels attempted to suppress it. However, parts of it were printed in the Frankfurter Zeitung , narrowly avoiding the increasingly invasive censorship by the government. Also, copies of the speech were circulated freely within Germany and to the foreign press. Papen told Hitler that unless the ban on the Marburg speech was lifted and Hitler declared himself willing to follow the line recommended by Papen in the speech, he would resign and would inform Hindenburg why he had resigned. Afterward, Hindenburg gave Hitler an ultimatum — unless Hitler acted immediately to end the disorder in Germany — he would declare martial law and hand the government to the army. Two weeks later, on the Night of the Long Knives , the SS and Gestapo murdered Hitler's enemies within the NSDAP as well as various past friends, associates of people that could not be killed directly, and several conservative opponents of the Nazi regime. During this blood purge Jung, von Bose, and Klausener were also murdered. Papen's office was ransacked and he himself held under house arrest but his life was spared. After the purge, Hitler formally accepted Papen's resignation as Vice Chancellor. Papen subsequently served as ambassador to Austria and later served as ambassador to Turkey during the war. During the Nuremberg Trials , Papen, who was one of the main defendants, cited the Marburg speech as evidence of his distance from the excesses of the Nazi government of the time. [ citation needed ] In the end, Papen was acquitted. "Rede des Vizekanzlers von Papen vor dem Universitätsbund, Marburg, am 17. Juni 1934", in: Edmund Forschbach: Edgar J. Jung. Ein konservativer Revolutionär 30. Juni 1934 , 1984, p. 154ff. "Rede des Vizekanzlers von Papen vor dem Universitätsbund, Marburg, am 17. Juni 1934", in: Sebastian Maaß: Die andere deutsche Revolution. Edgar Julius Jung und die metaphysischen Grundlagen der Konservativen Revolution , 2009, p. 134ff. "Vice-Chancellor Franz von Papen's Marburg Speech: A Call for More Freedom, June 17, 1934" (English-language translation), in: Louis L. Snyder, editor: Hitler's Third Reich; A Documentary History , Chicago: Nelson-Hall, 1981. pp. 173–177. "The Nazi Germany Sourcebook: AN ANTHOLOGY OF TEXTS" by Roderick Stackelberg & Sally A. Winkle
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https://api.wikimedia.org/core/v1/wikipedia/en/page/1967_Marburg_virus_outbreak/html
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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Diana Marburg
Miss Diana Marburg , also known as "The Oracle of Maddox Street ", is a palmist and female occult detective created by the writers L. T. Meade and Robert Eustace . The character is unusual for Meade, insofar that there is a supernatural element involved in her detective skills, though elements of this are taken from the authors' character John Bell in The Master of Mysteries . Diana Marburg first appeared in the New York edition of Pearson's Magazine in February 1902, in a story entitled 'The Dead Hand'. Two further stories were published, 'Finger Tips' (August 1902) and 'Sir Penn Caryll's Engagement' (December 1902). The stories were published in book form along with seven non-Marburg stories in The Oracle of Maddox Street (Ward, Lock & Co., 1904). [ unreliable source? ] The Marburg stories have since featured in a number of anthologies. The author Scott Dickerson has written three further adventures of Miss Marburg, narrated by her brother Rupert, along with versions of the originals, though with changed titles, published in his The Oracular Miss Marburg: Paranormal powers, woman detective--Victorian London! (The YOUNG & SMART Series Book T8). The book is only available as a Kindle edition. One of the new stories features the scientist Sir William Crookes and the bogus medium Florence Cook , both historical characters, and another features Arthur Conan Doyle and Harry Houdini.
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Marburger Schloss
The Marburger Schloss (or Marburg castle ), also known as Landgrafenschloss Marburg , is a castle in Marburg , Hesse , Germany , located on top of Schlossberg (287 m NAP ). Built in the 11th century as a fort, it became the first residence of Landgraviate of Hesse ( HRE ). The Marburg Colloquy was held here in 1529. Today the building is used as a museum (Marburger Universitätsmuseum für Kulturgeschichte, Wilhelmsbau, since 1981) and as an event site.The castle is located West of Marburg, Hesse, Germany, on top of Schlossberg ("Castle Hill").In 1945, the Marburg Files were compiled at Marburg Castle.
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Konrad von Marburg
Konrad von Marburg (sometimes anglicised as Conrad of Marburg ) (1180 – 30 July 1233) was a medieval German Catholic priest and nobleman. He is perhaps best known as the spiritual director of Elizabeth of Hungary .Konrad's early life is not well known, he may be of aristocratic descent, and he was described by contemporary church sources as well educated and highly knowledgeable. His contemporaries called him Magister, a proof that he had finished the course of studies at some university, perhaps Paris or Bologna. He was noted for his strong asceticism and his oppressive zeal in defending the church. Much of his early work within the church was related to the suppression of heresy, and he took an active part in the Albigensian Crusade in southern France. Pope Innocent III , who championed the Medieval Inquisition , was one of Konrad's early supporters. Eventually, however, Konrad returned to Germany , the land of his birth. In particular, Konrad was employed by Louis' wife, Elizabeth of Hungary , to whom Konrad acted as spiritual director . After receiving a commission from the Archbishop of Mainz , Siegfried II , Konrad set to work seeking out heresy in both Thuringia and Hesse , and quickly gained a reputation for being unreasonable and unjust. According to most accounts, Konrad accepted almost any accusation as true, and regarded suspects as guilty until proven innocent. Those accused of being heretics were quickly sought out by Konrad's mobs, and told to repent or else be burnt at the stake . Those accused of heresy were also encouraged to denounce others, with the implication that their own lives might be spared if they did so. Konrad included commoners, nobles and priests in his inquisition: Heinrich Minnike, Provost of Goslar , was one of Konrad's first targets, and was burnt at the stake. In one instance, he treated his penitent with extreme harshness, tricking a widow into some unwitting disobedience and then had her and her maids flogged. In 1231, Pope Gregory IX granted him permission to ignore standard church procedure for the investigation of heresy. The pope also issued the papal bull Vox in Rama in response to Konrad's allegations, condemning Luciferian. Konrad teamed up with Conrad Dorso and John the One-Eyed in the Upper Rhineland , burning many heretics with barely the semblance of a trial. In 1233, Konrad accused Henry II, Count of Sayn , of taking part in "Satanic orgies". Henry, however, appealed to an assembly of bishops in Mainz where they decided to postpone a verdict to the discontent of both parties. Konrad refused to accept the decision and demanded that a verdict be reached, but eventually gave up and left Mainz to return to Marburg . On the road, he was attacked by several knights , who killed both Konrad and his assistant, a Franciscan friar named Gerhard Lutzelkolb. After Konrad's death, Pope Gregory declared Konrad to have been an upholder of the Christian faith and ordered his killers punished. Perceptions in the German Empire however, were markedly less favorable, and the memory of Konrad was enough to turn opinion against the Italian Inquisition for many years. The reputation he amassed in the course of his years as an inquisitor, gradually spread throughout Europe, overcoming the local boundaries of his original area of activity; and was that of an overly harsh judge. He left an Epistola ad papam de miraculis Sanctae Elisabethae, which was first published at Cologne in 1653. The place where Konrad was killed, Hof Kapelle near Marburg, is marked with a stone (within the premises of a private farm); it was locally long believed to be haunted and is allegedly today, on certain days, the site of black rites.
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Peter Piot
Sir Peter Karel, Baron Piot , KCMG , FRCP , FFPH , FMedSci (born 17 February 1949) is a Belgian-British microbiologist known for his research into Ebola and AIDS . After helping discover the Ebola virus in 1976 and leading efforts to contain the first-ever recorded Ebola epidemic that same year, Piot became a pioneering researcher into AIDS. He has held key positions in the United Nations and World Health Organization involving AIDS research and management. He has also served as a professor at several universities worldwide. He is the author of 16 books and over 600 scientific articles.Piot was born in Leuven , Belgium. His father was a civil servant who worked with agricultural exports and his mother ran a construction company. Piot is the oldest of two brothers and a sister. After beginning in the school of engineering and physics at Ghent University studying physics, Piot changed to medicine. During medical school, Piot received a Diploma in Tropical Medicine (DTM) from the Institute of Tropical Medicine Antwerp in Antwerp. In 1974, he received an MD degree from Ghent University. In 1980, Piot received a PhD degree in clinical microbiology from the University of Antwerp . In 1976, while working at the Institute of Tropical Medicine, Piot was part of a team that observed a Marburg-like virus in a sample of blood taken from a sick nun working in Zaire . Piot and his colleagues subsequently traveled to Zaire as part of an International Commission set up by the Government of Zaire to help quell the outbreak. The International Commission made key discoveries into how the virus spread, and traveled from village to village, spreading information and putting the ill and those who had come into contact with them into quarantine. The epidemic was already waning when the International Commission arrived, thanks to measures taken by local and national authorities, and it finally stopped in three months, after it had killed almost 300 people. The events were dramatised by Mike Walker on BBC Radio 4 in December 2014 in a production by David Morley . Piot narrated the programme. Piot has received the majority of the credit for discovering Ebola, since in 1976, it was claimed he was the one to receive blood samples while working in a lab at the Institute for Tropical Medicine in Antwerp, Belgium. The samples were once claimed to be originally sent by Dr. Jean-Jacques Muyembe-Tamfum , a Congolese doctor who obtained the blood samples from those sickened with a mysterious disease in then-Zaire, later discovered to be Ebola. In 2012, Piot published a memoir entitled No Time to Lose which chronicles his professional work, including the discovery of the Ebolavirus; he mentions Muyembe in passing rather than as a co-discoverer. In a 2016 Journal of Infectious Disease article, co-signed by most of the actors from that first outbreak, including Peter Piot and Jean-Jacques Muyembe, the claims by both Piot and Muyembe to have played a significant role in the early discovery of Ebola have been refuted. Piot stated in 2019 that "my book was not an attempt to write the history of Ebola, but more my personal experience". In the 1980s, Piot participated in a series of collaborative projects in Burundi, Côte d'Ivoire, Kenya, Tanzania, and Zaire. Project SIDA in Kinshasa, Zaire was the first international project on AIDS in Africa and is widely acknowledged as having provided the foundations of science's understanding of HIV infection in Africa. He was a professor of microbiology , and of public health at the Prince Leopold Institute of Tropical Medicine , in Antwerp , and at the University of Nairobi , Vrije Universiteit Brussel , the Lausanne , and a visiting professor at the London School of Economics . He was also a senior fellow at the University of Washington in Seattle, a scholar in residence at the Ford Foundation , and a senior fellow at the Bill & Melinda Gates Foundation . From 1991 to 1994, Piot was president of the International AIDS Society . In 1992, he became assistant director of the World Health Organization 's Global Programme on HIV/AIDS. On 12 December 1994, he was appointed executive director of the Joint United Nations Programme on HIV/AIDS (UNAIDS) and Assistant-Secretary-General of the United Nations. From 2009 to 2010, Piot served as director of the Institute for Global Health at Imperial College London . In October 2010, Piot became the director of the London School of Hygiene & Tropical Medicine . In addition to his work at LSHTM, Piot is a member of the Institute of Medicine of the National Academy of Sciences of the United States and the Royal Academy of Medicine of Belgium, a Fellow of the Royal College of Physicians of London , UK and a Fellow of the Academy of Medical Sciences . In 2011, Amy Gutmann appointed him to serve on the International Research Panel at the Presidential Commission for the Study of Bioethical Issues . In 2014, in the face of an unprecedented Ebola epidemic in western Africa , Piot and other scientists called for the emergency release of the experimental ZMapp vaccine for use on humans before it had undergone clinical testing on humans. That year, he was appointed by Director General Margaret Chan to the World Health Organization 's Advisory Group on the Ebola Virus Disease Response, co-chaired by Sam Zaramba and David L. Heymann . He also chaired an independent panel convened by Harvard Global Health Institute and the London School of Hygiene & Tropical Medicine into the national and international response to the epidemic, which sharply criticised the response of the WHO and put forward ten recommendations for the body's reorganisation. In February 2020, he criticised the delay in declaring the 2019–20 novel coronavirus outbreak focused on Hubei , China, a Public Health Emergency of International Concern , and advocated a five-point scale for outbreaks, rather the current binary (emergency/no emergency) system. In 2020, Piot was appointed to the European Commission 's advisory panel on COVID-19 , co-chaired by Ursula von der Leyen and Stella Kyriakides . In the preparations for the Global Health Summit hosted by the European Commission and the G20 in May 2021, Piot co-chaired the event's High Level Scientific Panel. In October 2010, Piot became the director of the London School of Hygiene & Tropical Medicine . In addition to his work at LSHTM, Piot is a member of the Institute of Medicine of the National Academy of Sciences of the United States and the Royal Academy of Medicine of Belgium, a Fellow of the Royal College of Physicians of London , UK and a Fellow of the Academy of Medical Sciences . In 2011, Amy Gutmann appointed him to serve on the International Research Panel at the Presidential Commission for the Study of Bioethical Issues . In 2014, in the face of an unprecedented Ebola epidemic in western Africa , Piot and other scientists called for the emergency release of the experimental ZMapp vaccine for use on humans before it had undergone clinical testing on humans. That year, he was appointed by Director General Margaret Chan to the World Health Organization 's Advisory Group on the Ebola Virus Disease Response, co-chaired by Sam Zaramba and David L. Heymann . He also chaired an independent panel convened by Harvard Global Health Institute and the London School of Hygiene & Tropical Medicine into the national and international response to the epidemic, which sharply criticised the response of the WHO and put forward ten recommendations for the body's reorganisation. In February 2020, he criticised the delay in declaring the 2019–20 novel coronavirus outbreak focused on Hubei , China, a Public Health Emergency of International Concern , and advocated a five-point scale for outbreaks, rather the current binary (emergency/no emergency) system. In 2020, Piot was appointed to the European Commission 's advisory panel on COVID-19 , co-chaired by Ursula von der Leyen and Stella Kyriakides . In the preparations for the Global Health Summit hosted by the European Commission and the G20 in May 2021, Piot co-chaired the event's High Level Scientific Panel. In May 2020, Piot disclosed that he had had COVID-19 . Piot is fluent in English, French, and Dutch. He is married to the American anthropologist Heidi Larson . 2002: Jonathan Dimbleby (TV series) – episode: "The AIDS Crisis in Africa" 2006: Frontline (TV series documentary) – episode: "The Age of AIDS" 2006: 60 Minutes (TV series documentary) – episode: "The New Space Race/Fighting AIDS/Immortality" 2009: House of Numbers: Anatomy of an Epidemic (Documentary) 2014: Horizon: Ebola: The Search for a Cure (TV series documentary) 2017: Heart of the Matter (documentary short) 2017: Unseen Enemy (documentary)
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg_acute_multiple_sclerosis/html
Marburg acute multiple sclerosis
Marburg acute multiple sclerosis , also known as Marburg multiple sclerosis or acute fulminant multiple sclerosis , is considered one of the multiple sclerosis borderline diseases, which is a collection of diseases classified by some as MS variants and by others as different diseases. Other diseases in this group are neuromyelitis optica (NMO), Balo concentric sclerosis , and Schilder's disease . The graver course is one form of malignant multiple sclerosis , with patients reaching a significant level of disability in less than five years from their first symptoms, often in a matter of months. Sometimes Marburg MS is considered a synonym for tumefactive MS , but not for all authors. [ citation needed ]Marburg MS has been reported to be closer to anti-MOG associated ADEM than to standard MS It has been reported to appear sometimes post-partum Some anti-MOG cases satisfy the MS requirements (lesions disseminated in time and space) and are therefore traditionally considered MS cases. After the discovery of the anti-MOG disease this classification is into revision. Some anti-MOG cases satisfy the MS requirements (lesions disseminated in time and space) and are therefore traditionally considered MS cases. After the discovery of the anti-MOG disease this classification is into revision. It took its name from Otto Marburg . It can be diagnosed in vivo with an MRI scan. If Marburg disease occurs in the form of a single large lesion, it can be radiologically indistinguishable from a brain tumor or abscess. It is usually lethal, but it has been found to be responsive to Mitoxantrone and Alemtuzumab , and it has also been responsive to autologous stem cell transplantation . Recent evidence shows that Marburg's presents a heterogeneous response to medication, as does standard MS. Historically, acute MS was a fatal disease, with death occurring within a year of onset, often secondary to extensive brainstem demyelination. Treatments include plasma exchange and/or high-dose glucocorticoids(e.g., 1 g/day of methylprednisolone for 3-5 days). Patients that satisfy criteria for MS will be treated with immunomodulatory therapies, often favoring high efficacy monoclonal antibodies.Marburg variant of MS is an acute fulminant demyelinating process which in most cases progresses inexorably to death within 1–2 years. However, there are some reports of Marburg MS reaching stability by three years.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Schröck/html
Schröck
Schröck is a borough ( Ortsbezirk ) of Marburg in Hesse . Schröck has a population of 1,755 (2019) and was first mentioned around 1233 under the name of Scrikkede . The village has one primary school and various sporting places, such as a tennis hall and an outdoor sports arena.
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Botanischer Garten Marburg
The Botanischer Garten Marburg (20 hectares), also known as the Neuer Botanischer Garten Marburg , is a botanical garden maintained by the University of Marburg , located on Karl-von-Frisch-Straße, Marburg , Hesse , Germany , and open daily. An admission fee is charged. The garden was created between 1961-1977 to replace the Alter Botanischer Garten Marburg , dating from 1810. Its construction involved movement of some 80,000 m 3 of earth, creating a pond and a brook about 1 km long, as well as a major effort to build greenhouses. The garden was inaugurated in June 1977 to celebrate the university's 450th anniversary. Outdoor areas of the garden are organized as follows: In addition, the garden's greenhouses cover total area of 1,700 square meters as follows: tropical house (545 m², 12 m height); Canary Islands house (182 m² + 82 m², 7 m); tropical crop house (182 m², 7 m) with plants including Ananas comosus and Coffea arabica ; Amazon house (123 m², 6 m) containing aquatic plants of the Amazon region including Bruguiera sexangula and Victoria amazonica ; tropical fern house (182 m², 7 m); succulent house (227 m², 7 m); Australian outback house (182 m², 7 m); and carnivorous plant house (not open to the public).
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Woodlands, Marburg
Woodlands is a heritage-listed mansion at Seminary Road, Marburg , City of Ipswich , Queensland , Australia. It was designed by George Brockwell Gill and built from 1889 to 1940s. It is also known as Marburg Campus, Ipswich Grammar School and St Vincent's Seminary. It was added to the Queensland Heritage Register on 21 October 1992. Woodlands, an imposing, two-storeyed brick residence, was erected in 1889-91 for Thomas Lorimer Smith, saw miller, timber merchant, contractor, sugarcane grower, sugar mill proprietor, and active member of the Marburg community. It was designed by Ipswich architect George Brockwell Gill. Thomas had married Mary Stuart in 1881, and at Woodlands they raised a large family. Their first residence was a modest, single-storeyed timber house near the saw mill. In the late 1880s they commissioned Ipswich builder/architect Samuel Shenton to design an imposing two- storeyed brick residence, to be erected on the hill above the Woodlands mills. The Smith family established themselves in the Rosewood -Marburg district in the 1860s/early 1870s. Thomas' father, Charles, had arrived in Queensland from England in 1862, and in 1864 was joined by his wife and family. He established a saw mill at Sandy Creek, Walloon , on the outskirts of the Rosewood Scrub, in 1865, and c. 1866 took his eldest son, Thomas Lorimer Smith, into his saw milling business. Charles Smith was among the first to select land in the Rosewood Scrub, taking up about 1000 acres c. 1870 . This included 568 acres (portion 392, parish of Walloon) selected in September 1870, on part of which Woodlands mansion was erected 20 years later. In 1876 TL Smith entered into partnership with his father, and together they erected a new and larger saw mill on portion 392, close to the then emerging township of Marburg, in the heart of the Rosewood Scrub. The Marbug saw mill opened early in 1877. In the same year Charles retired, leaving the running of the mill to his son. The mill was destroyed by fire early in 1880, but was rebuilt within a few months. Charles Smith died in December 1880, his interest in the Marburg saw mill and land passing to his son Thomas. TL Smith named the property Woodlands, expanded the saw mill - adding a joinery plant - and in the early 1880s, as the district converted to agriculture, moved into sugar cultivation and manufacture. The first sugarcane was planted c. 1881 , a sugar mill was erected next to the saw mill in 1882, and the first crushing and sugar manufacture took place in 1883. TL Smith invested heavily in the sugar mill, erecting a sugar refinery in 1884, an electric light system in 1885 (illuminating the mills, offices, stables, and his private residence), a telephone line between the Marburg mills and Walloon (the nearest telegraph station) in 1885 and a large rum distillery near the mills in 1886. In 1888 he installed more powerful machinery in the sugar mills and distillery, and laid steel tramways on the Woodlands estate to transport sugar cane and other produce to the mills. By 1889, TL Smith's sugar mill and distillery were considered the most powerful and by far the most modern, in Southern Queensland. In March 1889, giving evidence before the Royal Commission into the Queensland Sugar Industry, TL Smith stated that he was employing 36 South Sea Islanders at Woodlands, which comprised about 1200 acres, with 250 acres under cane. He claimed to have invested £20-25,000 in the sugar mill, distillery, planting, fencing, and tramway. In the late 1880s, Smith also began to plant grapes on the Woodlands estate, intending to expand into the production of wines and brandies. In the 1880s and 1890s, TL Smith was the most influential landowner and employer in the Marburg district, and was actively involved in the progress of Marburg township (established early 1870s) and community. He was appointed a Justice of the Peace in 1884, and in 1885 erected the Marburg School of Arts, for which he supplied electric power from his saw mill for the opening celebrations. He also negotiated with the Edison Electric Light Company to supply power to several buildings in the township. He was a member of the Marburg School of Arts Committee, and in 1890 was appointed to the Church of England building committee, having donated an acre of land on the Marburg-Kirchheim Road for the erection of an Anglican church in the Rosewood Scrub. In the 1890s he encouraged the expansion of the local sugar industry, agreeing to purchase cane from other farmers in the Marburg district. Shenton had established himself in Ipswich by 1851 as a carpenter, builder and contractor, and was advertising as an architect and builder by 1874. He had been involved in local politics since 1863, and served as Mayor of Ipswich in 1871-72 and in 1889. From 1886 talented young London architect George Brockwell Gill was employed in Shenton's office, and took over the architectural practice when Shenton retired in 1889. It is understood that Woodlands was designed by Gill, rather than Shenton, whose designs prior to being joined by Gill had been modest and pragmatic in style. The Smith family later attributed the design to Gill, whose other notable works included Brynhyfryd (1889–90) at Blackstone (demolished), Ipswich Girls' Grammar School (1890–91) and Ipswich Technical College (1898-1900). Tenders for the construction of a mansion at Marburg for TL Smith were called by Shenton in January–February 1889. Construction took over 2 years to complete, the Smiths moving into their new home in July 1891. The bricks were made locally, likely on the property (as with brick-lined dams constructed near the sugar mill in 1883). Red cedar used in the panelling in the dining and drawing rooms reputedly came from Wivenhoe in the Brisbane River Valley and was milled at Woodlands. Cabinet maker and joiner Joseph Klee is understood to have worked on the timber panelling for over a year. In the 1890s, economic depression, falling sugar prices, unreliable rainfall, and government encouragement to dairy farmers, led to a decline in sugar cultivation in the Marburg district. TL Smith took out a substantial mortgage on his property in 1897, and in January 1906 the Woodlands Estate was subdivided and put up for sale by order of his mortgagees. At this time the estate comprised 29 improved scrub farms, a large sugar mill (to be sold with farm no.22), 1¾ miles of sugar tramway, 38 iron cane trucks, distillery, saw mill, milking herd, numerous small sheds, 12 small cottages and Woodlands Homestead, offered on about 7 acres with an orchard of fruit trees and olives. Several of the farms sold at this time, but the Smith family retained Woodlands residence and much surrounding land. The sugar mill was purchased by Marburg Sugar Co., the chief shareholders of which were Gibson Bros of Bingera , Bundaberg , but the era of the small mill was over - Marburg farmers were no longer keen to grow sugarcane, and the Marburg Sugar Mill closed c. 1919 . In 1925 TL Smith, still resident at Woodlands, was interviewed by the Brisbane press and a description of the house published: On the crest of an isolated hill the "lookout tower" rises some 50ft above the ground level, giving a beautiful view of the surrounding country. The house is of two stories, built of brick, covered with a cement coating. Doors and windows, of massive design to conform with the spacious rooms, are all of beautifully grained red cedar cut in the Brisbane Valley. Above the top story are two brick 10,000 gallon tanks, which receive all the water from the roof, and from these tanks the water is reticulated through the house, and provides flushing for a septic system. The house took four years to complete, most of the bricks being made in the vicinity. At present the area held is about 300 acres. . . . . Thomas Lorimer Smith died in 1931. Woodlands was retained by the Smith family for over a decade, until transferred in 1944 to the Corporation of the Roman Catholic Archdiocese of Brisbane , along with nearly 130 acres of the Woodlands estate. Archbishop Duhig had purchased the property in the hope of encouraging missionaries of the Society of the Divine Word , evacuated from New Guinea to Brisbane in May 1944, to stay in Queensland. The Society was founded in 1875 in Steyl , the Netherlands , and had established a base elsewhere in Australia early in the 20th century to provide support for its missionaries in New Guinea. The Divine Word missionaries accepted Duhig's offer, and at Woodlands established the first mission seminary in Queensland. The main residence was renovated, two timber-framed buildings were erected in the grounds for use as classrooms and dormitories, and the place opened as St Vincent's Seminary in 1945. In 1954 title to the property was transferred from the Catholic Church to The Society of the Divine Word. By 1986 the main building, then containing 8 bedrooms, 2 servants' bedrooms, sitting and dining rooms with full height cedar wall panelling, large sandstone cellar, and 8 fireplaces, remained largely in its original form. The grounds by this time included a 25-metre (82 ft) in-ground pool, two additional dormitory buildings, a chapel, and a small cemetery associated with St Vincent's Seminary, and in which 18 persons had been interred, including Dr Eucharist Sirois and his wife, who ran a private hospital in Marburg during the 1910s and 1920s. In 1986 St Vincent's Seminary closed and the property was sold to the Ipswich Grammar School , which uses the property for weekend activities, seminars, and conferences. In 2002, the school sold the property to a local family, who operate it as a function centre and boutique holiday accommodation. Woodlands is a large, ornate, rendered brick building with two main levels surrounded by verandahs, plus cellar, observation deck and tower. The roof comprises two hips, separated by a masonry balustraded tower section. A curved roof is set down on four sides over open verandahs, with cast-iron paired columns , valance, and upper level balustrade. The main roof eaves , decorated with zigzag fascia , project a small hip into the verandah roof over central doorways on the east and west. The southern elevation has a double-storey portico , aligned with the central masonry section, bearing the name Woodlands and the year 1868. (The date refers to the year Charles Smith first took up land in the Rosewood district, not the date of construction of the house.) Either side are two semi-circular pedimented frontis pieces. All have elaborately decorated crests, finials and bargeboards. A large bay window projects either side. This elevation, designed as a front entrance, stands close to steep terracing, overlooking secluded grotto areas. It opens into a vestibule some 2.4 metres (7 ft 10 in) wide, with early mosaic tiled floor. The building, however, is entered from the east, where the driveway encircles an expanse of lawn. This elevation is less formal with arched windows to the front dining room, and rectangular windows to service areas. External joinery to windows and doors is painted. The ground level verandah is concrete floored, and unlined above. Internally, a hallway about 1.5 metres (4 ft 11 in) wide runs east to west. Doors are four panelled with sidelights and semi-circular fanlights, of varying pattern and colour. Ground floor dining rooms and sitting room have plaster ceilings with elaborate circular surrounds to central lights. Doors are cedar panelled with rectangular fan lights over. Deep cornices and pelmets are of moulded cedar. The front dining room has walls of full height cedar, with 4-inch (100 mm) beaded vertical boarding above the panelling to dado height. The fireplace is dark grey marble. The sitting room has full height cedar panelling and a white marble fireplace. The formal dining room opposite has rendered walls with deep cedar skirting. The fireplace is painted. The adjoining office has an angled fireplace sheeted over. This room leads into a vaulted strong room in the northwest corner, rendered, with metal vent grilles . The kitchen is a large square room with recent ceramic tile floor and fittings c. 1960 s. Storerooms with rendered walls and tiled floors lead off under a wide-arched opening. The scullery in the northeast corner is of painted brickwork and hardboard ceiling, with recent mosaic tiled floors. The WC, between scullery and eastern entrance, has rendered walls. There are stairs leading up at the eastern end of the hall, and adjacent to the vestibule. Balustrades are of turned cedar with monumental and elaborate newel posts. The underside of the eastern stair is painted boarding. That adjacent to the vestibule, of cedar panelling. The upper level contains ten bedrooms, some of original dimensions, some divided by hardboard partitions, reusing in places, original panelled doors. Original walls are rendered, several with cornices and light surrounds matching the ground level rooms. The fireplace in the southwest bedroom is painted. The adjoining small bedroom is an exception, having window joinery painted internally. A sitting area above the ground level vestibule has a corrugated iron ceiling and moulded cornice . The door, and sashes to floor level, leading on to the southern verandah, are not early. Earlier glazed panels are in place above. The eastern door from hallway to verandah is of timber and glazed panels, with twin-paned fanlight of yellow patterned glass, and side lights of blue, above green bubble glass. The verandah is floored with 4-inch (100 mm) shot edged boarding. The roof is unlined. Central to this upper floor, a narrow winding stair, leading to the tower, has painted turned balusters and moulded rail. The tower overlooks, through arched openings, hipped roofs either side. Leading out to the masonry balustraded areas over the water tanks, are doors with semi-circular fan lights, boarded on the north, one panelled on the south. From the ground floor, a stair with turned cedar balusters descends to the cellar. Cellar walls are of rough sandstone with arched openings headed in cross-bracing in spaces between 12-inch (300 mm) joists. Along the eastern wall are low timber platforms. Woodlands is an outstanding grand residence in a rural setting, overlooking undulating open country to distant hills. It is associated with a picturesque hillside graveyard; large secluded grotto; olive grove and other plantings including Bunya pines ( Araucaria bidwillii ); and disused dairy buildings. There are three other buildings in the grounds, formerly associated with St Vincent's seminary: now Bougainvillaea House, Poinciana House and Jacaranda House. Woodlands was listed on the Queensland Heritage Register on 21 October 1992 having satisfied the following criteria. The place is important in demonstrating the evolution or pattern of Queensland's history. Woodlands is important in demonstrating the pattern of Queensland's history, being associated with early non-indigenous settlement of the Rosewood Scrub and the development of the Marburg district as a sugar-producing region in the late 19th century. The place demonstrates rare, uncommon or endangered aspects of Queensland's cultural heritage. It is a comparatively rare example of a substantial town mansion erected in a rural setting in Queensland, reflecting a way of life to which its builder, a successful entrepreneur of working-class background, aspired. The place is important in demonstrating the principal characteristics of a particular class of cultural places. The place survives remarkably intact, and is important in demonstrating the principal characteristics of a grand, two-storeyed brick residence with wide, ornate verandahs, observation tower, sandstone cellar, early water reticulation system, and set in substantial grounds [which include an olive grove, other significant plantings including Bunya pines (Araucaria bidwillii), and disused dairy buildings], and with fine vistas over rural surroundings. The place is important because of its aesthetic significance. The place has aesthetic significance, generated by the formal design, the use of rendered brick and stone, the large public rooms and fine joinery work and cedar panelling internally, the decorative verandahs with cast-iron posts, balustrading and valances, the garden setting [which includes a picturesque hillside graveyard and a large, secluded grotto], and the prominent ridge-top location. The place has landmark value from the main Ipswich-Toowoomba road. The place has a special association with the life or work of a particular person, group or organisation of importance in Queensland's history. The house is an excellent example of the "grand scale" domestic work of Ipswich architect George Brockwell Gill, and has a special association with saw-miller, timber merchant and sugar-mill proprietor Thomas Lorimer Smith and his family. As St Vincent's Seminary, the place has a special association with the work of the Society of the Divine Word in Queensland from 1945 to 1986. Two substantial timber-framed dormitory/classroom buildings and a later chapel (now kitchen-dining room) in the grounds are significant for their association with St Vincent's Seminary.
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Hesse
Hesse [lower-alpha 1] or Hessia [lower-alpha 2] ( German : Hessen [ ˈhɛsn̩ ] ⓘ ), officially the State of Hesse ( German: Land Hessen ), is a state in Germany . Its capital city is Wiesbaden , and the largest urban area is Frankfurt , which is also the country's principal financial centre . Two other major historic cities are Darmstadt and Kassel . With an area of 21,114.73 square kilometers and a population of over six million, it ranks seventh and fifth, respectively, among the sixteen German states. Frankfurt Rhine-Main , Germany's second-largest metropolitan area (after Rhine-Ruhr ), is mainly located in Hesse. As a cultural region , Hesse also includes the area known as Rhenish Hesse (Rheinhessen) in the neighbouring state of Rhineland-Palatinate . The German name Hessen , like the names of other German regions ( Schwaben "Swabia", Franken "Franconia", Bayern "Bavaria", Sachsen "Saxony" ), derives from the dative plural form of the name of the inhabitants or eponymous tribe , the Hessians ( Hessen , singular Hesse ). The geographical name represents a short equivalent of the older compound name Hessenland ("land of the Hessians"). The Old High German form of the name is recorded as Hessun (dative plural of Hessi ); in Middle Latin it appears as Hassonia , Hassia , Hessia . The name of the Hessians ultimately continues the tribal name of the Chatti . The ancient name Chatti by the 7th century is recorded as Chassi , and from the 8th century as Hassi or Hessi . An inhabitant of Hesse is called a "Hessian" (German: Hesse (masculine), plural Hessen , or Hessin (feminine), plural Hessinnen ). The American English term "Hessian" for 18th-century British auxiliary troops originates with Landgrave Frederick II of Hesse-Kassel hiring out regular army units to the government of Great Britain to fight in the American Revolutionary War . The English form Hesse was in common use by the 18th century, first in the hyphenated names of the states of Hesse-Cassel and Hesse-Darmstadt , but the latinate form Hessia remained in common English usage well into the 19th century. The European Commission uses the German form Hessen , even in English-language contexts, due to the policy of leaving regional names untranslated. The synthetic element hassium , number 108 on the periodic table , was named after the state of Hesse in 1997, following a proposal of 1992. The territory of Hesse was delineated only in 1945, as Greater Hesse , under American occupation . It corresponds loosely to the medieval Landgraviate of Hesse . In the 19th century, prior to the unification of Germany , the territory of what is now Hesse comprised the territories of Grand Duchy of Hesse (also known as Hesse-Darmstadt), the Duchy of Nassau , the free city of Frankfurt and the Electorate of Hesse (also known as Hesse-Kassel). The Central Hessian region was inhabited in the Upper Paleolithic . Finds of tools in southern Hesse in Rüsselsheim suggest the presence of Pleistocene hunters about 13,000 years ago. A fossil hominid skull that was found in northern Hesse, just outside the village of Rhünda, has been dated at 12,000 years ago. The Züschen tomb (German: Steinkammergrab von Züschen, sometimes also Lohne-Züschen) is a prehistoric burial monument, located between Lohne and Züschen , near Fritzlar , Hesse, Germany. Classified as a gallery grave or a Hessian-Westphalian stone cist ( hessisch-westfälische Steinkiste ), it is one of the most important megalithic monuments in Central Europe. Dating to c. 3000 BC , it belongs to the Late Neolithic Wartberg culture . An early Celtic presence in what is now Hesse is indicated by a mid-5th-century BC La Tène -style burial uncovered at Glauberg . The region was later settled by the Germanic Chatti tribe around the 1st century BC, and the name Hesse is a continuation of that tribal name. The ancient Romans had a military camp in Dorlar, and in Waldgirmes directly on the eastern outskirts of Wetzlar was a civil settlement under construction. Presumably, the provincial government for the occupied territories of the right bank of Germania was planned at this location. The governor of Germania, at least temporarily, likely had resided here. The settlement appears to have been abandoned by the Romans after the devastating Battle of the Teutoburg Forest failed in the year AD 9. The Chatti were also involved in the Revolt of the Batavi in AD 69. Hessia, from the early 7th century on, served as a buffer between areas dominated by the Saxons (to the north) and the Franks , who brought the area to the south under their control in the early sixth century and occupied Thuringia (to the east) in 531. Hessia occupies the northwestern part of the modern German state of Hesse; its borders were not clearly delineated. Its geographic center is Fritzlar ; it extends in the southeast to Hersfeld on the river Fulda, in the north to past Kassel and up to the rivers Diemel and Weser. To the west, it occupies the valleys of the rivers Eder and Lahn (the latter until it turns south). It measured roughly 90 kilometers north–south, and 80 north-west. The area around Fritzlar shows evidence of significant pagan belief from the 1st century on. Geismar was a particular focus of such activity; it was continuously occupied from the Roman period on, with a settlement from the Roman period, which itself had a predecessor from the 5th century BC. Excavations have produced a horse burial and bronze artifacts. A possible religious cult may have centered on a natural spring in Geismar, called Heilgenbron ; the name "Geismar" (possibly "energetic pool") itself may be derived from that spring. The village of Maden, Gudensberg [ de ] , now a part of Gudensberg near Fritzlar and less than ten miles from Geismar, was likely an ancient religious center; the basaltic outcrop of Gudensberg is named after Wodan, and a two-meter tall quartzite megalith called the Wotanstein is at the center of the village. By the mid-7th century, the Franks had established themselves as overlords, which is suggested by archeological evidence of burials, and they built fortifications in various places, including Christenberg . By 690, they took direct control over Hessia, apparently to counteract expansion by the Saxons, who built fortifications in Gaulskopf and Eresburg across the river Diemel, the northern boundary of Hessia. The Büraburg (which already had a Frankish settlement in the sixth century ) was one of the places the Franks fortified to resist the Saxon pressure, and according to John-Henry Clay, the Büraburg was "probably the largest man-made construction seen in Hessia for at least seven hundred years". Walls and trenches totaling one kilometer in length were made, and they enclosed "8 hectares of a spur that offered a commanding view over Fritzlar and the densely-populated heart of Hessia". Following Saxon incursions into Chattish territory in the 7th century, two gaue had been established; a Frankish one, comprising an area around Fritzlar and Kassel , and a Saxonian one. In the 9th century, the Saxon Hessengau also came under the rule of the Franconians. From 962 the land which would become Hesse was part of the Holy Roman Empire . In the 10th and 11th centuries it was mostly encompassed by the Western or Rhenish part of the stem duchy of Franconia . In the 12th century, Hessengau passed to the Landgraviate of Thuringia . As a result of the War of the Thuringian Succession (1247–1264) the former Thuringian lands were partitioned between the Wettin Margraviate of Meissen , which gained Thuringia proper, and the new Landgraviate of Hesse , which remained with the Ludovingians . From that point on the Ludovingian coat of arms came to represent both Thuringia and Hesse. It rose to prominence under Landgrave Philip the Magnanimous , who was one of the leaders of German Protestantism . After Philip's death in 1567, the territory was divided among his four sons from his first marriage (Philip was a bigamist ) into four lines: Hesse-Kassel (or Hesse-Cassel), Hesse-Darmstadt , Hesse-Rheinfels , and the also previously existing Hesse-Marburg . As the latter two lines died out quite quickly (1583 and 1605, respectively), Hesse-Kassel and Hesse-Darmstadt were the two core states within the Hessian lands. Several collateral lines split off during the centuries, such as in 1622, when Hesse-Homburg split off from Hesse-Darmstadt, and in 1760 when Hesse-Hanau split off from Hesse-Kassel. In the late 16th century, Kassel adopted Calvinism , while Darmstadt remained Lutheran and consequently the two lines often found themselves on opposing sides of conflicts, most notably in the disputes over Hesse-Marburg and in the Thirty Years' War , when Darmstadt fought on the side of the Emperor, while Kassel sided with Sweden and France . The Landgrave Frederick II (1720–1785) ruled Hesse-Kassel as a benevolent despot, from 1760 to 1785. He combined Enlightenment ideas with Christian values, cameralist plans for central control of the economy, and a militaristic approach toward diplomacy. He funded the depleted treasury of the poor government by loaning 19,000 soldiers in complete military formations to Great Britain to fight in North America during the American Revolutionary War , 1776–1783. These soldiers, commonly known as Hessians , fought under the British flag. The British used the Hessians in several conflicts, including in the Irish Rebellion of 1798 . For further revenue, the soldiers were loaned to other places as well. Most were conscripted, with their pay going to the Landgrave. In 1789 the French Revolution began and in 1794, during the War of the First Coalition , the French Republic occupied the Left Bank of the Rhine , including part of Lower Katzenelnbogen ( Niedergrafschaft Katzenelnbogen [ de ] , Hesse-Kassel's part of the former County of Katzenelnbogen which was held by the appanage Hesse-Rotenburg ). Emperor Francis II formally recognised the annexation of the Left Bank in the 1801 Treaty of Lunéville . This led in 1803 to the Reichsdeputationshauptschluss , a substantial reorganisation ( mediatisation ) of the states and territories of the Empire. Several exclaves of Mainz were mediatised to Hesse-Kassel and Hesse-Darmstadt , and Hesse-Darmstadt also gained the Duchy of Westphalia from Cologne , the parts of Worms on the right-bank of the Rhine, and the former Free City of Friedberg . Nassau-Weilburg gained the right-bank territories of Trier among other territories. Orange-Nassau gained the Prince-Bishopric of Fulda (as the Principality of Nassau-Orange-Fulda ). The Landgrave of Hesse-Kassel was also elevated to the status of Prince-Elector ( Kurfürst ), with his state thereby becoming the Electorate of Hesse or Electoral Hesse ( German: Kurhessen , Kur being the German-language term for the Empire's College of Electors ). In July 1806 Hesse-Darmstadt, Nassau-Weilburg, Nassau-Usingen , and the newly merged Principality of Isenburg became founding members of Napoleon 's Confederation of the Rhine . Hesse-Darmstadt expanded further in the resulting mediatisation, absorbing numerous small states (including Hesse-Homburg and much of the territory of the Houses of Solms [ de ] , Erbach [ de ] and Sayn-Wittgenstein ). It was also elevated by Napoleon to the status of Grand Duchy , becoming the Grand Duchy of Hesse . Orange-Nassau, which refused to join the Confederation, lost Siegen , Dillenburg , Hadamar and Beilstein to Berg and Fulda to the Prince-Primate of the Confederation (and former Elector of Mainz) Karl Theodor von Dalberg ; the remainder of its territory was merged with that of Nassau-Usingen and Nassau-Weilburg in August 1806 to form the Duchy of Nassau . Waldeck also joined the Confederation in 1807. The Holy Roman Empire was dissolved in August 1806 , rendering Hesse-Kassel's electoral privilege meaningless. Hesse-Kassel was occupied by the French in October 1806 and the remainder of Lower Katzenelnbogen was annexed to the French Empire as Pays réservé de Catzenellenbogen [ de ] . The rest of its territory was annexed to the Kingdom of Westphalia in 1807; Hesse-Hanau (a secundogeniture of Hesse-Kassel) was annexed to the Grand Duchy of Frankfurt in 1810 along with the other territories held by the Prince-primate: Frankfurt, Fulda, Aschaffenburg and Wetzlar . As a result of the German campaign of 1813 the Kingdom of Westphalia and the Grand Duchy of Frankfurt were dissolved and Hesse-Kassel and Hesse-Hanau were restored; Orange-Nassau was also restored in its territories previously lost to Berg. As a result of the 1815 Congress of Vienna Hesse-Kassel gained Fulda (roughly the western third of the former Prince-Bishopric, the rest of which went to Bavaria and Saxe-Weimar-Eisenach ) from Frankfurt and part of Isenburg, while several of its small northern exclaves were absorbed into Hanover , some small eastern areas were ceded to Saxe-Weimar-Eisenach and Lower Katzenelnbogen was ceded to Nassau. Hesse-Darmstadt lost the Duchy of Westphalia and the Sayn-Wittgensteiner lands to the Prussian Province of Westphalia but gained territory on the left bank of the Rhine centred on Mainz, which became known as Rhenish Hesse ( Rheinhessen ), and the remainder of Isenburg. Orange-Nassau, whose ruler was now also King William I of the Netherlands and Grand Duke of Luxembourg, was ceded to Prussia but most of its territory aside from Siegen was then ceded on to Nassau. Hesse-Homburg and the Free City of Frankfurt were also restored. While the other former Electors had gained other titles, becoming either Kings or Grand Dukes , the Elector of Hesse-Kassel alone retained the anachronistic title of Prince-Elector; a request to be recognised as "King of the Chatti " ( König der Katten ) was rejected by the Congress. Following the mediatisations and the Congress of Vienna significantly fewer states remained in the region that is now Hesse: the Hessian states, Nassau, Waldeck and Frankfurt. The Kingdoms of Prussia and Bavaria also held some territory in the region. The Congress also established the German Confederation , of which they all became members. Hesse-Hanau was (re-)absorbed into Hesse-Kassel in 1821. In the 1866 Austro-Prussian War the states of the region allied with Austria were defeated during the Campaign of the Main . Following Prussia's victory and dissolution of the German Confederation, Prussia annexed Electoral Hesse, Frankfurt, Hesse-Homburg, Nassau and small parts of Bavaria and the Grand Duchy of Hesse, which were then combined into the Province of Hesse-Nassau . The name Kurhessen survived, denoting the region around Kassel. The Grand Duchy of Hesse retained its autonomy in defeat because a greater part of the country was situated south of the river Main and it was feared that Prussian expansion beyond the Main might provoke France. However, Upper Hesse ( German: Oberhessen : the parts of Hesse-Darmstadt north of the Main around the town of Gießen ) was incorporated into the North German Confederation ( Norddeutscher Bund ), a tight federation of German states established by Prussia in 1867, while also remaining part of the Grand Duchy. In 1871, after France's defeat in the Franco-Prussian War , the whole of the Grand Duchy joined the German Empire . Around the turn of the 20th century, Darmstadt was one of the centres of the Jugendstil . Until 1907, the Grand Duchy of Hesse used the Hessian red and white lion barry as its coat-of-arms. The revolution of 1918 following the German defeat in WWI transformed Hesse-Darmstadt from a monarchy to a republic, which officially renamed itself the People's State of Hesse ( Volksstaat Hessen ). The state parliament, or Landtag consisted of 70 deputies elected on the basis of proportional representation . There were six Landtag elections between 1919 and 1932. Following the Nazi seizure of power in Berlin, the Landtag was formally abolished as a result of the " Law on the Reconstruction of the Reich " of 30 January 1934, which replaced the German federal system with a unitary state . The parts of Hesse-Darmstadt on the left bank of the Rhine (Rhenish Hesse), as well as those right-bank areas of Hesse-Darmstadt and Hesse-Nassau within 30 km (19 mi) of Koblenz or Mainz were occupied by French troops until 1930 under the terms of the Versailles peace treaty that officially ended World War I in 1919. The Kingdom of Prussia became the Free State of Prussia , of which Hesse-Nassau remained a province. In 1929 the Free State of Waldeck was dissolved and incorporated into Hesse-Nassau. In 1932 Wetzlar ( Landkreis Wetzlar [ de ] ), formerly an exclave of the Prussian Rhine Province situated between Hesse-Nassau and the Grand Duchy's Upper Hesse, was transferred to Hesse-Nassau. The former Hessian exclave of Rinteln ( Kreis Rinteln [ de ] , the Hessian part of the former County of Schaumburg ) was also detached and transferred to the Province of Hanover . On 1 July 1944 the Prussian Province of Hesse-Nassau was formally divided into the provinces of Kurhessen and Nassau . At the same time the former Hessian Schmalkalden exclaves ( Landkreis Herrschaft Schmalkalden [ de ] ), together with the Regierungsbezirk Erfurt [ de ] of the Province of Saxony , were transferred to Thuringia . The territories of the new provinces did not directly correspond with their pre-1866 namesakes but rather with the associated NSDAP Gaue : Gau Electoral Hesse and Gau Hesse-Nassau (excluding the areas which were part of the People's State of Hesse). After World War II , the Hessian territory west of the Rhine was again occupied by France , while the rest of the region was part of the US occupation zone . On 17 September 1945 the Wanfried agreement adjusted the border between American-occupied Kurhessen and Soviet-occupied Thuringia. The United States proclaimed the state of Greater Hesse ( Groß-Hessen ) on 19 September 1945, out of the People's State of Hesse and most of what had been the Prussian Provinces of Kurhessen and Nassau. The French incorporated their parts of Hesse (Rhenish Hesse) and Nassau (as Regierungsbezirk Montabaur ) into the newly founded state of Rhineland-Palatinate ( Rheinland-Pfalz ) on 30 August 1946. On 4 December 1946, Greater Hesse was officially renamed Hessen . Hesse in the 1940s received more than a million displaced ethnic Germans . Due to its proximity to the Inner German border , Hesse became an important location of NATO installations in the 1950s, especially military bases of the US V Corps and United States Army Europe . The first elected minister president of Hesse was Christian Stock , followed by Georg-August Zinn (both Social Democrats ). The German Social Democrats gained an absolute majority in 1962 and pursued progressive policies with the so-called Großer Hessenplan . The CDU gained a relative majority in the 1974 elections, but the Social Democrats continued to govern in a coalition with the FDP . Hesse was first governed by the CDU under Walter Wallmann during 1987–1991, replaced by a SPD-Greens coalition under Hans Eichel during 1991–1999. From 1999, Hesse was governed by the CDU under Roland Koch (retired 2010) and Volker Bouffier (incumbent as of 2020). Frankfurt during the 1960s to 1990s developed into one of the major cities of West Germany. As of 2016, 12% of the total population of Hesse lived in the city of Frankfurt.The Central Hessian region was inhabited in the Upper Paleolithic . Finds of tools in southern Hesse in Rüsselsheim suggest the presence of Pleistocene hunters about 13,000 years ago. A fossil hominid skull that was found in northern Hesse, just outside the village of Rhünda, has been dated at 12,000 years ago. The Züschen tomb (German: Steinkammergrab von Züschen, sometimes also Lohne-Züschen) is a prehistoric burial monument, located between Lohne and Züschen , near Fritzlar , Hesse, Germany. Classified as a gallery grave or a Hessian-Westphalian stone cist ( hessisch-westfälische Steinkiste ), it is one of the most important megalithic monuments in Central Europe. Dating to c. 3000 BC , it belongs to the Late Neolithic Wartberg culture . An early Celtic presence in what is now Hesse is indicated by a mid-5th-century BC La Tène -style burial uncovered at Glauberg . The region was later settled by the Germanic Chatti tribe around the 1st century BC, and the name Hesse is a continuation of that tribal name. The ancient Romans had a military camp in Dorlar, and in Waldgirmes directly on the eastern outskirts of Wetzlar was a civil settlement under construction. Presumably, the provincial government for the occupied territories of the right bank of Germania was planned at this location. The governor of Germania, at least temporarily, likely had resided here. The settlement appears to have been abandoned by the Romans after the devastating Battle of the Teutoburg Forest failed in the year AD 9. The Chatti were also involved in the Revolt of the Batavi in AD 69. Hessia, from the early 7th century on, served as a buffer between areas dominated by the Saxons (to the north) and the Franks , who brought the area to the south under their control in the early sixth century and occupied Thuringia (to the east) in 531. Hessia occupies the northwestern part of the modern German state of Hesse; its borders were not clearly delineated. Its geographic center is Fritzlar ; it extends in the southeast to Hersfeld on the river Fulda, in the north to past Kassel and up to the rivers Diemel and Weser. To the west, it occupies the valleys of the rivers Eder and Lahn (the latter until it turns south). It measured roughly 90 kilometers north–south, and 80 north-west. The area around Fritzlar shows evidence of significant pagan belief from the 1st century on. Geismar was a particular focus of such activity; it was continuously occupied from the Roman period on, with a settlement from the Roman period, which itself had a predecessor from the 5th century BC. Excavations have produced a horse burial and bronze artifacts. A possible religious cult may have centered on a natural spring in Geismar, called Heilgenbron ; the name "Geismar" (possibly "energetic pool") itself may be derived from that spring. The village of Maden, Gudensberg [ de ] , now a part of Gudensberg near Fritzlar and less than ten miles from Geismar, was likely an ancient religious center; the basaltic outcrop of Gudensberg is named after Wodan, and a two-meter tall quartzite megalith called the Wotanstein is at the center of the village. By the mid-7th century, the Franks had established themselves as overlords, which is suggested by archeological evidence of burials, and they built fortifications in various places, including Christenberg . By 690, they took direct control over Hessia, apparently to counteract expansion by the Saxons, who built fortifications in Gaulskopf and Eresburg across the river Diemel, the northern boundary of Hessia. The Büraburg (which already had a Frankish settlement in the sixth century ) was one of the places the Franks fortified to resist the Saxon pressure, and according to John-Henry Clay, the Büraburg was "probably the largest man-made construction seen in Hessia for at least seven hundred years". Walls and trenches totaling one kilometer in length were made, and they enclosed "8 hectares of a spur that offered a commanding view over Fritzlar and the densely-populated heart of Hessia". Following Saxon incursions into Chattish territory in the 7th century, two gaue had been established; a Frankish one, comprising an area around Fritzlar and Kassel , and a Saxonian one. In the 9th century, the Saxon Hessengau also came under the rule of the Franconians.From 962 the land which would become Hesse was part of the Holy Roman Empire . In the 10th and 11th centuries it was mostly encompassed by the Western or Rhenish part of the stem duchy of Franconia . In the 12th century, Hessengau passed to the Landgraviate of Thuringia . As a result of the War of the Thuringian Succession (1247–1264) the former Thuringian lands were partitioned between the Wettin Margraviate of Meissen , which gained Thuringia proper, and the new Landgraviate of Hesse , which remained with the Ludovingians . From that point on the Ludovingian coat of arms came to represent both Thuringia and Hesse. It rose to prominence under Landgrave Philip the Magnanimous , who was one of the leaders of German Protestantism . After Philip's death in 1567, the territory was divided among his four sons from his first marriage (Philip was a bigamist ) into four lines: Hesse-Kassel (or Hesse-Cassel), Hesse-Darmstadt , Hesse-Rheinfels , and the also previously existing Hesse-Marburg . As the latter two lines died out quite quickly (1583 and 1605, respectively), Hesse-Kassel and Hesse-Darmstadt were the two core states within the Hessian lands. Several collateral lines split off during the centuries, such as in 1622, when Hesse-Homburg split off from Hesse-Darmstadt, and in 1760 when Hesse-Hanau split off from Hesse-Kassel. In the late 16th century, Kassel adopted Calvinism , while Darmstadt remained Lutheran and consequently the two lines often found themselves on opposing sides of conflicts, most notably in the disputes over Hesse-Marburg and in the Thirty Years' War , when Darmstadt fought on the side of the Emperor, while Kassel sided with Sweden and France . The Landgrave Frederick II (1720–1785) ruled Hesse-Kassel as a benevolent despot, from 1760 to 1785. He combined Enlightenment ideas with Christian values, cameralist plans for central control of the economy, and a militaristic approach toward diplomacy. He funded the depleted treasury of the poor government by loaning 19,000 soldiers in complete military formations to Great Britain to fight in North America during the American Revolutionary War , 1776–1783. These soldiers, commonly known as Hessians , fought under the British flag. The British used the Hessians in several conflicts, including in the Irish Rebellion of 1798 . For further revenue, the soldiers were loaned to other places as well. Most were conscripted, with their pay going to the Landgrave.In 1789 the French Revolution began and in 1794, during the War of the First Coalition , the French Republic occupied the Left Bank of the Rhine , including part of Lower Katzenelnbogen ( Niedergrafschaft Katzenelnbogen [ de ] , Hesse-Kassel's part of the former County of Katzenelnbogen which was held by the appanage Hesse-Rotenburg ). Emperor Francis II formally recognised the annexation of the Left Bank in the 1801 Treaty of Lunéville . This led in 1803 to the Reichsdeputationshauptschluss , a substantial reorganisation ( mediatisation ) of the states and territories of the Empire. Several exclaves of Mainz were mediatised to Hesse-Kassel and Hesse-Darmstadt , and Hesse-Darmstadt also gained the Duchy of Westphalia from Cologne , the parts of Worms on the right-bank of the Rhine, and the former Free City of Friedberg . Nassau-Weilburg gained the right-bank territories of Trier among other territories. Orange-Nassau gained the Prince-Bishopric of Fulda (as the Principality of Nassau-Orange-Fulda ). The Landgrave of Hesse-Kassel was also elevated to the status of Prince-Elector ( Kurfürst ), with his state thereby becoming the Electorate of Hesse or Electoral Hesse ( German: Kurhessen , Kur being the German-language term for the Empire's College of Electors ). In July 1806 Hesse-Darmstadt, Nassau-Weilburg, Nassau-Usingen , and the newly merged Principality of Isenburg became founding members of Napoleon 's Confederation of the Rhine . Hesse-Darmstadt expanded further in the resulting mediatisation, absorbing numerous small states (including Hesse-Homburg and much of the territory of the Houses of Solms [ de ] , Erbach [ de ] and Sayn-Wittgenstein ). It was also elevated by Napoleon to the status of Grand Duchy , becoming the Grand Duchy of Hesse . Orange-Nassau, which refused to join the Confederation, lost Siegen , Dillenburg , Hadamar and Beilstein to Berg and Fulda to the Prince-Primate of the Confederation (and former Elector of Mainz) Karl Theodor von Dalberg ; the remainder of its territory was merged with that of Nassau-Usingen and Nassau-Weilburg in August 1806 to form the Duchy of Nassau . Waldeck also joined the Confederation in 1807. The Holy Roman Empire was dissolved in August 1806 , rendering Hesse-Kassel's electoral privilege meaningless. Hesse-Kassel was occupied by the French in October 1806 and the remainder of Lower Katzenelnbogen was annexed to the French Empire as Pays réservé de Catzenellenbogen [ de ] . The rest of its territory was annexed to the Kingdom of Westphalia in 1807; Hesse-Hanau (a secundogeniture of Hesse-Kassel) was annexed to the Grand Duchy of Frankfurt in 1810 along with the other territories held by the Prince-primate: Frankfurt, Fulda, Aschaffenburg and Wetzlar . As a result of the German campaign of 1813 the Kingdom of Westphalia and the Grand Duchy of Frankfurt were dissolved and Hesse-Kassel and Hesse-Hanau were restored; Orange-Nassau was also restored in its territories previously lost to Berg. As a result of the 1815 Congress of Vienna Hesse-Kassel gained Fulda (roughly the western third of the former Prince-Bishopric, the rest of which went to Bavaria and Saxe-Weimar-Eisenach ) from Frankfurt and part of Isenburg, while several of its small northern exclaves were absorbed into Hanover , some small eastern areas were ceded to Saxe-Weimar-Eisenach and Lower Katzenelnbogen was ceded to Nassau. Hesse-Darmstadt lost the Duchy of Westphalia and the Sayn-Wittgensteiner lands to the Prussian Province of Westphalia but gained territory on the left bank of the Rhine centred on Mainz, which became known as Rhenish Hesse ( Rheinhessen ), and the remainder of Isenburg. Orange-Nassau, whose ruler was now also King William I of the Netherlands and Grand Duke of Luxembourg, was ceded to Prussia but most of its territory aside from Siegen was then ceded on to Nassau. Hesse-Homburg and the Free City of Frankfurt were also restored. While the other former Electors had gained other titles, becoming either Kings or Grand Dukes , the Elector of Hesse-Kassel alone retained the anachronistic title of Prince-Elector; a request to be recognised as "King of the Chatti " ( König der Katten ) was rejected by the Congress. Following the mediatisations and the Congress of Vienna significantly fewer states remained in the region that is now Hesse: the Hessian states, Nassau, Waldeck and Frankfurt. The Kingdoms of Prussia and Bavaria also held some territory in the region. The Congress also established the German Confederation , of which they all became members. Hesse-Hanau was (re-)absorbed into Hesse-Kassel in 1821. In the 1866 Austro-Prussian War the states of the region allied with Austria were defeated during the Campaign of the Main . Following Prussia's victory and dissolution of the German Confederation, Prussia annexed Electoral Hesse, Frankfurt, Hesse-Homburg, Nassau and small parts of Bavaria and the Grand Duchy of Hesse, which were then combined into the Province of Hesse-Nassau . The name Kurhessen survived, denoting the region around Kassel. The Grand Duchy of Hesse retained its autonomy in defeat because a greater part of the country was situated south of the river Main and it was feared that Prussian expansion beyond the Main might provoke France. However, Upper Hesse ( German: Oberhessen : the parts of Hesse-Darmstadt north of the Main around the town of Gießen ) was incorporated into the North German Confederation ( Norddeutscher Bund ), a tight federation of German states established by Prussia in 1867, while also remaining part of the Grand Duchy. In 1871, after France's defeat in the Franco-Prussian War , the whole of the Grand Duchy joined the German Empire . Around the turn of the 20th century, Darmstadt was one of the centres of the Jugendstil . Until 1907, the Grand Duchy of Hesse used the Hessian red and white lion barry as its coat-of-arms. The revolution of 1918 following the German defeat in WWI transformed Hesse-Darmstadt from a monarchy to a republic, which officially renamed itself the People's State of Hesse ( Volksstaat Hessen ). The state parliament, or Landtag consisted of 70 deputies elected on the basis of proportional representation . There were six Landtag elections between 1919 and 1932. Following the Nazi seizure of power in Berlin, the Landtag was formally abolished as a result of the " Law on the Reconstruction of the Reich " of 30 January 1934, which replaced the German federal system with a unitary state . The parts of Hesse-Darmstadt on the left bank of the Rhine (Rhenish Hesse), as well as those right-bank areas of Hesse-Darmstadt and Hesse-Nassau within 30 km (19 mi) of Koblenz or Mainz were occupied by French troops until 1930 under the terms of the Versailles peace treaty that officially ended World War I in 1919. The Kingdom of Prussia became the Free State of Prussia , of which Hesse-Nassau remained a province. In 1929 the Free State of Waldeck was dissolved and incorporated into Hesse-Nassau. In 1932 Wetzlar ( Landkreis Wetzlar [ de ] ), formerly an exclave of the Prussian Rhine Province situated between Hesse-Nassau and the Grand Duchy's Upper Hesse, was transferred to Hesse-Nassau. The former Hessian exclave of Rinteln ( Kreis Rinteln [ de ] , the Hessian part of the former County of Schaumburg ) was also detached and transferred to the Province of Hanover . On 1 July 1944 the Prussian Province of Hesse-Nassau was formally divided into the provinces of Kurhessen and Nassau . At the same time the former Hessian Schmalkalden exclaves ( Landkreis Herrschaft Schmalkalden [ de ] ), together with the Regierungsbezirk Erfurt [ de ] of the Province of Saxony , were transferred to Thuringia . The territories of the new provinces did not directly correspond with their pre-1866 namesakes but rather with the associated NSDAP Gaue : Gau Electoral Hesse and Gau Hesse-Nassau (excluding the areas which were part of the People's State of Hesse). After World War II , the Hessian territory west of the Rhine was again occupied by France , while the rest of the region was part of the US occupation zone . On 17 September 1945 the Wanfried agreement adjusted the border between American-occupied Kurhessen and Soviet-occupied Thuringia. The United States proclaimed the state of Greater Hesse ( Groß-Hessen ) on 19 September 1945, out of the People's State of Hesse and most of what had been the Prussian Provinces of Kurhessen and Nassau. The French incorporated their parts of Hesse (Rhenish Hesse) and Nassau (as Regierungsbezirk Montabaur ) into the newly founded state of Rhineland-Palatinate ( Rheinland-Pfalz ) on 30 August 1946. On 4 December 1946, Greater Hesse was officially renamed Hessen . Hesse in the 1940s received more than a million displaced ethnic Germans . Due to its proximity to the Inner German border , Hesse became an important location of NATO installations in the 1950s, especially military bases of the US V Corps and United States Army Europe . The first elected minister president of Hesse was Christian Stock , followed by Georg-August Zinn (both Social Democrats ). The German Social Democrats gained an absolute majority in 1962 and pursued progressive policies with the so-called Großer Hessenplan . The CDU gained a relative majority in the 1974 elections, but the Social Democrats continued to govern in a coalition with the FDP . Hesse was first governed by the CDU under Walter Wallmann during 1987–1991, replaced by a SPD-Greens coalition under Hans Eichel during 1991–1999. From 1999, Hesse was governed by the CDU under Roland Koch (retired 2010) and Volker Bouffier (incumbent as of 2020). Frankfurt during the 1960s to 1990s developed into one of the major cities of West Germany. As of 2016, 12% of the total population of Hesse lived in the city of Frankfurt.In 1789 the French Revolution began and in 1794, during the War of the First Coalition , the French Republic occupied the Left Bank of the Rhine , including part of Lower Katzenelnbogen ( Niedergrafschaft Katzenelnbogen [ de ] , Hesse-Kassel's part of the former County of Katzenelnbogen which was held by the appanage Hesse-Rotenburg ). Emperor Francis II formally recognised the annexation of the Left Bank in the 1801 Treaty of Lunéville . This led in 1803 to the Reichsdeputationshauptschluss , a substantial reorganisation ( mediatisation ) of the states and territories of the Empire. Several exclaves of Mainz were mediatised to Hesse-Kassel and Hesse-Darmstadt , and Hesse-Darmstadt also gained the Duchy of Westphalia from Cologne , the parts of Worms on the right-bank of the Rhine, and the former Free City of Friedberg . Nassau-Weilburg gained the right-bank territories of Trier among other territories. Orange-Nassau gained the Prince-Bishopric of Fulda (as the Principality of Nassau-Orange-Fulda ). The Landgrave of Hesse-Kassel was also elevated to the status of Prince-Elector ( Kurfürst ), with his state thereby becoming the Electorate of Hesse or Electoral Hesse ( German: Kurhessen , Kur being the German-language term for the Empire's College of Electors ). In July 1806 Hesse-Darmstadt, Nassau-Weilburg, Nassau-Usingen , and the newly merged Principality of Isenburg became founding members of Napoleon 's Confederation of the Rhine . Hesse-Darmstadt expanded further in the resulting mediatisation, absorbing numerous small states (including Hesse-Homburg and much of the territory of the Houses of Solms [ de ] , Erbach [ de ] and Sayn-Wittgenstein ). It was also elevated by Napoleon to the status of Grand Duchy , becoming the Grand Duchy of Hesse . Orange-Nassau, which refused to join the Confederation, lost Siegen , Dillenburg , Hadamar and Beilstein to Berg and Fulda to the Prince-Primate of the Confederation (and former Elector of Mainz) Karl Theodor von Dalberg ; the remainder of its territory was merged with that of Nassau-Usingen and Nassau-Weilburg in August 1806 to form the Duchy of Nassau . Waldeck also joined the Confederation in 1807. The Holy Roman Empire was dissolved in August 1806 , rendering Hesse-Kassel's electoral privilege meaningless. Hesse-Kassel was occupied by the French in October 1806 and the remainder of Lower Katzenelnbogen was annexed to the French Empire as Pays réservé de Catzenellenbogen [ de ] . The rest of its territory was annexed to the Kingdom of Westphalia in 1807; Hesse-Hanau (a secundogeniture of Hesse-Kassel) was annexed to the Grand Duchy of Frankfurt in 1810 along with the other territories held by the Prince-primate: Frankfurt, Fulda, Aschaffenburg and Wetzlar . As a result of the German campaign of 1813 the Kingdom of Westphalia and the Grand Duchy of Frankfurt were dissolved and Hesse-Kassel and Hesse-Hanau were restored; Orange-Nassau was also restored in its territories previously lost to Berg. As a result of the 1815 Congress of Vienna Hesse-Kassel gained Fulda (roughly the western third of the former Prince-Bishopric, the rest of which went to Bavaria and Saxe-Weimar-Eisenach ) from Frankfurt and part of Isenburg, while several of its small northern exclaves were absorbed into Hanover , some small eastern areas were ceded to Saxe-Weimar-Eisenach and Lower Katzenelnbogen was ceded to Nassau. Hesse-Darmstadt lost the Duchy of Westphalia and the Sayn-Wittgensteiner lands to the Prussian Province of Westphalia but gained territory on the left bank of the Rhine centred on Mainz, which became known as Rhenish Hesse ( Rheinhessen ), and the remainder of Isenburg. Orange-Nassau, whose ruler was now also King William I of the Netherlands and Grand Duke of Luxembourg, was ceded to Prussia but most of its territory aside from Siegen was then ceded on to Nassau. Hesse-Homburg and the Free City of Frankfurt were also restored. While the other former Electors had gained other titles, becoming either Kings or Grand Dukes , the Elector of Hesse-Kassel alone retained the anachronistic title of Prince-Elector; a request to be recognised as "King of the Chatti " ( König der Katten ) was rejected by the Congress. Following the mediatisations and the Congress of Vienna significantly fewer states remained in the region that is now Hesse: the Hessian states, Nassau, Waldeck and Frankfurt. The Kingdoms of Prussia and Bavaria also held some territory in the region. The Congress also established the German Confederation , of which they all became members. Hesse-Hanau was (re-)absorbed into Hesse-Kassel in 1821.In the 1866 Austro-Prussian War the states of the region allied with Austria were defeated during the Campaign of the Main . Following Prussia's victory and dissolution of the German Confederation, Prussia annexed Electoral Hesse, Frankfurt, Hesse-Homburg, Nassau and small parts of Bavaria and the Grand Duchy of Hesse, which were then combined into the Province of Hesse-Nassau . The name Kurhessen survived, denoting the region around Kassel. The Grand Duchy of Hesse retained its autonomy in defeat because a greater part of the country was situated south of the river Main and it was feared that Prussian expansion beyond the Main might provoke France. However, Upper Hesse ( German: Oberhessen : the parts of Hesse-Darmstadt north of the Main around the town of Gießen ) was incorporated into the North German Confederation ( Norddeutscher Bund ), a tight federation of German states established by Prussia in 1867, while also remaining part of the Grand Duchy. In 1871, after France's defeat in the Franco-Prussian War , the whole of the Grand Duchy joined the German Empire . Around the turn of the 20th century, Darmstadt was one of the centres of the Jugendstil . Until 1907, the Grand Duchy of Hesse used the Hessian red and white lion barry as its coat-of-arms.The revolution of 1918 following the German defeat in WWI transformed Hesse-Darmstadt from a monarchy to a republic, which officially renamed itself the People's State of Hesse ( Volksstaat Hessen ). The state parliament, or Landtag consisted of 70 deputies elected on the basis of proportional representation . There were six Landtag elections between 1919 and 1932. Following the Nazi seizure of power in Berlin, the Landtag was formally abolished as a result of the " Law on the Reconstruction of the Reich " of 30 January 1934, which replaced the German federal system with a unitary state . The parts of Hesse-Darmstadt on the left bank of the Rhine (Rhenish Hesse), as well as those right-bank areas of Hesse-Darmstadt and Hesse-Nassau within 30 km (19 mi) of Koblenz or Mainz were occupied by French troops until 1930 under the terms of the Versailles peace treaty that officially ended World War I in 1919. The Kingdom of Prussia became the Free State of Prussia , of which Hesse-Nassau remained a province. In 1929 the Free State of Waldeck was dissolved and incorporated into Hesse-Nassau. In 1932 Wetzlar ( Landkreis Wetzlar [ de ] ), formerly an exclave of the Prussian Rhine Province situated between Hesse-Nassau and the Grand Duchy's Upper Hesse, was transferred to Hesse-Nassau. The former Hessian exclave of Rinteln ( Kreis Rinteln [ de ] , the Hessian part of the former County of Schaumburg ) was also detached and transferred to the Province of Hanover . On 1 July 1944 the Prussian Province of Hesse-Nassau was formally divided into the provinces of Kurhessen and Nassau . At the same time the former Hessian Schmalkalden exclaves ( Landkreis Herrschaft Schmalkalden [ de ] ), together with the Regierungsbezirk Erfurt [ de ] of the Province of Saxony , were transferred to Thuringia . The territories of the new provinces did not directly correspond with their pre-1866 namesakes but rather with the associated NSDAP Gaue : Gau Electoral Hesse and Gau Hesse-Nassau (excluding the areas which were part of the People's State of Hesse).After World War II , the Hessian territory west of the Rhine was again occupied by France , while the rest of the region was part of the US occupation zone . On 17 September 1945 the Wanfried agreement adjusted the border between American-occupied Kurhessen and Soviet-occupied Thuringia. The United States proclaimed the state of Greater Hesse ( Groß-Hessen ) on 19 September 1945, out of the People's State of Hesse and most of what had been the Prussian Provinces of Kurhessen and Nassau. The French incorporated their parts of Hesse (Rhenish Hesse) and Nassau (as Regierungsbezirk Montabaur ) into the newly founded state of Rhineland-Palatinate ( Rheinland-Pfalz ) on 30 August 1946. On 4 December 1946, Greater Hesse was officially renamed Hessen . Hesse in the 1940s received more than a million displaced ethnic Germans . Due to its proximity to the Inner German border , Hesse became an important location of NATO installations in the 1950s, especially military bases of the US V Corps and United States Army Europe . The first elected minister president of Hesse was Christian Stock , followed by Georg-August Zinn (both Social Democrats ). The German Social Democrats gained an absolute majority in 1962 and pursued progressive policies with the so-called Großer Hessenplan . The CDU gained a relative majority in the 1974 elections, but the Social Democrats continued to govern in a coalition with the FDP . Hesse was first governed by the CDU under Walter Wallmann during 1987–1991, replaced by a SPD-Greens coalition under Hans Eichel during 1991–1999. From 1999, Hesse was governed by the CDU under Roland Koch (retired 2010) and Volker Bouffier (incumbent as of 2020). Frankfurt during the 1960s to 1990s developed into one of the major cities of West Germany. As of 2016, 12% of the total population of Hesse lived in the city of Frankfurt.The only state to straddle west and central portions of Germany where the eight ordinal directions (compass points) and the centre is considered, Hesse borders six other states. These are, from north, clockwise: Lower Saxony , Thuringia , Bavaria , Baden-Württemberg , Rhineland-Palatinate , and North Rhine-Westphalia . The most populous towns and cities of Hesse are in the southwest, the Frankfurt Rhein-Main Region namely Frankfurt am Main , Wiesbaden , Darmstadt , Offenbach , Hanau , Giessen , Wetzlar , and Rüsselsheim am Main . Outside, but very near the south-west corner of Hesse are four populous, highly technologised, places: Worms , Ludwigshafen , Mannheim , and Heidelberg . Other large Hessian towns are Fulda in the east , Kassel and Marburg an der Lahn in the north and Limburg an der Lahn in the west. All of the "on the river" suffixes are locally and, informally far beyond, omitted of these cities. The plain between the rivers Main, Rhine, and lower Neckar, and the Odenwald ridge of low mountains or very high hills is called the Ried which continues to north, across the Main, as the Wetterau. Both plains which are quite densely populated also have a substantial built environment such as the country's largest airport, contrasting with the more forested, hillier middle and northern thirds of Hesse. The longest rivers in Hesse are the Eder and moreover its distributary the Fulda draining most of the north, the Lahn in the centre-west and, as to those navigable by large vessels, the Main and very broad Rhine in the south. The countryside is hilly and the topographical map, inset, names 14 short, low to medium-height mountain ranges including the Rhön , the Westerwald , the Taunus , the Vogelsberg , the Knüll and the Spessart . The notable range forming the southern taper of Hesse (shared with a narrowing of the Ried, the Rhine's eastern plain) and briefly spanning the middle Neckar valley which begins directly east of Heidelberg (thus also in Baden-Württemberg ) is the Odenwald . Forming a mid-eastern tiny projection into mostly Thuringia is the uppermost part of the Ulster , commanding the west valley side of which is the Hessian highest point, Wasserkuppe at 950m above sea level – in the Rhön. The Rhine forms the long southwest border of Hesse. Two notables oxbow lakes , the Stockstadt-Erfelder Altrhein and Lampertheimer Altrhein are in the south-west fringe. Hesse, 42% forest, is by that measure the greenest state in Germany. Hesse is a unitary state governed directly by the Hessian government in the capital city Wiesbaden, partially through regional vicarious authorities called Regierungspräsidien . Municipal parliaments are, however, elected independently from the state government by the Hessian people. Local municipalities enjoy a considerable degree of home rule . The state is divided into three administrative provinces ( Regierungsbezirke ): Kassel in the north and east, Gießen in the centre, and Darmstadt in the south, the latter being the most populous region with the Frankfurt Rhine-Main agglomeration in its central area. The administrative regions have no legislature of their own, but are executive agencies of the state government. Hesse is divided into 21 districts (Kreise) and five independent cities, each with their own local governments. They are, shown with abbreviations as used on vehicle number plates: Independent cities: The term "Rhenish Hesse" ( German : Rheinhessen ) refers to the part of the former Grand Duchy of Hesse-Darmstadt located west of the Rhine . It has not been part of the State of Hesse since 1946 due to divisions in the aftermath of World War II. This province is now part of the State of Rhineland-Palatinate . It is a hilly countryside largely devoted to vineyards; therefore, it is also called the "land of the thousand hills". Its larger towns include Mainz , Worms , Bingen , Alzey , Nieder-Olm , and Ingelheim . Many inhabitants commute to work in Mainz, Wiesbaden, or Frankfurt.The state is divided into three administrative provinces ( Regierungsbezirke ): Kassel in the north and east, Gießen in the centre, and Darmstadt in the south, the latter being the most populous region with the Frankfurt Rhine-Main agglomeration in its central area. The administrative regions have no legislature of their own, but are executive agencies of the state government. Hesse is divided into 21 districts (Kreise) and five independent cities, each with their own local governments. They are, shown with abbreviations as used on vehicle number plates: Independent cities:The term "Rhenish Hesse" ( German : Rheinhessen ) refers to the part of the former Grand Duchy of Hesse-Darmstadt located west of the Rhine . It has not been part of the State of Hesse since 1946 due to divisions in the aftermath of World War II. This province is now part of the State of Rhineland-Palatinate . It is a hilly countryside largely devoted to vineyards; therefore, it is also called the "land of the thousand hills". Its larger towns include Mainz , Worms , Bingen , Alzey , Nieder-Olm , and Ingelheim . Many inhabitants commute to work in Mainz, Wiesbaden, or Frankfurt.Hesse has been a parliamentary republic since 1918, except during Nazi rule (1933–1945). The German federal system has elements of exclusive federal competences, shared competences, and exclusive competences of the states. Hesse is famous for having a rather brisk style in its politics with the ruling parties being either the center-right Christian Democratic Union (CDU) or the center-left Social Democratic Party of Germany (SPD). Due to the Hessian electoral laws, the biggest party normally needs a smaller coalition partner. As Hesse is a partly sovereign federated state , its constitution combines the offices of the head of state and head of government in one office called the Minister-President (German: Ministerpräsident ) which is comparable to the office of a prime minister . In the 2018 state elections the two leading parties, CDU and SPD, lost 11.3% (7 seats) and 10.9% (8 seats) of the vote respectively. The Green party, a member of Hesse's previous governing coalition with CDU, gained 8.7% (16 seats). The largest gains during the election were made by Alternative for Germany (AfD) at 13.1%. As AfD had not passed the 5% threshold in the 2013 state election , this marked its first entry into the Hessian parliament ( Hessischer Landtag ). The two other parties also made gains. The major losses of the two leading parties (whose coalition made up the federal cabinet during the election) closely mirrors the results of the 2018 state elections in Bavaria . In the current parliament the conservative CDU holds 40 seats, the centre-left SPD and the leftist Green party each hold 29 seats, the right-wing AfD holds 19 seats, the liberal FDP party holds 11 seats and the socialist party The Left holds 9 seats. As a member state of the German federation, Hesse does not have a diplomatic service of its own. However, Hesse operates representation offices in such foreign countries as the United States, China, Hungary, Cuba, Russia, Poland, and Iran. These offices are mostly used to represent Hessian interests in cultural and economic affairs. Hesse has also permanent representation offices in Berlin at the federal government of Germany and in Brussels at the institutions of the European Union . The flag colors of Hesse are red and white, which are printed on a Hessian sack. The civil flag of Hesse resembles that of Monaco 's and, particularly, Indonesia 's. The Hessian coat of arms shows a lion rampant striped with red and white. The official anthem of Hesse is called " Hessenlied " ("Song of Hesse") and was written by Albrecht Brede (music) and Carl Preser (lyrics). As Hesse is a partly sovereign federated state , its constitution combines the offices of the head of state and head of government in one office called the Minister-President (German: Ministerpräsident ) which is comparable to the office of a prime minister .In the 2018 state elections the two leading parties, CDU and SPD, lost 11.3% (7 seats) and 10.9% (8 seats) of the vote respectively. The Green party, a member of Hesse's previous governing coalition with CDU, gained 8.7% (16 seats). The largest gains during the election were made by Alternative for Germany (AfD) at 13.1%. As AfD had not passed the 5% threshold in the 2013 state election , this marked its first entry into the Hessian parliament ( Hessischer Landtag ). The two other parties also made gains. The major losses of the two leading parties (whose coalition made up the federal cabinet during the election) closely mirrors the results of the 2018 state elections in Bavaria . In the current parliament the conservative CDU holds 40 seats, the centre-left SPD and the leftist Green party each hold 29 seats, the right-wing AfD holds 19 seats, the liberal FDP party holds 11 seats and the socialist party The Left holds 9 seats.As a member state of the German federation, Hesse does not have a diplomatic service of its own. However, Hesse operates representation offices in such foreign countries as the United States, China, Hungary, Cuba, Russia, Poland, and Iran. These offices are mostly used to represent Hessian interests in cultural and economic affairs. Hesse has also permanent representation offices in Berlin at the federal government of Germany and in Brussels at the institutions of the European Union . The flag colors of Hesse are red and white, which are printed on a Hessian sack. The civil flag of Hesse resembles that of Monaco 's and, particularly, Indonesia 's. The Hessian coat of arms shows a lion rampant striped with red and white. The official anthem of Hesse is called " Hessenlied " ("Song of Hesse") and was written by Albrecht Brede (music) and Carl Preser (lyrics). Hesse has a population of over 6 million, nearly 4 million of which is concentrated in the Rhein-Main region (German: Rhein-Main Gebiet ) in the south of the state, an area that includes the most populous city, Frankfurt am Main , the capital Wiesbaden , and Darmstadt and Offenbach . The population of Hesse is predicted to shrink by 4.3% by 2030, with the biggest falls in the north of the state, especially in the area around the city of Kassel . Frankfurt is the fastest growing city with a predicted rise in population of 4.8% by 2030. Frankfurt's growth is driven by its importance as a financial centre and it receives immigrants from all over the world: in 2015 over half of the city's population had an immigrant background. Source: Births January–March 2017 = 14,537 Births January–March 2018 = 14,202 Deaths January–March 2017 = 19,289 Deaths January–March 2018 = 18,831 Natural growth January–March 2017 = −4,752 Natural growth January–March 2018 = −4,629 Three different languages or dialect groups are spoken in Hesse: The Far North is part of the Low Saxon language area, divided into a tiny Eastphalian and a larger Westphalian dialect area. Most of Hesse belongs to the West Middle German dialect zone. There is some disagreement as to whether all Hessian dialects south of the Benrath line may be subsumed under one dialect group: Rhine Franconian, or whether most dialects should be regarded as a dialect group of its own: Hessian, whereas only South Hessian is part of Rhine Franconian. Hessian proper can be split into Lower Hessian in the north, East Hessian in the East around Fulda and Central Hessian, which covers the largest area of all dialects in Hesse. In the extreme Northeast, the Thuringian dialect zone extends into Hesse, whereas in the Southeast, the state border to Bavaria is not fully identical to the dialect border between East Franconian and East Hessian. Since approximately World War II, a spoken variety of Standard German with dialect substrate has been superseding the traditional dialects mentioned so far. This development knows a north-to-south movement, the north being early to supplant the traditional language, whereas in the south, there is still a considerable part of the population that communicates in South Hessian. In most of the areas, however, the traditional language is close to extinction, whereas until the first half of the 20th century, almost the entire population spoke dialect in almost all situations. The Upper Class started to speak Standard German beginning in the late 19th century, so for decades, the traditional language served as a sociolect. The prominent written language in Hesse has been Standard German since the 16th century. Before, the Low Saxon part used Middle Low German , the rest of the Land Early Modern German as prominent written languages. These had supplanted Latin in the High Middle Ages . In 2016 Christianity was the most widespread religion in the state (63%). In 2011, 40% of Hessians belonged to the Protestant Church in Hesse and Nassau or Evangelical Church of Hesse Electorate-Waldeck (members of the Protestant Church in Germany ), 25% adhered to the Roman Catholic Church , while other Christians constituted some 3%; the next most common religion of the Hessian population was Islam , adhered to by 7%. Source: Births January–March 2017 = 14,537 Births January–March 2018 = 14,202 Deaths January–March 2017 = 19,289 Deaths January–March 2018 = 18,831 Natural growth January–March 2017 = −4,752 Natural growth January–March 2018 = −4,629Three different languages or dialect groups are spoken in Hesse: The Far North is part of the Low Saxon language area, divided into a tiny Eastphalian and a larger Westphalian dialect area. Most of Hesse belongs to the West Middle German dialect zone. There is some disagreement as to whether all Hessian dialects south of the Benrath line may be subsumed under one dialect group: Rhine Franconian, or whether most dialects should be regarded as a dialect group of its own: Hessian, whereas only South Hessian is part of Rhine Franconian. Hessian proper can be split into Lower Hessian in the north, East Hessian in the East around Fulda and Central Hessian, which covers the largest area of all dialects in Hesse. In the extreme Northeast, the Thuringian dialect zone extends into Hesse, whereas in the Southeast, the state border to Bavaria is not fully identical to the dialect border between East Franconian and East Hessian. Since approximately World War II, a spoken variety of Standard German with dialect substrate has been superseding the traditional dialects mentioned so far. This development knows a north-to-south movement, the north being early to supplant the traditional language, whereas in the south, there is still a considerable part of the population that communicates in South Hessian. In most of the areas, however, the traditional language is close to extinction, whereas until the first half of the 20th century, almost the entire population spoke dialect in almost all situations. The Upper Class started to speak Standard German beginning in the late 19th century, so for decades, the traditional language served as a sociolect. The prominent written language in Hesse has been Standard German since the 16th century. Before, the Low Saxon part used Middle Low German , the rest of the Land Early Modern German as prominent written languages. These had supplanted Latin in the High Middle Ages .In 2016 Christianity was the most widespread religion in the state (63%). In 2011, 40% of Hessians belonged to the Protestant Church in Hesse and Nassau or Evangelical Church of Hesse Electorate-Waldeck (members of the Protestant Church in Germany ), 25% adhered to the Roman Catholic Church , while other Christians constituted some 3%; the next most common religion of the Hessian population was Islam , adhered to by 7%. The Hessian government has overall responsibility for the education within the state. Hesse has follow universities: None of Hesse's universities are included in German Excellence Universities . There are many international schools in Hesse, primarily centred in and around Frankfurt. Hesse is the only state in Germany where students have to study all three stanzas of the " Das Deutschlandlied ". A single existing big science facility in Hesse is GSI Helmholtz Centre for Heavy Ion Research in Darmstadt-Wixhausen with 1,520 employees. The second one Facility for Antiproton and Ion Research is in construction till 2025. In space research there are 2 European organization European Space Operations Center and European Organisation for the Exploitation of Meteorological Satellites in Darmstadt .The Hessian government has overall responsibility for the education within the state. Hesse has follow universities: None of Hesse's universities are included in German Excellence Universities . There are many international schools in Hesse, primarily centred in and around Frankfurt. Hesse is the only state in Germany where students have to study all three stanzas of the " Das Deutschlandlied ". A single existing big science facility in Hesse is GSI Helmholtz Centre for Heavy Ion Research in Darmstadt-Wixhausen with 1,520 employees. The second one Facility for Antiproton and Ion Research is in construction till 2025. In space research there are 2 European organization European Space Operations Center and European Organisation for the Exploitation of Meteorological Satellites in Darmstadt .A single existing big science facility in Hesse is GSI Helmholtz Centre for Heavy Ion Research in Darmstadt-Wixhausen with 1,520 employees. The second one Facility for Antiproton and Ion Research is in construction till 2025. In space research there are 2 European organization European Space Operations Center and European Organisation for the Exploitation of Meteorological Satellites in Darmstadt .Hesse has a rich and varied cultural history, with many important cultural and historical centres and several UNESCO world-heritage sites. Darmstadt has a rich cultural heritage as the former seat of the Landgraves and Grand Dukes of Hesse. It is known as centre of the art nouveau Jugendstil and modern architecture and there are also several important examples of 19th century architecture influenced by British and Russian imperial architecture due to close family ties of the Grand Duke's family to the reigning dynasties in London and Saint Petersburg in the Grand Duchy period . Darmstadt is an important centre for music, home of the Darmstädter Ferienkurse for contemporary classical music and the Jazz Institute Darmstadt, Europe's largest public jazz archive. Frankfurt am Main is a major international cultural centre. Over 2 million people visit the city's approximately 60 exhibition centres every year. Amongst its most famous art galleries are the Schirn Kunsthalle , a major centre for international modern art, and the Städel , whose large collections include over 3000 paintings, 4000 photographs, and 100,000 drawings including works by Picasso , Monet , Rembrandt and Dürer . Goethe was born in Frankfurt and there is a museum in his birthplace . Frankfurt has many music venues, including an award-winning opera house , the Alte Oper , and the Jahrhunderthalle . Its several theatres include the English Theatre, the largest English-speaking theatre on the European continent. Kassel has many palaces and parks, including Bergpark Wilhelmshöhe , a Baroque landscape park and UNESCO World Heritage site. The Brothers Grimm lived and worked in Kassel for 30 years and the recently opened Grimmwelt museum explores their lives, works and influence and features their personal copies of the Children's and Household Tales , which are on the UNESCO World Heritage "Memory of the World" Document register. The Fridericianum , built in 1779, is one of the oldest public museums in Europe. Kassel is also home to the documenta , a large modern art exhibition that has taken place every five years since the 1950s. The Hessian Ministry of the Arts supports numerous independent cultural initiatives, organisations, and associations as well as artists from many fields including music, literature, theatre and dance, cinema and the new media, graphic art, and exhibitions. International cultural projects aim to further relations with European partners. From an archaeological point of view, the old watercourses of Hesse provide evidence of the wider history of the landscape and their protection has required cooperation. Hesse has several UNESCO World Heritage sites. These include: Frankfurt hosts the following professional sports teams or clubs: Frankfurt is host to the classic cycle race Eschborn-Frankfurt City Loop (known as Rund um den Henninger-Turm from 1961 to 2008). The city hosts also the annual Frankfurt Marathon and the Ironman Germany . Outside Frankfurt, notable professional sports teams include Kickers Offenbach , SV Darmstadt 98 , Marburg Mercenaries , Gießen 46ers , MT Melsungen , VfB Friedberg , and the Kassel Huskies . The Hessian state broadcasting corporation is called HR ( Hessischer Rundfunk ). HR is a member of the federal ARD broadcasting association. HR provides a statewide TV channel as well as a range of regional radio stations (HR 1, HR 2, HR 3, HR 4, you fm and HR info). Besides the state run HR, privately run TV stations exist and are an important line of commerce. Among the commercial radio stations that are active in Hesse, Hit Radio FFH, Planet Radio, Harmony FM, Radio BOB and Antenne Frankfurt are the most popular.Darmstadt has a rich cultural heritage as the former seat of the Landgraves and Grand Dukes of Hesse. It is known as centre of the art nouveau Jugendstil and modern architecture and there are also several important examples of 19th century architecture influenced by British and Russian imperial architecture due to close family ties of the Grand Duke's family to the reigning dynasties in London and Saint Petersburg in the Grand Duchy period . Darmstadt is an important centre for music, home of the Darmstädter Ferienkurse for contemporary classical music and the Jazz Institute Darmstadt, Europe's largest public jazz archive. Frankfurt am Main is a major international cultural centre. Over 2 million people visit the city's approximately 60 exhibition centres every year. Amongst its most famous art galleries are the Schirn Kunsthalle , a major centre for international modern art, and the Städel , whose large collections include over 3000 paintings, 4000 photographs, and 100,000 drawings including works by Picasso , Monet , Rembrandt and Dürer . Goethe was born in Frankfurt and there is a museum in his birthplace . Frankfurt has many music venues, including an award-winning opera house , the Alte Oper , and the Jahrhunderthalle . Its several theatres include the English Theatre, the largest English-speaking theatre on the European continent. Kassel has many palaces and parks, including Bergpark Wilhelmshöhe , a Baroque landscape park and UNESCO World Heritage site. The Brothers Grimm lived and worked in Kassel for 30 years and the recently opened Grimmwelt museum explores their lives, works and influence and features their personal copies of the Children's and Household Tales , which are on the UNESCO World Heritage "Memory of the World" Document register. The Fridericianum , built in 1779, is one of the oldest public museums in Europe. Kassel is also home to the documenta , a large modern art exhibition that has taken place every five years since the 1950s. The Hessian Ministry of the Arts supports numerous independent cultural initiatives, organisations, and associations as well as artists from many fields including music, literature, theatre and dance, cinema and the new media, graphic art, and exhibitions. International cultural projects aim to further relations with European partners. From an archaeological point of view, the old watercourses of Hesse provide evidence of the wider history of the landscape and their protection has required cooperation. Hesse has several UNESCO World Heritage sites. These include:Frankfurt hosts the following professional sports teams or clubs: Frankfurt is host to the classic cycle race Eschborn-Frankfurt City Loop (known as Rund um den Henninger-Turm from 1961 to 2008). The city hosts also the annual Frankfurt Marathon and the Ironman Germany . Outside Frankfurt, notable professional sports teams include Kickers Offenbach , SV Darmstadt 98 , Marburg Mercenaries , Gießen 46ers , MT Melsungen , VfB Friedberg , and the Kassel Huskies .The Hessian state broadcasting corporation is called HR ( Hessischer Rundfunk ). HR is a member of the federal ARD broadcasting association. HR provides a statewide TV channel as well as a range of regional radio stations (HR 1, HR 2, HR 3, HR 4, you fm and HR info). Besides the state run HR, privately run TV stations exist and are an important line of commerce. Among the commercial radio stations that are active in Hesse, Hit Radio FFH, Planet Radio, Harmony FM, Radio BOB and Antenne Frankfurt are the most popular.With Hesse's largest city Frankfurt am Main being home of the European Central Bank (ECB), the German Bundesbank and the Frankfurt Stock Exchange , Hesse is home to the financial capital of mainland Europe. Furthermore, Hesse has always been one of the largest and healthiest economies in Germany. Its GDP in 2013 exceeded €236 billion (about US$316 billion). This makes Hesse itself one of the largest economies in Europe and the 38th largest in the world. According to GDP-per-capita figures, Hesse is the wealthiest state (after the city-states Hamburg and Bremen ) in Germany with approx. US$52,500. Frankfurt is crucial as a financial center , with both the European Central Bank and the Deutsche Bundesbank 's headquarters located there. Numerous smaller banks and Deutsche Bank , DZ Bank , KfW Bank , Commerzbank are also headquartered in Frankfurt, with the offices of several international banks also being housed there. Frankfurt is also the location of the most important German stock exchange, the Frankfurt Stock Exchange. Insurance companies have settled mostly in Wiesbaden . The city's largest private employer is the R+V Versicherung , with about 3,900 employees, other major employers are DBV-Winterthur , the SV SparkassenVersicherung and the Delta Lloyd Group . The Rhine-Main Region has the second largest industrial density in Germany after the Ruhr area . The main economic fields of importance are the chemical and pharmaceutical industries with Sanofi , Merck , Heraeus , Stada , Messer Griesheim , Bayer Crop Science , SGL Carbon , Celanese , Cabot , Clariant , Akzo Nobel , Kuraray , Ineos , LyondellBasell , Allessa [ de ] and Evonik Industries . But also other consumer goods are produced by Procter & Gamble , Coty and Colgate Palmolive . The Rhine-Main Region is not restricted only to Hesse, smaller part is in Rhineland-Palatinate . There situated 2 important pharma companies: BioNTech (HQ), which found the first mRNA vaccine against COVID-19 in the world (licensed to Pfizer ), and Boehringer Ingelheim , close to Hesse's border in Mainz and Ingelheim respectively. It supports from Max Planck Institute for Heart and Lung Research , Max Planck Institute for Brain Research and Paul Ehrlich Institute . Also in other part of Hesse there is important pharma and medical manufacturers, especially in Marburg where there is industry park based on ex-Behring Werke: BioNTech (mRNA vaccines), CSL Behring , Temmler and Melsungen with B. Braun . Pharma activity in Marburg is also supported from research facilities: Max Planck Institute for Terrestrial Microbiology , Center for undiagnosed and rare diseases [ de ] , Institute of Virology (Marburg) [ de ] (researh of Ebolavirus and Marburgvirus ; Parasitology ) with BSL4-Labor , Marburg Heavy Ion Beam Therapy Center [ de ] . Merck controls ca. 60% of world's liquid crystal market. Heraeus , Umicore and Evonik Industries manufacture different type of catalysts from Platinum metals , Vanadium , Neodymium , Manganese , Copper etc. In east Fulda there is the tire plant ( Fulda Reifen ). 2 other tire plants are in Korbach from Continental and Hanau from Goodyear . Specialised metallurgical industry focused on platinum metals has been represented by Heraeus and Umicore and magnetic materials have been a focus of Vacuumschmelze based in Hanau . Also in Hanau there used to be a plant producing nuclear fuel (classical uranium, but also MOX fuel ), but the production has stopped and the facility has been mothballed. Heraeus continues to manufacture irradiation sources from Cobalt and Iridium . In the mechanical and automotive engineering field Opel in Rüsselsheim is worth mentioning. After acquisition Opel by Stellantis , it is in rapid decline of production and employment. Which has also negative effect on automotive parts supplier, Continental will close a plant in Karben and cut jobs at other location in Hesse. In northern Hesse, in Baunatal , Volkswagen AG has a large factory that manufactures spare parts, not far-away from it there is also a Daimler Truck plant, which produces an axes. Alstom , after takeover of Bombardier , has a large plant that manufactures Traxx locomotives in Kassel . Industrial printers ( Manroland , Gallus Holding ), x-ray airport check equipment ( Smiths ), handling and loading equipment ( Dematic ), chemical equipment ( Air Liquide Global E&C Solutions ), vacuum pumps ( Pfeiffer Vacuum ), vacuum industrial furnace (ALD Vacuum Technologies), textile machines (Karl Mayer), shavers ( Braun ), medical ( Fresenius , Sirona ) and industrial (Schenck Process, Samson ) apparatuses are produced in Rhine-Main Region. Manufacturing of heating boilers and heat pumps are typical for Hesse and represented with Bosch Thermotechnik [ de ] and Viessmann . Vistec produces electron-beam lithography systems for semiconductor industry in Weilburg , also there is manufacturing of inspection, testing and measurement equipment for semiconductor fabrication process from KLA-Tencor . Leica Microsystems manufactures different types of microscopes, inclusive they with special light microscopic optics, which are used in wafer and photo mask testing. PVA TePla from Wettenberg is specialist for crystal growing process (Si, Ge, GaAs, GaP, InP) with Czochralski Process , Float-Zone Process , High-Temperature Chemical Vapor Deposition , Vertical Gradient Freeze equipment, quality inspection apparatus, plasma and vacuum machine. ABB Robotics is in Friedberg . Satisloh is a machine manufacturer in Wetzlar for the production of lenses and components for the optical industry. The company operating Frankfurt Airport is one of the largest employers in Hesse with nearly 22,000 employees. Aerospace cluster contains also Rolls-Royce's aviation engine work in Oberursel and APU manufacturing plant and service center of Honeywell in Raunheim . Companies with an international reputation are located outside the Rhine-Main region in Wetzlar . There is the center of the optical, electrical and precision engineering industries, Leitz , Leica , Minox , Hensoldt ( Zeiss ) and Brita with several plants in central Hesse. Oculus Optikgeräte manufactures Scheimpflug tomographs for examining the anterior segment of the eye, topographers for measuring the anterior surface of the cornea, tonometers for assessing the biomechanical properties of the cornea, a wide-angle observation system for vitreous body surgery, universal trial goggles for subjective refraction, various perimeters for visual field testing and vision testing devices for testing eyesight. Electrical transformers are produced by Hitachi ABB Power Grids in Hanau and Siemens Energy in Frankfurt-am-Main . SMA Solar Technology manufactures an inverters for photovoltaic systems. Rittal is specialized on electrical enclosure situated in Herborn and Eschenburg . Power semiconductors from IXYS in Lampertheim and UV and infrared lamps from Heraeus . Many IT and telecommunications companies are located in Hesse, many of them in Frankfurt and Darmstadt, like Software AG (Darmstadt), T-Systems (Frankfurt and Darmstadt), Deutsche Telekom (laboratories in Darmstadt), DB Systel (Frankfurt), Lufthansa Systems (Raunheim near Frankfurt) and DE-CIX (Frankfurt). Sweet making is typical, there are 2 big factories: Ferrero , Stadtallendorf and Baronie (Sarotti), Hattersheim am Main . Frankfurter Sausage is famous, but there is also other sorts like Frankfurter Rindswurst , Ahle Wurst . Beverage industry is well-developed and manufactures sparkling wine ( Sekt ), white wine ( Riesling ), mineral waters ( Selters ), beers ( Radeberger ) and cider . In Frankfurt-Oberrad exists growing of wild herbs for green sauce and monument. The leather industry was predominantly based in Offenbach , but is now extinct, existing only in museums. The same happened with Frankfurt's fur industry and Hanau's jewelry industry. The Hochtaunuskreis has the lowest unemployment rate at 3.8% while the independent city of Kassel has the highest rate nationally at 12.1%. In October 2018 the unemployment rate stood at 4.4% and was lower than the national average. With Hesse's largest city Frankfurt am Main being home of the European Central Bank (ECB), the German Bundesbank and the Frankfurt Stock Exchange , Hesse is home to the financial capital of mainland Europe. Furthermore, Hesse has always been one of the largest and healthiest economies in Germany. Its GDP in 2013 exceeded €236 billion (about US$316 billion). This makes Hesse itself one of the largest economies in Europe and the 38th largest in the world. According to GDP-per-capita figures, Hesse is the wealthiest state (after the city-states Hamburg and Bremen ) in Germany with approx. US$52,500. Frankfurt is crucial as a financial center , with both the European Central Bank and the Deutsche Bundesbank 's headquarters located there. Numerous smaller banks and Deutsche Bank , DZ Bank , KfW Bank , Commerzbank are also headquartered in Frankfurt, with the offices of several international banks also being housed there. Frankfurt is also the location of the most important German stock exchange, the Frankfurt Stock Exchange. Insurance companies have settled mostly in Wiesbaden . The city's largest private employer is the R+V Versicherung , with about 3,900 employees, other major employers are DBV-Winterthur , the SV SparkassenVersicherung and the Delta Lloyd Group .The Rhine-Main Region has the second largest industrial density in Germany after the Ruhr area . The main economic fields of importance are the chemical and pharmaceutical industries with Sanofi , Merck , Heraeus , Stada , Messer Griesheim , Bayer Crop Science , SGL Carbon , Celanese , Cabot , Clariant , Akzo Nobel , Kuraray , Ineos , LyondellBasell , Allessa [ de ] and Evonik Industries . But also other consumer goods are produced by Procter & Gamble , Coty and Colgate Palmolive . The Rhine-Main Region is not restricted only to Hesse, smaller part is in Rhineland-Palatinate . There situated 2 important pharma companies: BioNTech (HQ), which found the first mRNA vaccine against COVID-19 in the world (licensed to Pfizer ), and Boehringer Ingelheim , close to Hesse's border in Mainz and Ingelheim respectively. It supports from Max Planck Institute for Heart and Lung Research , Max Planck Institute for Brain Research and Paul Ehrlich Institute . Also in other part of Hesse there is important pharma and medical manufacturers, especially in Marburg where there is industry park based on ex-Behring Werke: BioNTech (mRNA vaccines), CSL Behring , Temmler and Melsungen with B. Braun . Pharma activity in Marburg is also supported from research facilities: Max Planck Institute for Terrestrial Microbiology , Center for undiagnosed and rare diseases [ de ] , Institute of Virology (Marburg) [ de ] (researh of Ebolavirus and Marburgvirus ; Parasitology ) with BSL4-Labor , Marburg Heavy Ion Beam Therapy Center [ de ] . Merck controls ca. 60% of world's liquid crystal market. Heraeus , Umicore and Evonik Industries manufacture different type of catalysts from Platinum metals , Vanadium , Neodymium , Manganese , Copper etc. In east Fulda there is the tire plant ( Fulda Reifen ). 2 other tire plants are in Korbach from Continental and Hanau from Goodyear .Specialised metallurgical industry focused on platinum metals has been represented by Heraeus and Umicore and magnetic materials have been a focus of Vacuumschmelze based in Hanau . Also in Hanau there used to be a plant producing nuclear fuel (classical uranium, but also MOX fuel ), but the production has stopped and the facility has been mothballed. Heraeus continues to manufacture irradiation sources from Cobalt and Iridium .In the mechanical and automotive engineering field Opel in Rüsselsheim is worth mentioning. After acquisition Opel by Stellantis , it is in rapid decline of production and employment. Which has also negative effect on automotive parts supplier, Continental will close a plant in Karben and cut jobs at other location in Hesse. In northern Hesse, in Baunatal , Volkswagen AG has a large factory that manufactures spare parts, not far-away from it there is also a Daimler Truck plant, which produces an axes. Alstom , after takeover of Bombardier , has a large plant that manufactures Traxx locomotives in Kassel . Industrial printers ( Manroland , Gallus Holding ), x-ray airport check equipment ( Smiths ), handling and loading equipment ( Dematic ), chemical equipment ( Air Liquide Global E&C Solutions ), vacuum pumps ( Pfeiffer Vacuum ), vacuum industrial furnace (ALD Vacuum Technologies), textile machines (Karl Mayer), shavers ( Braun ), medical ( Fresenius , Sirona ) and industrial (Schenck Process, Samson ) apparatuses are produced in Rhine-Main Region. Manufacturing of heating boilers and heat pumps are typical for Hesse and represented with Bosch Thermotechnik [ de ] and Viessmann . Vistec produces electron-beam lithography systems for semiconductor industry in Weilburg , also there is manufacturing of inspection, testing and measurement equipment for semiconductor fabrication process from KLA-Tencor . Leica Microsystems manufactures different types of microscopes, inclusive they with special light microscopic optics, which are used in wafer and photo mask testing. PVA TePla from Wettenberg is specialist for crystal growing process (Si, Ge, GaAs, GaP, InP) with Czochralski Process , Float-Zone Process , High-Temperature Chemical Vapor Deposition , Vertical Gradient Freeze equipment, quality inspection apparatus, plasma and vacuum machine. ABB Robotics is in Friedberg . Satisloh is a machine manufacturer in Wetzlar for the production of lenses and components for the optical industry.The company operating Frankfurt Airport is one of the largest employers in Hesse with nearly 22,000 employees. Aerospace cluster contains also Rolls-Royce's aviation engine work in Oberursel and APU manufacturing plant and service center of Honeywell in Raunheim .Companies with an international reputation are located outside the Rhine-Main region in Wetzlar . There is the center of the optical, electrical and precision engineering industries, Leitz , Leica , Minox , Hensoldt ( Zeiss ) and Brita with several plants in central Hesse. Oculus Optikgeräte manufactures Scheimpflug tomographs for examining the anterior segment of the eye, topographers for measuring the anterior surface of the cornea, tonometers for assessing the biomechanical properties of the cornea, a wide-angle observation system for vitreous body surgery, universal trial goggles for subjective refraction, various perimeters for visual field testing and vision testing devices for testing eyesight. Electrical transformers are produced by Hitachi ABB Power Grids in Hanau and Siemens Energy in Frankfurt-am-Main . SMA Solar Technology manufactures an inverters for photovoltaic systems. Rittal is specialized on electrical enclosure situated in Herborn and Eschenburg . Power semiconductors from IXYS in Lampertheim and UV and infrared lamps from Heraeus .Many IT and telecommunications companies are located in Hesse, many of them in Frankfurt and Darmstadt, like Software AG (Darmstadt), T-Systems (Frankfurt and Darmstadt), Deutsche Telekom (laboratories in Darmstadt), DB Systel (Frankfurt), Lufthansa Systems (Raunheim near Frankfurt) and DE-CIX (Frankfurt).Sweet making is typical, there are 2 big factories: Ferrero , Stadtallendorf and Baronie (Sarotti), Hattersheim am Main . Frankfurter Sausage is famous, but there is also other sorts like Frankfurter Rindswurst , Ahle Wurst . Beverage industry is well-developed and manufactures sparkling wine ( Sekt ), white wine ( Riesling ), mineral waters ( Selters ), beers ( Radeberger ) and cider . In Frankfurt-Oberrad exists growing of wild herbs for green sauce and monument.The leather industry was predominantly based in Offenbach , but is now extinct, existing only in museums. The same happened with Frankfurt's fur industry and Hanau's jewelry industry.The Hochtaunuskreis has the lowest unemployment rate at 3.8% while the independent city of Kassel has the highest rate nationally at 12.1%. In October 2018 the unemployment rate stood at 4.4% and was lower than the national average. Hesse has a dense highway network with a total of 24 motorways. The internationally important motorway routes through Hesse are the A3, A5, and A7. Close to Frankfurt Airport is the Frankfurter Kreuz , Germany's busiest and one of Europe's busiest motorway junctions, where the motorways A3 (Arnhem-Cologne-Frankfurt-Nuremberg-Passau) and A5 (Hattenbach-Frankfurt-Karlsruhe-Basel) intersect. The A5 becomes as wide as four lanes in each direction near the city of Frankfurt am Main, and during the rush-hour, it is possible to use the emergency lanes on the A3 and A5 motorway in the Rhine-Main Region , adding additional lanes. Other major leading Hesse highways are the A4 , the A44 , the A45 , the Federal Highway A66 and the A67 . There are also a number of smaller motorways and major trunk roads, some of which are dual carriageways . Hesse is accessed by many major rail lines, including the high-speed lines Cologne–Frankfurt (op.speed 300 km/h) and Hanover–Würzburg . Other north-south connections traverse major east–west routes from Wiesbaden and Mainz to Frankfurt and from Hanau and Aschaffenburg to Fulda and Kassel. The Frankfurt Central Station is the most important hub for German trains, with over 1,100 trains per day. The region around Frankfurt has an extensive S-Bahn network, the S-Bahn Rhein-Main , which is complemented by many regional train connections. In the rest of the country, the rail network is less extensive. Since 2007, the region around Kassel has been served by the RegioTram , a tram-train -concept similar to the Karlsruhe model . Frankfurt Airport is by far the largest airport in Germany with more than 57 million passengers each year, is and among the world's ten largest. Frankfurt Egelsbach Airport lies to the south, and is frequented by general aviation and private planes. Kassel Airport offers a few flights to holiday destinations, but has struggled to compete. There are also a number of sports airfields. Low-cost airlines , especially Ryanair , use Frankfurt-Hahn Airport as a major base, although the airport is actually located about 100 km from Frankfurt in the neighbouring state of Rhineland-Palatinate . The DFS ( German air traffic control ) has its headquarters in Langen .Hesse has a dense highway network with a total of 24 motorways. The internationally important motorway routes through Hesse are the A3, A5, and A7. Close to Frankfurt Airport is the Frankfurter Kreuz , Germany's busiest and one of Europe's busiest motorway junctions, where the motorways A3 (Arnhem-Cologne-Frankfurt-Nuremberg-Passau) and A5 (Hattenbach-Frankfurt-Karlsruhe-Basel) intersect. The A5 becomes as wide as four lanes in each direction near the city of Frankfurt am Main, and during the rush-hour, it is possible to use the emergency lanes on the A3 and A5 motorway in the Rhine-Main Region , adding additional lanes. Other major leading Hesse highways are the A4 , the A44 , the A45 , the Federal Highway A66 and the A67 . There are also a number of smaller motorways and major trunk roads, some of which are dual carriageways .Hesse is accessed by many major rail lines, including the high-speed lines Cologne–Frankfurt (op.speed 300 km/h) and Hanover–Würzburg . Other north-south connections traverse major east–west routes from Wiesbaden and Mainz to Frankfurt and from Hanau and Aschaffenburg to Fulda and Kassel. The Frankfurt Central Station is the most important hub for German trains, with over 1,100 trains per day. The region around Frankfurt has an extensive S-Bahn network, the S-Bahn Rhein-Main , which is complemented by many regional train connections. In the rest of the country, the rail network is less extensive. Since 2007, the region around Kassel has been served by the RegioTram , a tram-train -concept similar to the Karlsruhe model .Frankfurt Airport is by far the largest airport in Germany with more than 57 million passengers each year, is and among the world's ten largest. Frankfurt Egelsbach Airport lies to the south, and is frequented by general aviation and private planes. Kassel Airport offers a few flights to holiday destinations, but has struggled to compete. There are also a number of sports airfields. Low-cost airlines , especially Ryanair , use Frankfurt-Hahn Airport as a major base, although the airport is actually located about 100 km from Frankfurt in the neighbouring state of Rhineland-Palatinate . The DFS ( German air traffic control ) has its headquarters in Langen .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Henry_III,_Landgrave_of_Upper_Hesse/html
Henry III, Landgrave of Upper Hesse
Henry III, Landgrave of Upper Hesse , called "the Rich" (15 October 1440 – 13 January 1483) was the second son of Louis I of Hesse and his wife Anna of Saxony . Upon the death of his father Louis I in 1458, Henry received Upper Hesse and his brother Louis II received Lower Hesse . He succeeded to the title of Landgrave of Hesse-Marburg in 1458. His nickname "the Rich" is indicative of his fortune in territory and tolls on the Rhine received by his marriage to Anna, daughter and heir of Philipp , the last Count of Katzenelnbogen and his wife Anne of Württemberg.Henry was the second son of Landgrave Ludwig I of Hesse and his wife Anna of Saxony . Ludwig I had stipulated in his will that Henry and his brother Ludwig (1438–1471) should share the landgraviate equally between them, but did not concretize this provision until his death. Ludwig II initially decided on Lower Hesse and left Marburg and the land on the Lahn to Heinrich, where he ruled as Heinrich III. He received his nickname "the Rich" due to his marriage to Anna of Katzenelnbogen (daughter of Philipp I ) and the territorial gains associated with it, which also came with considerable financial gain, including the lucrative revenues from Rhine customs . The dispute over the exact division of the landgraviate between the two brothers dragged on for more than ten years. Several appraisals and arbitration awards had no effect. After initial encroachments, the conflict finally escalated in 1468/69 into an open feud , the so-called Hessian Brother War . A peace brokered by the third brother, Hermann , later archbishop of Köln , initiated renewed partition negotiations. The result was another agreement at a Diet of the Hessian Landstände in Spieskappel Monastery, on the traditional border between Lower and Upper Hesse, in 1470. Again, some points remained unresolved. However, further discussion was unnecessary, since Ludwig II died already in 1471. Henry III took over the guardianship of Ludwig II's two sons and ruled over Lower and Upper Hesse until his death in 1483. The Marburg line became extinct with Heinrich's son, Wilhelm III, in 1500, and its possessions fell by inheritance to the Kassel line.His daughter Elisabeth (1466–1523) would go on to marry John V, Count of Nassau-Siegen and they would become grandparents to William the Silent . His younger daughter, Mathilde (1473–1524), would go on to marry John II, Duke of Cleves and they would become grandparents to Queen Anne of Cleves . Henry's only son to reach adulthood succeeded as William III (Wilhelm III, Landgraf von Hessen-Marburg) (1471–1500). In 1498, William ΙΙΙ married Elisabeth , the daughter of Philip, Elector Palatine . William ΙΙΙ left no legitimate heir and the title passed to his cousin, William II, Landgrave of Hesse , son of Louis II, Landgrave of Lower Hesse . Henry also had an illegitimate daughter, Contzel (* before 1471; †before 1508), with a woman named Christina (Steyna), the wife of the painter Johannes Dietz (†1480) of Marburg. Contzel married Ludwig Orth (about 1460–1523), the several-times mayor of Marburg, and their descendants include Johann Wolfgang von Goethe .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg,_Queensland/html
Marburg, Queensland
Download coordinates as: Marburg is a rural town in the City of Ipswich and a locality split between the City of Ipswich and the Somerset Region , both in Queensland , Australia. In the 2016 census , the town had a population of 873 people. Marburg is located approximately 50 kilometres (31 mi) west-south-west from Brisbane city. The land has an elevation of between approximately 80 and 120 metres above sea level. A small creek, the Black Snake creek, runs through Marburg. It is named after the Red-bellied Black Snake . Rosewood–Marburg Road enters from the south. German settlers arrived around the 1860s in the region, which is part of the land of the Indigenous Jagera people . The district was initially named Sally Owens Plains , but the town itself takes its present name from Marburg in Hesse , Germany. The story goes that the settlers used to respond with 'ober dar' when asked where they lived. Eventually they named their settlement after the German town of Marburg, which was well known at the time. The timber, sugar cane and dairy industries put Marburg on its feet and the town grew over time. About 46 acres, sub-divided into 200 allotments, were offered for sale by auction on 29 November 1884. Advertising included details of the clearing of the Rosewood Scrub, of close-by townships, and the future rail and telegraph services, following "the establishment of the police station". In 1900 Marburg had a courthouse, police barracks, a post office, two hotels, five churches, a State school, a School of Arts, several stores, a blacksmith, a butter factory, a sugar factory and a rum distillery. At that time nearly 80 percent of Marburg's population came from Germany or were of German descent. Frederick State School opened on 18 March 1879. In 1888, the name was changed to Marburg State School. From 1920 to 1934, it incorporated a rural school, which taught practical skills needed for farming. In 1977, a pre-school centre was added. Marburg Post Office opened on 1 October 1879 (a receiving office named Frederick had been open from 1878), was renamed Townshend in 1917 during World War 1 and reverted to Marburg in 1919. On 4 July 1891, All Saints' Anglican Church was officially dedicated by Bishop William Webber . It was built at 2-6 Seminary Road ( 27°33′58″S 152°36′42″E / 27.5662°S 152.6117°E / -27.5662; 152.6117 ( All Saints' Anglican Church (original site) ) ) adjacent to the present Warrego Highway on 2 acres (0.81 ha) of land donated by Thomas Lorimer Smith, the owner of the mansion Woodlands , also in Seminary Road. It was designed by architect George Brockwell Gill of Ipswich and built by W. Luder for £225. On Wednesday 9 November 1892, Bishop Webber returned to consecrate the church's burial ground. Not being located in the town itself led to requests to relocate the church. In 1956, land was bought in Queen Street and a church hall was built on the site, opening in February 1959, but the church remained at its original location. However, in the 1970s, the plan to make the Warrego Highway four lanes wide required the resumption of part of the church's land. The last service was held at the original location on 22 May 1977 after which it was moved onto the Queen Street site beside the hall. On 22 October 1979, the church re-opened with a service conducted by Reverend John Magee. The cemetery remains at the original site. Marburg grew rapidly in the first half of the twentieth century, as the main road from Brisbane to Toowoomba passed through the town's centre. Marburg became popular as a stopover for travellers. Marburg was the administrative centre for local government in the area, composing Walloon Division (1879-1903) and Shire of Walloon (1903-1917). In 1912, the Marburg branch railway line from Rosewood to Marburg was opened but only a few years later the railway began to suffer from the competition of highway traffic. It still survived until 1965 when the line was closed. There were two stations within the locality (from north to south): Because of an anti-German sentiment of some State politicians the name of Marburg was changed during the First World War into Townshend , a name change the locals did not support. Dr. Sirois, the local General Practician at the time, was instrumental in having the name Marburg be re-introduced after the war in 1920, which created a storm of protest but the name Marburg prevailed. When the Warrego Highway was built in the 1960s, most of the traffic from Brisbane to Toowoomba bypassed Marburg, and subsequently the town has become less populated. In the 2011 census , Marburg had a population of 567 people. In the 2016 census , Marburg had a population of 873 people. Marburg has a number of heritage-listed sites, including:Marburg State School is a government primary (Prep-6) school for boys and girls at Louisa Street ( 27°33′45″S 152°35′38″E / 27.5624°S 152.5939°E / -27.5624; 152.5939 ( Marburg State School ) ). In 2017, the school had an enrolment of 52 students with 5 teachers (4 full-time equivalent) and 6 non-teaching staff (4 full-time equivalent). Marburg has active community groups such as the Marburg and District Resident's Association, the Rosewood Scrub Historical Society , the Marburg Harness Racing Club, the Marburg Show Society and show grounds. The town hosts the Marburg Fire and Rescue Station, the Marburg Rural Fire Brigade, and the Marburg branch of the State Emergency Services. Weekly Sunday services are held at All Saints' Anglican Church at 111 Queen Street ( 27°33′56″S 152°35′48″E / 27.5656°S 152.5966°E / -27.5656; 152.5966 ( All Saints' Anglican Church ) ). A street library was installed in the park in the centre of the town by the Marburg Residents Association. It includes a reading room in the form of a typical Australian outhouse .'Woodlands' is Marburg's finest building. It is an example of the nineteenth century plantation owner's residence and for its historic significance in relation to the development of various primary industries in Queensland. It was built between 1888 and 1891 by Thomas Lorrimar Smith who was the owner of the sawmill, sugarmill, distillery and other business interests in the region. At present the property serves as a centre for functions such as weddings, business meetings and conferences. The Marburg Black Snake Creek Festival is an annual event held in October and features musicians and other attractions. The 'Band in the Park' is an initiative of the Marburg and District Resident's Association on the first Friday of the month at 6.30 pm. Marburg is well known for its 'Marburg Dances' which take place every Saturday night in the hall on the show grounds. Harness racing takes place regularly on the Marburg race course at the show grounds.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg_Picture_Index/html
Marburg Picture Index
The Bildindex der Kunst und Architektur ( English: Image Index of Art and Architecture ) is an open online database of 2.2 million photographs of 1.7 million artworks and architectural objects. The owner and operator of the database is the " Deutsches Dokumentationszentrum für Kunstgeschichte " ("German Documentation Center for Art History"), known formally as " Bildarchiv Foto Marburg " ("Image Archive Photo Marburg"). In addition to its own image holdings, around 1 million images from 50 partner institutions are also available online. Not all images are of German objects. In 1976 the institution purchased thousands of photographs of the Du magazine of the Swiss publishing house Conzett & Huber . Between 1977 and 2008, 1.4 million photographs from 15 different institutions were made available on microfiche by Bildarchiv Foto Marburg as the " Marburger Index : Inventar der Kunst in Deutschland " ("Marburger Index : Inventory of Art in Germany"). Published digital reproductions of these microfiche photographs from the original partner institutions now form the basis of the image index.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Warrego_Highway_state-controlled_roads/html
Warrego Highway state-controlled roads
Warrego Highway state-controlled roads presents information about how the Warrego Highway is described for administrative and funding purposes by the Queensland Department of Transport and Main Roads, and about the state-controlled roads that intersect with it.The Warrego Highway runs from Ipswich to Charleville in Queensland , Australia. It is a state-controlled road, divided into seven sections for administrative and funding purposes. Six of the seven sections (numbers 18A to 18F) are part of the National Highway , while section 18G is a regional road. The sections are: 18A – Ipswich to Toowoomba 18B – Toowoomba to Dalby 18C – Dalby to Miles 18D – Miles to Roma 18E – Roma to Mitchell 18F – Mitchell to Morven 18G – Morven to CharlevilleThe following state-controlled roads intersect with section 18A: Riverview–Moggill Ferry Road River Road (Queensland) Mount Crosby Road Ipswich–Warrego Highway Connection Road Brisbane Valley Highway Haigslea–Amberley Road Rosewood–Marburg Road Laidley–Plainland Road Forest Hill–Fernvale Road Gatton–Esk Road Gatton–Helidon Road Toowoomba Second Range Crossing Murphys Creek Road New England Highway Details of above roads not described in another article are shown below. Riverview–Moggill Ferry Road (Riverview Road) Riverview–Moggill Ferry Road (Riverview Road) is a state-controlled district road (number 916). It runs from the Warrego Highway in Riverview to Moggill Ferry Road (Moggill Sub–Arterial Road) in Riverview, a distance of 2.0 kilometres (1.2 mi) . It does not intersect with any state-controlled roads. River Road (Queensland) River Road (Queensland) is a state-controlled district road (number 309). It runs from the Warrego Highway in Riverview to the Cunningham Highway in Dinmore , a distance of 1.5 kilometres (0.93 mi) . It intersects with Ipswich–Cunningham Highway Connection Road (Brisbane Road) in Dinmore. Mount Crosby Road Mount Crosby Road is a state-controlled district road (number 3042), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Warrego Highway Connection Road (Downs Street) in North Ipswich to the Moggill Sub–Arterial Road ( Moggill Road ) in Pinjarra Hills , a distance of 19.6 kilometres (12.2 mi) . This road carries the State Route 37 shield. It intersects with the Warrego Highway on the North Tivoli / Chuwar boundary. Ipswich–Warrego Highway Connection Road Ipswich–Warrego Highway Connection Road is a state-controlled district road (number 302), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Cunningham Highway Connection Road (Brisbane Street / Limestone Street) in Ipswich to the Warrego Highway in Brassall , a distance of 7.4 kilometres (4.6 mi) . This road carries the State Route 38 shield. It intersects with Mount Crosby Road in North Ipswich . Haigslea–Amberley Road Haigslea–Amberley Road is a state-controlled district road (number 3041), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway on the Haigslea / Ironbark / Walloon tripoint to the Ipswich–Rosewood Road in Amberley , a distance of 9.5 kilometres (5.9 mi) . It intersects with Karrabin–Rosewood Road in Walloon . Rosewood–Marburg Road Rosewood–Marburg Road is a state-controlled district road (number 303), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Rosewood Road in Rosewood to the Warrego Highway in Marburg , a distance of 10.5 kilometres (6.5 mi) . It intersects with Rosewood–Laidley Road and Karrabin–Rosewood Road in Rosewood. Laidley–Plainland Road Laidley–Plainland Road is a state-controlled district road (number 311), part of which is rated as a local road of regional significance (LRRS). It runs from the Rosewood–Laidley Road in Laidley to the Warrego Highway in Plainland , a distance of 8.6 kilometres (5.3 mi) . It intersects with Gatton–Laidley Road in Laidley. Murphys Creek Road Murphys Creek Road is a state-controlled district road (number 4104), rated as a local road of regional significance (LRRS). It runs from the New England Highway in Blue Mountain Heights to the former Warrego Highway ( Toowoomba Connection Road ) – (see below) in Postmans Ridge , a distance of 24.6 kilometres (15.3 mi) . It does not intersect with any state-controlled roads. A project to replace the Rocky Creek Bridge, built in 1928, was completed in October 2022 at a cost of $11 million. Riverview–Moggill Ferry Road (Riverview Road) Riverview–Moggill Ferry Road (Riverview Road) is a state-controlled district road (number 916). It runs from the Warrego Highway in Riverview to Moggill Ferry Road (Moggill Sub–Arterial Road) in Riverview, a distance of 2.0 kilometres (1.2 mi) . It does not intersect with any state-controlled roads. River Road (Queensland) River Road (Queensland) is a state-controlled district road (number 309). It runs from the Warrego Highway in Riverview to the Cunningham Highway in Dinmore , a distance of 1.5 kilometres (0.93 mi) . It intersects with Ipswich–Cunningham Highway Connection Road (Brisbane Road) in Dinmore. Mount Crosby Road Mount Crosby Road is a state-controlled district road (number 3042), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Warrego Highway Connection Road (Downs Street) in North Ipswich to the Moggill Sub–Arterial Road ( Moggill Road ) in Pinjarra Hills , a distance of 19.6 kilometres (12.2 mi) . This road carries the State Route 37 shield. It intersects with the Warrego Highway on the North Tivoli / Chuwar boundary. Ipswich–Warrego Highway Connection Road Ipswich–Warrego Highway Connection Road is a state-controlled district road (number 302), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Cunningham Highway Connection Road (Brisbane Street / Limestone Street) in Ipswich to the Warrego Highway in Brassall , a distance of 7.4 kilometres (4.6 mi) . This road carries the State Route 38 shield. It intersects with Mount Crosby Road in North Ipswich . Haigslea–Amberley Road Haigslea–Amberley Road is a state-controlled district road (number 3041), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway on the Haigslea / Ironbark / Walloon tripoint to the Ipswich–Rosewood Road in Amberley , a distance of 9.5 kilometres (5.9 mi) . It intersects with Karrabin–Rosewood Road in Walloon . Rosewood–Marburg Road Rosewood–Marburg Road is a state-controlled district road (number 303), rated as a local road of regional significance (LRRS). It runs from the Ipswich–Rosewood Road in Rosewood to the Warrego Highway in Marburg , a distance of 10.5 kilometres (6.5 mi) . It intersects with Rosewood–Laidley Road and Karrabin–Rosewood Road in Rosewood. Laidley–Plainland Road Laidley–Plainland Road is a state-controlled district road (number 311), part of which is rated as a local road of regional significance (LRRS). It runs from the Rosewood–Laidley Road in Laidley to the Warrego Highway in Plainland , a distance of 8.6 kilometres (5.3 mi) . It intersects with Gatton–Laidley Road in Laidley. Murphys Creek Road Murphys Creek Road is a state-controlled district road (number 4104), rated as a local road of regional significance (LRRS). It runs from the New England Highway in Blue Mountain Heights to the former Warrego Highway ( Toowoomba Connection Road ) – (see below) in Postmans Ridge , a distance of 24.6 kilometres (15.3 mi) . It does not intersect with any state-controlled roads. A project to replace the Rocky Creek Bridge, built in 1928, was completed in October 2022 at a cost of $11 million. Officially, section 18A follows what is now known as Toowoomba Connection Road to its intersection with the New England Highway in Toowoomba , where section 18B commences. The Toowoomba Second Range Crossing is now part of the National Highway, and is gazetted as road 319. It is planned to gazette the Toowoomba Connection Road as number 315.The following state-controlled roads intersect with section 18B: Details of above roads not described in another article are shown below. Charlton Connection Road Charlton Connection Road (Troys Road) is a state-controlled district road (number 320). It runs from the former Warrego Highway ( Toowoomba Connection Road ) in Charlton to Toowoomba–Cecil Plains Road in Charlton, a distance of 1.5 kilometres (0.93 mi) . It does not intersect with any state-controlled roads. Charlton Connection Road Charlton Connection Road (Troys Road) is a state-controlled district road (number 320). It runs from the former Warrego Highway ( Toowoomba Connection Road ) in Charlton to Toowoomba–Cecil Plains Road in Charlton, a distance of 1.5 kilometres (0.93 mi) . It does not intersect with any state-controlled roads. The following state-controlled roads intersect with section 18C: Details of above roads not described in another article are shown below. Warra–Canaga Creek Road Warra–Canaga Creek Road is a state-controlled district road (number 4201), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Warra to Chinchilla–Wondai Road on the Canaga / Langlands midpoint, a distance of 30.9 kilometres (19.2 mi) . It does not intersect with any state-controlled roads. Auburn Road (Queensland) Auburn Road (Queensland) is a state-controlled district road (number 4261), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Chinchilla to Auburn Road in Auburn , a distance of 104 kilometres (65 mi) . It does not intersect with any state-controlled roads. Auburn Road continues north as a local road to Sujeewong , where it transitions to Redbank Road. This continues north to an intersection with Eidsvold–Theodore Road in Eidsvold West . Warra–Canaga Creek Road Warra–Canaga Creek Road is a state-controlled district road (number 4201), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Warra to Chinchilla–Wondai Road on the Canaga / Langlands midpoint, a distance of 30.9 kilometres (19.2 mi) . It does not intersect with any state-controlled roads. Auburn Road (Queensland) Auburn Road (Queensland) is a state-controlled district road (number 4261), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Chinchilla to Auburn Road in Auburn , a distance of 104 kilometres (65 mi) . It does not intersect with any state-controlled roads. Auburn Road continues north as a local road to Sujeewong , where it transitions to Redbank Road. This continues north to an intersection with Eidsvold–Theodore Road in Eidsvold West . The following state-controlled roads intersect with section 18D: Details of above roads not described in another article are shown below. Jackson–Wandoan Road Jackson–Wandoan Road is a state-controlled district road (number 4302), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Jackson to the Leichhardt Highway in Wandoan , a distance of 81.2 kilometres (50.5 mi) . It does not intersect with any state-controlled roads. Jackson–Wandoan Road Jackson–Wandoan Road is a state-controlled district road (number 4302), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Jackson to the Leichhardt Highway in Wandoan , a distance of 81.2 kilometres (50.5 mi) . It does not intersect with any state-controlled roads. The following state-controlled roads intersect with section 18E: Mitchell–Forestvale Road Mitchell–St George Road Details of the above roads are shown below. Mitchell–Forestvale Road Mitchell–Forestvale Road is a state-controlled district road (number 4403), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Mitchell to Mount Moffatt Road in Forestvale , a distance of 67.8 kilometres (42.1 mi) . It does not intersect with any state-controlled roads. Mitchell–St George Road Mitchell–St George Road is a state-controlled district road (number 355), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Mitchell to the Balonne Highway in St George , a distance of 203 kilometres (126 mi) . It does not intersect with any state-controlled roads. Mitchell–Forestvale Road Mitchell–Forestvale Road is a state-controlled district road (number 4403), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Mitchell to Mount Moffatt Road in Forestvale , a distance of 67.8 kilometres (42.1 mi) . It does not intersect with any state-controlled roads. Mitchell–St George Road Mitchell–St George Road is a state-controlled district road (number 355), rated as a local road of regional significance (LRRS). It runs from the Warrego Highway in Mitchell to the Balonne Highway in St George , a distance of 203 kilometres (126 mi) . It does not intersect with any state-controlled roads. Section 18F ends at an intersection with the Landsborough Highway in Morven , and section 18G ends at an intersection with the Mitchell Highway in Charleville .The following state-controlled roads, not described in another article, are associated with the intersecting roads described above, or their terminating roads: Karrabin–Rosewood Road Rosewood–Laidley Road Mulgowie Road Gatton–Laidley Road Karrabin–Rosewood Road Karrabin–Rosewood Road is a state-controlled district road (number 3002), rated as a local road of regional significance (LRRS). It runs from Toongarra Road in Wulkuraka to Rosewood–Laidley Road in Rosewood , a distance of 14.7 kilometres (9.1 mi) . It intersects with Haigslea-Amberley Road in Walloon , and with Rosewood–Marburg Road and Ipswich–Rosewood Road in Rosewood. Rosewood–Laidley Road Rosewood–Laidley Road is a state-controlled district road (number 308), part of which is rated as a local road of regional significance (LRRS). It runs from Karrabin–Rosewood Road in Rosewood to Laidley–Plainland Road in Laidley , a distance of 23.6 kilometres (14.7 mi) . It intersects with Rosewood–Marburg Road and Ipswich–Rosewood Road in Rosewood, and with Mulgowie Road and Gatton–Laidley Road in Laidley. Mulgowie Road Mulgowie Road is a state-controlled district road (number 3083), part of which is rated as a local road of regional significance (LRRS). It runs from Rosewood–Laidley Road in Laidley to Mulgowie Road in Townson , a distance of 28.0 kilometres (17.4 mi) . It does not intersect with any state-controlled roads. Gatton–Laidley Road Gatton–Laidley Road is a state-controlled district road (number 312), part of which is rated as a local road of regional significance (LRRS). It runs from Gatton–Helidon Road in Gatton to Rosewood–Laidley Road in Laidley , a distance of 15.1 kilometres (9.4 mi) . It intersects with Forest Hill–Fernvale Road in Forest Hill and Laidley–Plainland Road in Laidley. Karrabin–Rosewood Road Karrabin–Rosewood Road is a state-controlled district road (number 3002), rated as a local road of regional significance (LRRS). It runs from Toongarra Road in Wulkuraka to Rosewood–Laidley Road in Rosewood , a distance of 14.7 kilometres (9.1 mi) . It intersects with Haigslea-Amberley Road in Walloon , and with Rosewood–Marburg Road and Ipswich–Rosewood Road in Rosewood. Rosewood–Laidley Road Rosewood–Laidley Road is a state-controlled district road (number 308), part of which is rated as a local road of regional significance (LRRS). It runs from Karrabin–Rosewood Road in Rosewood to Laidley–Plainland Road in Laidley , a distance of 23.6 kilometres (14.7 mi) . It intersects with Rosewood–Marburg Road and Ipswich–Rosewood Road in Rosewood, and with Mulgowie Road and Gatton–Laidley Road in Laidley. Mulgowie Road Mulgowie Road is a state-controlled district road (number 3083), part of which is rated as a local road of regional significance (LRRS). It runs from Rosewood–Laidley Road in Laidley to Mulgowie Road in Townson , a distance of 28.0 kilometres (17.4 mi) . It does not intersect with any state-controlled roads. Gatton–Laidley Road Gatton–Laidley Road is a state-controlled district road (number 312), part of which is rated as a local road of regional significance (LRRS). It runs from Gatton–Helidon Road in Gatton to Rosewood–Laidley Road in Laidley , a distance of 15.1 kilometres (9.4 mi) . It intersects with Forest Hill–Fernvale Road in Forest Hill and Laidley–Plainland Road in Laidley.
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Marbach, Marburg
Marbach is a borough ( Ortsbezirk ) of Marburg in Hesse . Marbach has a current population of approx. 3,400 inhabitants.Marbach was mentioned in 1272 with the name Marpah . Also it was noticed in the register of the city of Marburg in 1374, where Marbach was a small village of the Landgraves of Thuringia , beside the other districts Ockershausen , Wehrda and Cappel .
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James Marburg
James Marburg (born 27 December 1982) is an Australian retired rower. He is a dual Olympian, Olympic silver medallist and has represented Australia at five World Rowing Championships.Marburg attended St Patrick's College, Ballarat. He undertook undergraduate studies at Royal Melbourne Institute of Technology and legal studies at University of Melbourne .Marburg's senior rowing was done from the Melbourne University Boat Club. He was selected in the Victorian state representative eights who raced for the King's Cup at the Australian Rowing Championships on eight consecutive occasions from 2005 to 2012. Those Victorian crews saw King's Cup victories in 2006 and 2007. In 2006 he teamed up with Cameron McKenzie-McHarg to win the Australian national coxless pair championship beating out the fancied veteran duo of Drew Ginn and Duncan Free .He gained selection in Australian VIIIs who competed at the 2006 and 2007 World Championships and considered that he was in contention for the Beijing Olympics. In 2008 Marburg was selected in the men's coxless four, with Francis Hegerty , Matt Ryan and Cameron McKenzie-McHarg . The crew won their event at the 2008 World Rowing Cup I in Lucerne , Switzerland . The crew then turned their attention to the Olympic Qualification Regatta in Poznan. Ryan was struck down by illness and had to be replaced for the race by Terrence Alfred and the crew achieved qualification for the Olympic Games. In Beijing, the crew led for a large part of the race before placing second behind the race favourites from Great Britain to take the silver medal. Marburg was selected in an unchanged men's coxless four for the 2009 World Rowing Championships in Poznan , Poland and won a silver medal. The following year he moved into the VIII which won bronze at the Lake Karapiro , New Zealand at the 2010 World Championships . In 2011 he was again selected into the VIII which placed fourth at the 2011 World Championships in Bled , Slovenia . For the 2012 Summer Olympics , Marburg was selected into the men's pair with team-mate Brodie Buckland . The pair reached the final of the men's pair, placing fifth. Following the London games he retired from rowing. Marburg began his legal career as a solicitor at King & Wood Mallesons Melbourne in 2014. Since 2020 he has been a senior associate at Clayton Utz Melbourne.
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The Hot Zone
The Hot Zone: A Terrifying True Story is a best-selling 1994 nonfiction thriller by Richard Preston about the origins and incidents involving viral hemorrhagic fevers , particularly ebolaviruses and marburgviruses . The basis of the book was Preston's 1992 New Yorker article "Crisis in the Hot Zone". The filoviruses —including Ebola virus , Sudan virus , Marburg virus , and Ravn virus —are Biosafety Level 4 agents, extremely dangerous to humans because they are very infectious, have a high fatality rate, and most have no known prophylactic measures , treatments, or cures. Along with describing the history of the devastation caused by two of these Central African diseases, Ebola virus disease and Marburg virus disease , Preston described a 1989 incident in which a relative of Ebola virus, Reston virus , was discovered at a primate quarantine facility in Reston, Virginia , less than 15 miles (24 km) away from Washington, D.C.The book is in four sections: The book starts with "Charles Monet" visiting Kitum Cave during a camping trip to Mount Elgon in Central Africa. Not long after, he begins to suffer from a number of symptoms, including vomiting, diarrhea and red eye. He is taken to Nairobi Hospital for treatment, but his condition deteriorates further, and he goes into a coma while in the waiting room. This particular filovirus is called Marburg virus. Dr. Nancy Jaax had been promoted to work in the Level 4 Biosafety containment area at the United States Army Medical Research Institute of Infectious Diseases, and is assigned to research Ebola virus. While preparing food for her family at home, she cuts her right hand. Later, while working on a dead monkey infected with Ebola virus, one of the gloves on the hand with the open wound tears, and she is almost exposed to contaminated blood, but does not get infected. Nurse Mayinga is also infected by a nun and goes to Ngaleima Hospital in Kinshasa for treatment, where she succumbs to the disease. In Reston, Virginia, less than fifteen miles (24 km) away from Washington, D.C., a company called Hazelton Research once operated a quarantine center for monkeys that were destined for laboratories. In October 1989, when an unusually high number of their monkeys began to die, their veterinarian decided to send some samples to Fort Detrick (USAMRIID) for study. Early during the testing process in biosafety level 3 , when one of the flasks appeared to be contaminated with harmless pseudomonas bacterium , two USAMRIID scientists exposed themselves to the virus by wafting the flask. The virus found at the facility was a mutated form of the original Ebola virus and was initially mistaken for simian hemorrhagic fever virus . They later determine that, while the virus is lethal to monkeys, humans can be infected with it without any health effects at all. This virus is now known as Reston virus. Finally, the author goes to Africa to explore Kitum Cave. On the way, he discusses the role of AIDS in the present, as the Kinshasa Highway that he travels on was sometimes called the "AIDS Highway" after its early appearance in the region. Equipped with a hazmat suit , he enters the cave and finds a large number of animals, one of which might be the virus carrier. At the conclusion of the book, he travels to the quarantine facility in Reston. He finds the building abandoned and deteriorating. He concludes the book by claiming that Ebola will be back.The discovery of the Reston virus was made in November 1989 by Thomas W. Geisbert, an intern at United States Army Medical Research Institute of Infectious Diseases. Dr. Peter B. Jahrling isolated the filovirus further. The Center for Disease Control and Prevention conducted blood tests of the 178 animal handlers. While six tested positive, they did not exhibit any symptoms. The Reston virus was found to have low pathogenicity in humans. This was further supported later when a handler infected himself during a necropsy of an infected monkey, as the handler did not show symptoms of the virus after the incubation period. The Hot Zone was listed as one of around 100 books that shaped a century of science by American Scientist . Many reviews of The Hot Zone exemplify the impact the book had on the public's view of emerging viruses. A review in the British Medical Journal captures the paranoia and public panic described in this book. The reviewer was left "wondering when and where this enigmatic agent will appear next and what other disasters may await human primates". This can also be seen in a review in the Public Health Reports which highlights the "seriousness of our current situation" and "our ability to respond to a major health threat". The Hot Zone is described as a "romantic account of environmental transgression". Reactions to this book could be seen not only in the public's view of emerging viruses, but in the changes in the Centers for Disease Control and Prevention . In addition to the funding of public health infrastructure during the early 1970s, there were many public discussions of biodefense. This book continued to fuel the emerging diseases campaign. By connecting international health to national security , this campaign used The Hot Zone as a method of justifying increased intervention in the global phenomena of disease. The Hot Zone elicited a major response by the World Health Organization (WHO) by shedding light on the Ebola Zaire outbreak . [ clarification needed ] Teams of experts were immediately released. [ clarification needed ] Many countries tightened their borders, issued warnings to custom officials, quarantined travelers, and issued travel advisories. In his blurb , horror writer Stephen King called the first chapter "one of the most horrifying things I've read in my whole life". When asked whether any book "scared the pants off you" writer Suzanne Collins answered " The Hot Zone , by Richard Preston. I just read it a few weeks ago. Still recovering." The Hot Zone has received criticism for sensationalizing the effects of Ebola virus. In their memoir Level 4: Virus Hunters of the CDC (1996), former CDC scientists Joseph B. McCormick and Susan Fisher-Hoch lambasted Preston for claiming that Ebola dissolves organs, stating that although it causes great blood loss in tissues the organs remain structurally intact. McCormick and Fisher-Hoch also dispute Preston's version of the CDC's actions in the Reston virus incident. [ citation needed ] In an interview about his book Ebola: The Natural and Human History of a Deadly Virus (2014), David Quammen claimed that The Hot Zone had "vivid, gruesome details" that gave an "exaggerated idea of Ebola over the years" causing "people to view this disease as though it was some sort of preternatural phenomenon". In January 1993, 20th Century Fox producer Lynda Obst won a bidding war for the film rights to Preston's 1992 New Yorker article, which was still being transitioned into book form. In response to being outbid, Warner Bros. producer Arnold Kopelson immediately began working on a similarly themed production. This competing film, Outbreak , would ultimately be a factor in the collapse of Fox's planned production, Crisis in The Hot Zone . Directors considered for Crisis in The Hot Zone included Wolfgang Petersen (who would later direct Outbreak ), Michael Mann , and Ridley Scott . Scott eventually signed on to direct the film in February 1994. Screenwriter James V. Hart was also signed to adapt the book. In late April 1994, Fox announced they had signed Robert Redford and Jodie Foster to star in the film. Crisis in The Hot Zone , however, was never made. Foster dropped out of the film just before filming was to begin and production was delayed, with Meryl Streep , Sharon Stone , and Robin Wright touted as possible replacements. In August 1994, Redford also dropped out of the film; a few days after Redford left it was announced that pre-production had been shut down. On October 16, 2014, The Hollywood Reporter announced that Ridley Scott again planned to adapt the book, this time as a television miniseries for NatGeo . Kelly Souders, Brian Peterson , and Jeff Vintar wrote the pilot. Julianna Margulies starred as Nancy Jaax. Filming began in September 2018. Lynda Obst again produced the series. The series first aired from May 27 to May 29, 2019, and was later renewed for a second season.In January 1993, 20th Century Fox producer Lynda Obst won a bidding war for the film rights to Preston's 1992 New Yorker article, which was still being transitioned into book form. In response to being outbid, Warner Bros. producer Arnold Kopelson immediately began working on a similarly themed production. This competing film, Outbreak , would ultimately be a factor in the collapse of Fox's planned production, Crisis in The Hot Zone . Directors considered for Crisis in The Hot Zone included Wolfgang Petersen (who would later direct Outbreak ), Michael Mann , and Ridley Scott . Scott eventually signed on to direct the film in February 1994. Screenwriter James V. Hart was also signed to adapt the book. In late April 1994, Fox announced they had signed Robert Redford and Jodie Foster to star in the film. Crisis in The Hot Zone , however, was never made. Foster dropped out of the film just before filming was to begin and production was delayed, with Meryl Streep , Sharon Stone , and Robin Wright touted as possible replacements. In August 1994, Redford also dropped out of the film; a few days after Redford left it was announced that pre-production had been shut down. On October 16, 2014, The Hollywood Reporter announced that Ridley Scott again planned to adapt the book, this time as a television miniseries for NatGeo . Kelly Souders, Brian Peterson , and Jeff Vintar wrote the pilot. Julianna Margulies starred as Nancy Jaax. Filming began in September 2018. Lynda Obst again produced the series. The series first aired from May 27 to May 29, 2019, and was later renewed for a second season.
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Marburg railway line
Download coordinates as: The Marburg Branch Railway is a branch line of the Main Line railway (from Brisbane to Toowoomba ) in Queensland , Australia. It branches near Rosewood , which is about 20 kilometres west of Ipswich . Previously known as Rosewood Gate, a railway gatekeeper was appointed to Rosewood in 1866. A waiting room and stationmaster's house were built in 1875 and a station office built in 1880 was replaced with the current building in 1918. Agricultural land to the north of Rosewood was not directly serviced by the Brisbane Valley railway line and, in December 1909, parliament approved the construction of a branch line to run about 15 kilometres to Marburg . The Marburg locality was originally known as First Plain, then as Frederick after the name of an early settler, and lastly as Marburg after a Prussian town of the same name. During World War I the town was known as Townshend but the Marburg name was reinstated in 1920. The line opened on 18 December 1911. The route was (from north to south): A daily service to Ipswich departed Marburg each morning and returned in the evening. It was a two-hour journey by rail and over time the faster road trip prevailed. Coal mines in the region kept the line viable until they progressively closed. The branch closed in stages – from Marburg to Birru in 1964, to Kunkala in 1970, Cabanda in 1973 and to Perry's Knob in 1979. The Rosewood Railway Museum now uses the upper section of the line. It has a display at Kunkala station.
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Emil von Behring
Emil von Behring ( German pronunciation: [ ˈeːmiːl fɔn ˈbeːʁɪŋ ] ⓘ ; Emil Adolf von Behring ), born Emil Adolf Behring (15 March 1854 – 31 March 1917), was a German physiologist who received the 1901 Nobel Prize in Physiology or Medicine , the first one awarded in that field, for his discovery of a diphtheria antitoxin . He was widely known as a "saviour of children", as diphtheria used to be a major cause of child death. His work with the disease, as well as tetanus, has come to bring him most of his fame and acknowledgment. He was honoured with Prussian nobility in 1901, henceforth being known by the surname "von Behring."Behring was born in Hansdorf, Kreis Rosenberg, Province of Prussia (now Ławice , Iława County , Poland ). His father was a schoolmaster; the family had 13 children. Between 1874 and 1878, he studied medicine at the Kaiser-Wilhelm-Akademie in Berlin , an academy for military doctors, since his family could not afford the university. As a military doctor, he studied the action of iodoform . Due to his work on Neurotomia opticociliaris (or optociliary neurotomy), Behring became a doctor from the institute and later was able to pass his exam for licensed work in his area of Marburg. In 1878, his service required him to be sent to Poland where he focused on septic diseases. His potential was becoming well known to many. This led to his commanded return to Prussia to study with Robert Koch. He was employed by the military as he received his grants and money from the Prussian army. For each semester of education, he owed one year of service as a military surgeon. This accumulated to two years, from 1881 to 1883 as he served under the Second Hussar regiment. A lesser known part of his studies was his research in ophthalmology and how he furthered the understanding of the eye and its diseases. He wrote a paper during his time at Wicherkiewicz's hospital in Poznan from 1881 to 1883 on an eye tumor case that ended up with the patient dying from leukemia , but it did allow for much needed research on treatments for the eye and what the preferred pathways for surgery would be. He learned under some of the great ophthalmologists such as Carl Ernst Schweigger and Wilhelm Uhthoff, leading to his interest in the subject and his writing his doctoral dissertation on it. In 1890 he published an article with Kitasato Shibasaburō reporting that they had developed "antitoxins" against both diphtheria and tetanus . They had injected diphtheria and tetanus toxins into guinea-pigs , goats and horses; when these animals developed immunity, they derived antitoxins (now known to contain antibodies ) from their serum . This process would be called serum therapy by him at the time as he described it as a way to induce permanent immunity or "to stimulate the body's internal disinfection". These antitoxins could protect against and cure the diseases in non-immunized animals. In 1892 he started the first human trials of the diphtheria antitoxin, but they were unsuccessful. Successful treatment started in 1894, after the production and quantification of antitoxin had been optimized. During 1894, Behring was also awarded the Cameron Prize for Therapeutics of the University of Edinburgh . In 1895 he became Professor of Hygienics within the Faculty of Medicine at the University of Marburg , a position held for the rest of his life. He and the pharmacologist Hans Horst Meyer had their laboratories in the same building, and Behring stimulated Meyer's interest in the mode of action of tetanus toxin . Behring won the first Nobel Prize in Physiology or Medicine in 1901 for the development of serum therapies against diphtheria. He was elected a Foreign Honorary Member of the American Academy of Arts and Sciences in 1902. In 1904 he founded the Behringwerke in Marburg, a company to produce antitoxins and vaccines. At the International Tuberculosis Congress in 1905 he announced that he had discovered "a substance proceeding from the virus of tuberculosis". This substance, which he designated "T C", plays the important part in the immunizing action of his "bovivaccine", which prevents bovine tuberculosis . He tried unsuccessfully to obtain a protective and therapeutic agents for humans. Behring died at Marburg , Hessen-Nassau , on 31 March 1917. His name survived in the Dade Behring organisation (now part of the Siemens Healthineers ), in CSL Behring , a manufacturer of plasma-derived biotherapies, in Novartis Behring and in the Emil von Behring Prize of the University of Marburg , the highest endowed medicine award in Germany. His Nobel Prize medal is now kept on display at the International Red Cross and Red Crescent Museum in Geneva . Von Behring is believed to have cheated Paul Ehrlich out of recognition and financial reward in relation to collaborative research in diphtheria. The two men developed a diphtheria serum by repeatedly injecting the deadly toxin into a horse. The serum was used effectively during an epidemic in Germany. A chemical company preparing to undertake commercial production and marketing of the diphtheria serum offered a contract to both men, but von Behring manoeuvered to claim all the considerable financial rewards for himself. To add insult to injury, only Behring received the first Nobel Prize in Medicine, in 1901, for his contributions. However, Ehrlich went on to win the 1908 Nobel Prize in Medicine for his contribution to immunology. Von Behring is believed to have cheated Paul Ehrlich out of recognition and financial reward in relation to collaborative research in diphtheria. The two men developed a diphtheria serum by repeatedly injecting the deadly toxin into a horse. The serum was used effectively during an epidemic in Germany. A chemical company preparing to undertake commercial production and marketing of the diphtheria serum offered a contract to both men, but von Behring manoeuvered to claim all the considerable financial rewards for himself. To add insult to injury, only Behring received the first Nobel Prize in Medicine, in 1901, for his contributions. However, Ehrlich went on to win the 1908 Nobel Prize in Medicine for his contribution to immunology. On 29 December 1896 Behring married the then twenty-year-old Else Spinola (1876-1936), who was a daughter of Bernhard Spinola [ de ] , the director of the Charité hospital in Berlin, and a Jewish -born mother – Elise Spinola, born Bendix – who had converted to Christianity upon her marriage. They had six sons. They held their honeymoon at villa "Behring" on Capri 1897, where Behring owned a vacation home. In 1909–1911, the Russian writer Maxim Gorky lived at this villa.Die Blutserumtherapie (1892) Die Geschichte der Diphtherie (1893) Bekämpfung der Infektionskrankheiten (1894) Beiträge zur experimentellen Therapie (1906) E. v. Behring's Gesammelte Abhandlungen (1915) Digital edition by the University and State Library Düsseldorf
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Landgraviate of Hesse-Darmstadt
The Landgraviate of Hesse-Darmstadt ( German : Landgrafschaft Hessen-Darmstadt ) was a State of the Holy Roman Empire , ruled by a younger branch of the House of Hesse . It was formed in 1567 following the division of the Landgraviate of Hesse among the four sons of Landgrave Philip I . The residence of the landgraves was in Darmstadt , hence the name. As a result of the Napoleonic Wars , the landgraviate was elevated to the Grand Duchy of Hesse following the Empire's dissolution in 1806.Like many petty German states, the landgraviate comprised a number of disconnected pockets of land (exclaves). These included the southern Starkenburg territory with the Darmstadt residence and the northern province of Upper Hesse with Alsfeld , Giessen , Grünberg , the northwestern hinterland estates around Gladenbach , Biedenkopf and Battenberg as well as the exclave of Vöhl in Lower Hesse .The Landgraviate of Hesse-Darmstadt came into existence in 1567, when George , youngest of the four sons of Landgrave Philip I "the Magnanimous", received the Hessian lands in the former upper County of Katzenelnbogen . His eldest brother William IV received the Landgraviate of Hesse-Kassel , while the second son Louis IV obtained Hesse-Marburg , and the third Philipp II became Landgrave of Hesse-Rheinfels . The Hesse-Rheinfels line became extinct on Philip's death in 1583. When, in 1604, the childless Landgrave Louis IV of Hesse-Marburg died at Marburg Castle , a succession dispute to his lands, along with the sectarian differences between Calvinist Hesse-Kassel and Lutheran Hesse-Darmstadt, led to a bitter, decades-long rivalry. Because the University of Marburg had become Calvinist under the rule of Landgrave Maurice of Hesse-Kassel , his cousin Louis V of Hesse-Darmstadt founded the Lutheran University of Giessen in 1607. The inheritance conflict was continued in the broader context of the Thirty Years' War , in which Hesse-Kassel sided with the Protestant estates and Hesse-Darmstadt sided with the Habsburg emperor. The Hesse-Homburg and Hesse-Rotenburg estates seceded from the opponents in 1622 and 1627. Though Hesse-Darmstadt and Hesse-Kassel reached an agreement in 1627, the quarrels rekindled, resulting inter alia in the Siege of Dorsten and culminating in a series of open battles from 1645, when the Kassel Landgravine Amalie Elisabeth besieged Marburg. The conflict was finally settled on the eve of the 1648 Peace of Westphalia , more than eighty years after the division of the estates. Large parts of the disputed Upper Hesse territory, including Marburg, fell to the elder Kassel line, while Hesse-Darmstadt retained Giessen and Biedenkopf . In 1736, the Landgraves of Hesse-Darmstadt inherited the estates of the extinct Counts of Hanau-Lichtenberg , again contested by their Kassel cousins. Hesse-Darmstadt gained a great deal of territory by the secularizations and mediatizations authorized by the Reichsdeputationshauptschluss of 1803. Most notable was the acquisition of the Duchy of Westphalia , formerly owned by the Prince-Archbishop of Cologne , as well as territories from the Prince-Archbishop of Mainz and the Prince-Bishop of Worms . In 1806, upon the dissolution of the Holy Roman Empire and the dispossession of his cousin, Elector William I of Hesse-Kassel , Landgrave Louis X joined the Napoleonic Confederation of the Rhine and took the title of Grand Duke of Hesse .The Hesse-Rheinfels line became extinct on Philip's death in 1583. When, in 1604, the childless Landgrave Louis IV of Hesse-Marburg died at Marburg Castle , a succession dispute to his lands, along with the sectarian differences between Calvinist Hesse-Kassel and Lutheran Hesse-Darmstadt, led to a bitter, decades-long rivalry. Because the University of Marburg had become Calvinist under the rule of Landgrave Maurice of Hesse-Kassel , his cousin Louis V of Hesse-Darmstadt founded the Lutheran University of Giessen in 1607. The inheritance conflict was continued in the broader context of the Thirty Years' War , in which Hesse-Kassel sided with the Protestant estates and Hesse-Darmstadt sided with the Habsburg emperor. The Hesse-Homburg and Hesse-Rotenburg estates seceded from the opponents in 1622 and 1627. Though Hesse-Darmstadt and Hesse-Kassel reached an agreement in 1627, the quarrels rekindled, resulting inter alia in the Siege of Dorsten and culminating in a series of open battles from 1645, when the Kassel Landgravine Amalie Elisabeth besieged Marburg. The conflict was finally settled on the eve of the 1648 Peace of Westphalia , more than eighty years after the division of the estates. Large parts of the disputed Upper Hesse territory, including Marburg, fell to the elder Kassel line, while Hesse-Darmstadt retained Giessen and Biedenkopf .In 1736, the Landgraves of Hesse-Darmstadt inherited the estates of the extinct Counts of Hanau-Lichtenberg , again contested by their Kassel cousins. Hesse-Darmstadt gained a great deal of territory by the secularizations and mediatizations authorized by the Reichsdeputationshauptschluss of 1803. Most notable was the acquisition of the Duchy of Westphalia , formerly owned by the Prince-Archbishop of Cologne , as well as territories from the Prince-Archbishop of Mainz and the Prince-Bishop of Worms . In 1806, upon the dissolution of the Holy Roman Empire and the dispossession of his cousin, Elector William I of Hesse-Kassel , Landgrave Louis X joined the Napoleonic Confederation of the Rhine and took the title of Grand Duke of Hesse .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Cappel,_Marburg/html
Cappel, Marburg
Cappel ( German pronunciation: [ ˈkapl̩ ] ⓘ ) is a borough ( Ortsbezirk ) of Marburg in Hesse .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/List_of_Hessian_royal_consorts/html
List of Hessian royal consorts
This is a list of the Landgravine, Electress and Grand Duchess of Hesse , the consorts of the Landgrave of Hesse and its successor states; and finally of the Electors and Grand Dukes of Hesse.The only Landgravine of Upper Hesse was Anna of Katzenelnbogen (1443–1494) who married Henry III in 1458. One could say that Anna of Brunswick was a Landgravine of Upper Hesse when it was united with Lower Hesse after 1500.The only Landgravine of Upper Hesse was Anna of Katzenelnbogen (1443–1494) who married Henry III in 1458. One could say that Anna of Brunswick was a Landgravine of Upper Hesse when it was united with Lower Hesse after 1500.
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg_Hotel/html
Marburg Hotel
Marburg Hotel is a heritage-listed hotel at Edmond Street, Marburg , City of Ipswich , Queensland , Australia. It was built from c. 1881 to c. 1890 . It was added to the Queensland Heritage Register on 21 October 1992. The Marburg Hotel, initially single-storeyed, was erected probably early in 1881 for Marburg farmer and Walloon publican, Weigand Raabe. The 0.81 hectares (2.0 acres) site was registered in his wife's name in mid-1880; a mortgage of £ 180 was taken out in January 1881; and by June 1881 races and sports were being held at Weigand Raabe's Marburg Hotel. It was among the first buildings in the town, and was the first hotel. The Marburg district was developed principally by German settlers, who in the early 1870s cleared farms from the dense Rosewood Scrub. By late 1885 the district supported a population of approximately 5,000, and the town boasted a Court House, School of Arts, primary school, two hotels and electricity supplied from TL Smith's Woodlands sawmill. Following Weigand Raabe's death in 1883, the hotel was placed under trusteeship. In mid-1884 Auguste Raabe, his widow, renewed the hotel license, and married Otto Sakrzewski, a Marburg storekeeper and carpenter, who then held the license from mid-1885 until mid-1887. Thomas Mortimer was licensee from mid-1887 until mid-1890, at which time Sakrzewski was appointed trustee and renewed the license. Sakrzewski raised a £ 600 mortgage on the property in 1890, and the second storey may have been added then. The Sakrzewski family held the license until 1921, and the freehold remained theirs until 1925, having been sold to Otto's brother, Albert, c. 1915 . The hotel then passed through several owners, lessees and licensees until purchased by Queensland Brewery Ltd in 1936. It has remained Marburg's sole hotel since 1947. In 1986 the freehold was acquired by the Bowden family, who have been licensees of the Marburg Hotel since c. 1944 . The Marburg Hotel remains one of the oldest buildings in the town. It has operated continuously as a hotel since 1881, and was a highway landmark and popular stopping place for travellers from 1923 to 1969, when the Brisbane - Toowoomba highway passed through Marburg. This two-storeyed timber building, with a corrugated iron hipped roof , is located on the corner of Queen and Edmond Streets in the centre of Marburg, opposite the former Queensland National Bank and First World War memorial (now the Marburg Community Centre and First World War Memorial ). Both street facades have double-height full length verandahs which are supported by timber posts. Both street facades also have cross braced exposed timber framing, but the rear walls are clad in chamferboard . First floor verandahs have decorative cast iron work with the verandah floor sloping outwards to a noticeable degree. The verandah roof is formed by a curved corrugated iron awning which has sagged in places along its length. Ground floor verandahs have large advertising signage in the position of the original valance. Entry to the public bar is from the verandah via the front corner door. The building sits on timber stumps. At the rear there is a single-storeyed chamferboard kitchen house, attached to the building via a covered breezeway and open deck. The ground floor contains hotel facilities and has been substantially altered. The first floor contains accommodation, most of which is of original plan form. Internal walls are of single skin tongue and groove board. Internal doors have fanlights above on the ground floor and fretwork panels above on the first floor. Rooms open onto the verandahs via french doors , and rooms at the rear of the building have sash windows with pressed metal window hoods. Marburg Hotel was listed on the Queensland Heritage Register on 21 October 1992 having satisfied the following criteria. The place is important in demonstrating the evolution or pattern of Queensland's history. Marburg Hotel, erected c. 1881 with additions c. 1890 . is important in demonstrating the evolution of part of Queensland's history, being associated with the emergence of Marburg as the centre of a flourishing agricultural community in the 1880s. The place is important in demonstrating the principal characteristics of a particular class of cultural places. It is important in demonstrating some of the principle characteristics of a late 19th century Queensland rural hotel, in the intactness of the setting, street elevations and upper floor. The place is important because of its aesthetic significance. It exhibits a range of aesthetic characteristics valued by the Marburg community, including the contribution through scale, form and material to the streetscapes off Queen and Edmond streets, and the landmark quality of the building, being an expression of the centre of the town. The place has a strong or special association with a particular community or cultural group for social, cultural or spiritual reasons. It has a strong and special association with the Marburg community, being: an integral part of Marburg social and recreational life since 1881 and part of an historic precinct in the centre of Marburg, which includes the nearby former Queensland National Bank and First World War memorial (now the Marburg Community Centre and First World War Memorial ), and the former Walloon Shire Council Office (now the Rosewood Scrub Historical Society Building ).
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Literaturpreis der Universitätsstadt Marburg und des Landkreises Marburg-Biedenkopf
Literaturpreis der Universitätsstadt Marburg und des Landkreises Marburg-Biedenkopf is a literary prize of Hesse . This article about a German literary award is a stub . You can help Wikipedia by expanding it .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg_Süd_station/html
Marburg Süd station
Marburg Süd railway station ( German : Marburg Südbahnhof ) is a train station in the south of Marburg in Hesse on the Main-Weser Railway .
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Elisabethschule Marburg
The Elisabethschule is a Gymnasium in Marburg .The Elisabethschule was founded in 1879 as Höhere Töchterschule . It was a school only for girls in this time. The first school building was located in the Universitätsstraße in the centre of Marburg. During the 1950s the new building in the Leopold-Lucas-Straße in Marburg Ockershausen was established. Since 1969 also boys were allowed to attend the school. Between 1936 and 1938 all jewish school girls and teachers were forced to leave the school. In 1993 a memorial was established in the form of a star of David for the 66 jewish victims of the school (pupils and teachers) caused by the Nazi regime.The first foreign language is English starting in 5th grade. In the 6th grade French or Latin is offered and in the 8th grade the student can choose another modern language like Spanish .The Elisabethschule has a partnership with the Redland High School for Girls in Bristol , England and with some other schools in Europe.50°48′N 8°45′E / 50.800°N 8.750°E / 50.800; 8.750
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Michelbach, Marburg
Michelbach ( German: [ ˈmɪçl̩ˌbax ] ⓘ ) is a borough ( Ortsbezirk ) of Marburg in Hesse .
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https://api.wikimedia.org/core/v1/wikipedia/en/page/Marburg_Central_Collecting_Point/html
Marburg Central Collecting Point
The Marburg Central Collecting Point , also known as the Marburg Central Art Collecting Point , was the first art depot in Post-World War II Germany . It was established by the U.S. Office of Military Government in the university town of Marburg to collect art looted or evacuated from museums, libraries, archives, castles, etc. before and during World War II and return them to their rightful owners. The Collecting Point existed between May 1945 and mid-August 1946.In 1943 , the American government established the American Commission for the Protection and Salvage of Artistic and Historic Monuments in War Areas . This commission, unofficially called the Roberts Commission after its chairman Supreme Court Justice Owen J. Roberts , had lists drawn up of monuments in Europe that were worthy of protection and were to be secured against further damage immediately after the withdrawal of military units. For practical implementation, a special military section called the Monuments, Fine Arts, and Archives program , or MFA&A for short, was founded, whose art protection officers were informally referred to as "Monuments Men" because of their activities. In addition, the unit was to collect the cultural assets that had been looted from the occupied countries, primarily by the Reichsleiter Rosenberg Taskforce , and return them to their original owners. In the fall of 1944, the first officers following the Allied front line, which was slowly shifting eastward from France, reached German soil. George L. Stout and Walker Hancock became aware of a large cache of artifacts in a former iron ore mine near Siegen during their stay in war-torn Aachen . During their subsequent visit to the Hain mine in early April 1945, the two officers discovered in a separate and guarded room nearly 600 paintings, hundreds of sculptures and other objects that were already attacked by mold due to the prevailing high humidity. To secure the artworks, Stout and Hancock decided to evacuate them as quickly as possible. However, because this was not immediately possible due to the ongoing state of war, they continued their inspection trip. After a stopover in Marburg, they parted ways. While Stout continued south, Hancock turned east and on April 29, 1945, he discovered in a potash mine in Bernterode , in addition to works of art, the Prussian Crown Jewels , the military standard collection, and the sarcophagi of Frederick the Great , Frederick William I , former German President Paul von Hindenburg and his wife Gertrud. In order to prevent the collection from falling into the hands of the Soviet Union , in whose occupation zone the mine was located, the American military government ordered its immediate evacuation. On May 9, 1945, the first objects from the Bernterode depot arrived in Marburg and the Central Collecting Point began its official activities. Several factors were decisive for the choice of the university town in central Hesse : Marburg was located in the American occupation zone , relatively close to other depots in central Germany that were known in the meantime, and had only minor war damage. Moreover, as early as April 1945, during his inspection tour of Hesse and Thuringia , Hancock had registered three buildings in the city that were suitable for this purpose: The Jubilee building of the university, which is still the seat of the university museum and the institutes of cultural studies together with their collections, the Marburg Castle , and the State Archives , which was inaugurated in 1938. It was there that Hancock set up his office immediately after his return following the unconditional surrender , having had the building occupied by an American military unit vacated and placed "Off Limits." With the help of the remaining employees of the State Archives and six workers assigned by the employment office, the objects arriving almost daily were magazined. For the inventory of the artworks, Hancock asked for assistance from Richard Hamann , who was both head of the Art history seminar and of the Foto Marburg Bildarchiv (picture archive) and willingly made his staff available. The Art history department was commissioned to prepare index cards for each object and to annotate them with photographs taken by the Bildarchiv. It was Hamann who, together with the mayor of the time, Eugen Siebecke, and the university rector, Julius Ebbinghaus, advocated the organization of an exhibition with the Collecting Point objects to the military government. After the permission was granted, a first exhibition of 30 masterpieces of European painting opened in the University Museum on November 15, 1945. More followed in the museum as well as in the State Archives until the dissolution of the Collecting Point. To secure the historically significant buildings in Hesse and to provide further support for the collection of objects, Hancock also recruited the working staff of Friedrich Bleibaum, the former provincial conservator of monuments of Hesse. Bleibaum had been active in securing buildings and evacuating valuable Hessian holdings during World War II and remained responsible for these areas on behalf of the Americans, for example, for the works of art he himself had stowed in the bunkers at Bad Wildungen . The most important goal at the Collecting Point was the restitution of the collected holdings, which they primarily suspected to be looted property. For this reason, art protection representatives such as the Belgian Raymond M. Lemaire , the American Edith Standen and the French Rose Valland came to Marburg and sifted through the artworks for suspected looted objects. But contrary to expectations of finding looted objects everywhere in Germany, apparently only a few such objects came to light in Marburg. A total of approximately 200 works, including the treasure from Metz Cathedral , arrived in Marburg from various depots and were returned to their original owners or taken to the Wiesbaden Central Collecting Point for further examination. It must be noted here, however, that due to a lack of personnel and time, no active provenance research could be conducted in Marburg, so that sometimes objects wrongfully acquired by museums or private individuals during Nazism remained undiscovered. The majority of the more than 4,000 art objects, more than 14,000 books and 17,500 shelf meters of file material came from German museums, churches, archives or private collections, including various Berlin and Rhineland collections, the Museum Folkwang in Essen , the Kunsthalle Düsseldorf etc. After it became clear that the Marburg State Archives did not have the necessary capacity to store the shipments that were still expected, and that the separation of objects at various locations in Hesse (at the Collecting Points in Marburg and Wiesbaden, the Offenbach Archival Depot , and the Bad Wildungen depot) did not seem advisable for security and personnel reasons, the MFA&A officers responsible for Hesse decided to merge the art collecting points in Wiesbaden . Beginning in the spring of 1946, objects from Marburg were transferred to the Museum Wiesbaden , where the U.S. military government had established another Art Collecting Point under the art protection officer Walter Farmer and which offered a larger storage capacity. At the same time, those objects that the American troops had illegally evacuated from the British occupation zone were moved to Düsseldorf and Dyck castle (this mainly concerned the objects from the Siegen ore mine). As a final measure, the four sarcophagi from the Bernterode depot were transferred to the St. Elizabeth's Church in Marburg in the secret "Operation Bodysnatch," while the military standards went to America as political booty. Immediately after this operation, Francis Bilodeau, who had followed Hancock as director in December 1945, announced the end of the Marburg Collecting Point on August 17, 1946.The most important goal at the Collecting Point was the restitution of the collected holdings, which they primarily suspected to be looted property. For this reason, art protection representatives such as the Belgian Raymond M. Lemaire , the American Edith Standen and the French Rose Valland came to Marburg and sifted through the artworks for suspected looted objects. But contrary to expectations of finding looted objects everywhere in Germany, apparently only a few such objects came to light in Marburg. A total of approximately 200 works, including the treasure from Metz Cathedral , arrived in Marburg from various depots and were returned to their original owners or taken to the Wiesbaden Central Collecting Point for further examination. It must be noted here, however, that due to a lack of personnel and time, no active provenance research could be conducted in Marburg, so that sometimes objects wrongfully acquired by museums or private individuals during Nazism remained undiscovered. The majority of the more than 4,000 art objects, more than 14,000 books and 17,500 shelf meters of file material came from German museums, churches, archives or private collections, including various Berlin and Rhineland collections, the Museum Folkwang in Essen , the Kunsthalle Düsseldorf etc. After it became clear that the Marburg State Archives did not have the necessary capacity to store the shipments that were still expected, and that the separation of objects at various locations in Hesse (at the Collecting Points in Marburg and Wiesbaden, the Offenbach Archival Depot , and the Bad Wildungen depot) did not seem advisable for security and personnel reasons, the MFA&A officers responsible for Hesse decided to merge the art collecting points in Wiesbaden . Beginning in the spring of 1946, objects from Marburg were transferred to the Museum Wiesbaden , where the U.S. military government had established another Art Collecting Point under the art protection officer Walter Farmer and which offered a larger storage capacity. At the same time, those objects that the American troops had illegally evacuated from the British occupation zone were moved to Düsseldorf and Dyck castle (this mainly concerned the objects from the Siegen ore mine). As a final measure, the four sarcophagi from the Bernterode depot were transferred to the St. Elizabeth's Church in Marburg in the secret "Operation Bodysnatch," while the military standards went to America as political booty. Immediately after this operation, Francis Bilodeau, who had followed Hancock as director in December 1945, announced the end of the Marburg Collecting Point on August 17, 1946.The MFA&A was chronically understaffed. Only Walker Hancock, assisted at times by New York conservator Sheldon Keck , and his successor Francis Bilodeau operated in Marburg. Hancock was thus dependent on local support, which is why he drew on personnel from the State Archives, the university, the State Monuments Office, and the Building Department. Even though the collaborations lasted only about 15 months, the cooperation that Hancock reported allowed the Marburg Central Collecting Point to become a methodological model for the collecting centers subsequently established in Munich Central Collecting Point and Wiesbaden. Representatives of the other art repositories, such as Walter Farmer (head of the Wiesbaden Collecting Point) and Gustav André (working at the British Zonal Fine Arts Repository), traveled to the university town in central Hesse to see the procedures at the Collecting Point and to exchange ideas about the joint work.In the German-American feature film " The Monuments Men ", which was released in 2014, the prequel that led to the founding of the Marburg Art Collecting Point is the subject of discussion. After the visit to the Siegen mine, however, the film abruptly switches to the events in Bavaria that led to the establishment of the Munich Collecting Point.
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Maribor
Maribor ( UK : / ˈ m ær ɪ b ɔːr / MARR -ib-or , US : / ˈ m ɑːr -/ MAR - , Slovene: [ ˈmáːɾibɔɾ ] ⓘ ; also known by other historical names ) is the second-largest city in Slovenia and the largest city of the traditional region of Lower Styria . It is also the seat of the City Municipality of Maribor , the seat of the Drava statistical region and the Eastern Slovenia region. Maribor is also the economic, administrative, educational, and cultural centre of eastern Slovenia. Maribor was first mentioned as a castle in 1164, as a settlement in 1209, and as a city in 1254. Like most Slovene ethnic territory , Maribor was under Habsburg rule until 1918, when Rudolf Maister and his men secured the city for the State of Slovenes, Croats and Serbs , which then joined the Kingdom of Serbia to form the Kingdom of Yugoslavia . In 1991 Maribor became part of independent Slovenia. Maribor, along with the Portuguese city of Guimarães , was selected as the European Capital of Culture for 2012.Maribor was attested in historical sources as Marpurch c. 1145 (and later as Marchburch , Marburc , and Marchpurch ), and is a compound of Middle High German march ' march (borderland) ' + burc 'fortress'. In modern times, the town's German name was Marburg an der Drau ( pronounced [ ˈmaʁbʊʁk ʔan deːɐ̯ ˈdʁaʊ̯ ] ; literally, 'Marburg on the Drava '). The Slovene name Maribor is an artificial Slovenized creation, coined by Stanko Vraz in 1836. Vraz created the name in the spirit of Illyrianism by analogy with the name Brandenburg (cf. Lower Sorbian Bramborska ). Locally, the town was known in Slovene as Marprk or Marprog . The name Maribor was accepted among Slovenes in 1861, when Lovro Toman published a song named Mar i bor , giving the name a Slovene compound Mar ('to care') + i ('and') + bor ('to fight for'). In addition to its Slovene and German names, the city is also known as Marburgum in Latin and Marburgo in Italian. Archbishop of Salzburg (1164–1555) Habsburg Monarchy (1555–1804) Austrian Empire (1804–1867) Austria-Hungary (1867–1918) State of Slovenes, Croats and Serbs (1918) Kingdom of Yugoslavia (1918–1941) Nazi Germany (1941–1945; annexed ) SFR Yugoslavia (1945–1991) Slovenia 1991–Present The oldest known remnants of settlement in the Maribor area date back to the 5th millennium BC, at the time of the Chalcolithic . With the construction of Maribor's western bypass, larger settlements were discovered dating from the 44th to 42nd century BC. Another settlement from around the same period was also discovered in Spodnje Hoče , a town right next to Maribor and another below Melje Hill near Malečnik . Another settlement below Melje Hill was also found dating to the 4th millennium BC. A more intense period of settlement of the Maribor area occurred in the 3rd millennium BC with the advent of the Bronze Age . In the 13th to 12th century BC, in the age of the Urnfield culture , new settlements were found in Pekel . Around 1000 BC, new settlers moved to the Maribor area. An urnfield cemetery was found from that period in today's Mladinska ulica and another necropolis was also found in Pobrežje . With the Iron Age and the Hallstatt Culture , new settlements began to appear on hills. One of them was Poštela in the Pohorje Mountains. Poštela was an old town that was abandoned in the 6th century BC and inhabited again in the 2nd century BC. During Roman times , the area where Maribor later developed was part of the province of Noricum , right on the border with Pannonia . During that period, Roman agricultural estates known as villae rusticae filled the area around Radvanje , Betnava , Bohova , and Hoče. The best-known of them was in today's Borova Vas neighborhood of Maribor. An important trade route was also established in the area, connecting Celeia and Flavia Solva in one direction with Poetovio and central Noricum on the other. After the fall of the Roman Empire, the Maribor area was settled by the Slavs . A Slavic cemetery was found in Radvanje dating to the 10th century AD. The area of what later became Maribor was first part of Samo's Empire and later the area stood on the border between Carantania and Lower Pannonia . In 843 the area was absorbed into the Frankish Empire . In the Frankish Empire, the area again stood on the border, this time between the Frankish Empire and the Principality of Hungary . To protect the Frankish Empire from Hungarian raids, a castle was built on Pyramid Hill . The castle was mentioned for the first time on 20 October 1164 as Castrum Marchburch . A settlement soon began to grow below the castle. Maribor was first mentioned as a market near the castle in 1204, and it received town privileges in 1254. It is likely that the castle stood before 1164 because Bernard of Trixien , the count of the region, already used the title Bernhard von Marchpurg 'Bernard of Maribor' in 1124. The town began to grow rapidly after the victory of Rudolf I of the Habsburg dynasty over King Otakar II of Bohemia in 1278. The town built fortifications, and trade, viticulture, and crafts started to grow. The town had a monopoly over the entire region and also controlled the viticulture trade with Carinthia . The first churches were built, and also around this time the first Jews arrived. The Jews built their own ghetto in the southeastern part of town, where they also built the Maribor Synagogue . Most Slovenians lived in the northwestern part of town on what is now Slovenian Street ( Slovenska ulica ). In 1478, a second castle was built on the northeastern side of the town, today known as Maribor Castle . In 1480 and in 1481, Matthias Corvinus besieged the town but failed to conquer it on both occasions. In 1496, Maximilian I issued a decree to expel all Jews from Maribor and Styria . In 1515, the Maribor Town Hall was built and a few years later, in 1532, Maribor again came under siege, this time by the Ottoman Empire . In the battle that became known as the Siege of Maribor , a 100,000-strong Ottoman army under the leadership of Suleiman the Magnificent attacked the town, which was defended only by the local garrison and its citizens. Despite all the odds, Maribor was defended and the legend of the Maribor shoemaker who raised the sluice gates and flooded the Ottoman army is still popular today. In the 17th century, numerous fires razed the town. The biggest ones occurred in 1601, 1645, 1648, and 1700. As a consequence, the town was rebuilt numerous times. In addition to fires, the plague decimated the town's population. The largest plague epidemics occurred in 1646, 1664, and 1680. Due to the plague, the town lost 35 percent of its population. In gratitude for the end of the plague, a plague column was built in 1681, with the original being replaced in 1743. In 1846, the Southern Railway was built through the town, which resulted in great economic growth and territorial expansion. In 1859, Anton Martin Slomšek , a bishop of the Diocese of Lavant , transferred the seat of the diocese to Maribor, and he further encouraged the use of Slovene. With the transfer, Maribor also received its first higher school. Four years later, Maribor was connected with Carinthia with the construction of the railway from Maribor to Prevalje . The first daily Slovenian newspaper, called Slovenski narod , was established in 1868 on today's Slomšek Square ( Slomškov trg ). On 4 April 1883, the first electric light in Slovene ethnic territory was installed on Castle Square ( Grajski trg ). The renowned electrical engineer Nikola Tesla lived in Maribor from 1878 to 1879, where he received his first job. Maribor National Hall was built in 1899, and it became a political, cultural, and economic centre for all Styrian Slovenes. In 1900, the city itself had a population that was 82.3% Austrian German (19,298 people) and 17.3% Slovene (4,062 people; based on the language spoken at home); : 4 most of the city's capital and public life was in Austrian German hands. However, the county excluding the city had only 10,199 Austrian Germans and 78,888 Slovene inhabitants, meaning the city was completely surrounded by majority-Slovene ethnic territory. : 210, 300 Some former independent settlements that later became part of the city had more ethnic Slovenes than Austrian Germans (e.g., Krčevina, Radvanje, Tezno), whereas others had more Austrian Germans than ethnic Slovenes (e.g., Pobrežje and Studenci). : 202–206 In 1913, a new bridge was opened over the Drava River, today known as the Old Bridge . In World War I , the 47th Infantry Regiment of the Austro-Hungarian Army was based in the city and also fought on the Isonzo front . During the First World War many Slovenes in Carinthia and Styria were detained on suspicion of being enemies of the Austrian Empire. This led to distrust between Austrian Germans and Slovenes. After the collapse of the Austrian-Hungarian Empire in 1918, Maribor was claimed by both the State of Slovenes, Croats and Serbs and German Austria . On 1 November 1918, a meeting was held by Colonel Anton Holik in the Melje barracks, where it was decided that the city would be part of German Austria. Ethnic Slovene Major Rudolf Maister , who was present at the meeting, denounced the decision and organised Slovenian military units that were able to seize control of the city. All Austrian officers and soldiers were disarmed and demobilised to the new state of German Austria. The German city council then held a secret meeting, where it was decided to do whatever possible to regain Maribor for German Austria. They organised a military unit called the Green Guard ( Schutzwehr ), and approximately 400 well-armed soldiers of this unit opposed the pro-Slovenian and pro- Yugoslav Major Maister. Slovenian troops surprised and disarmed the Green Guard early on the morning of 23 November. Thereafter, the city remained in Slovenian hands. On 27 January 1919, Austrian Germans gathered to await the United States peace delegation at the city's marketplace were fired upon by Slovenian troops. Nine citizens were killed and eighteen were seriously wounded; : 142 who had actually ordered the shooting has never been unequivocally established. German sources accused Maister's troops of shooting without cause. In turn Slovene witnesses such as Maks Pohar claimed that the Austrian Germans attacked the Slovenian soldiers guarding the town hall, one even discharging a revolver and hitting one Slovenian soldier in the bayonet. : 141 The German-language media called the incident Marburg's Bloody Sunday . As Maribor was now firmly in the hands of the Slovenian forces and surrounded completely by Slovenian territory; the city had been recognised as part of the Kingdom of Serbs, Croats and Slovenes without a plebiscite in the Treaty of Saint-Germain of 10 September 1919 between the victors and German Austria. For his actions in Maribor and later in the Austro-Slovene conflict in Carinthia , Rudolf Maister is today considered a Slovenian national hero. After 1918, most of Maribor's Austrian Germans left the Kingdom of Serbs, Croats and Slovenes for Austria . A policy of cultural assimilation was pursued in Yugoslavia against the Austrian German minority similar to the Germanization policy followed by Austria against its Slovene minority in Carinthia . From 1922 to 1929, Maribor was the seat of the Maribor Oblast , a subdivision within Yugoslavia and was later part of the Drava Banovina . Up until World War II , Maribor was considered the fastest-developing city in the country. In 1941 Lower Styria , the predominantly Slovene part of Styria, was annexed by Nazi Germany. German troops marched into the town at 9 pm on 8 April 1941. On 26 April Adolf Hitler , who encouraged his followers to "make this land German again", visited Maribor and a grand reception was organised in the city castle by the local Germans. Immediately after the occupation, Nazi Germany began mass expulsions of Slovenes to the Independent State of Croatia , Serbia , and later to the concentration and work camps in Germany. The Nazi goal was to Germanize the population of Lower Styria after the war. Slovene patriots were taken hostage and many were later shot in the prisons of Maribor and Graz. This led to organised resistance by Slovene partisans . The first act of resistance in Maribor and occupied Slovenia occurred only three days after Hitler's visit, when Slovene communists and SKOJ members burned two German cars. Maribor was the site of a German prisoner-of-war camp from 1941 to 1945 for many British, Australian, and New Zealand troops who had been captured in Crete in 1941 . In 1944, the largest mass rescue of POWs of the war in Europe took place when 105 Allied prisoners from the camp were freed by Slovene partisans in the Raid at Ožbalt . The city, a major industrial centre with an extensive armament industry, was systematically bombed by the Allies in the closing years of World War II . A total of 29 bombing raids devastated some 47% of the city area, killing 483 civilians and leaving over 4,200 people homeless. Over 2,600 people died in Maribor during the war. By the end of the war, Maribor was the most war-damaged major town of Yugoslavia. The remaining German-speaking population, except those who had actively supported the resistance during the war, was summarily expelled at the end of the war in May 1945. At the same time Croatian Home Guard members and their relatives who tried to escape from Yugoslavia were executed by the Yugoslav Army . The existence of nine mass graves in and near Maribor was revealed after Slovenia's independence. After the Second World War, Maribor became part of SR Slovenia , within SFR Yugoslavia . A major process of renewal and reconstruction began in the city. Maribor soon after became the industrial centre of Slovenia and the whole of Yugoslavia, hosting many known companies such as the Maribor Automobile Factory among others. The first clash between the Yugoslav People's Army and the Slovenian Territorial Defence in Slovenia's war of independence happened in nearby Pekre and on the streets of Maribor resulting in the conflicts first casualty. After Slovenia seceded from Yugoslavia in 1991, the loss of the Yugoslav market severely strained the city's economy, which was based on heavy industry. The city saw a record unemployment rate of nearly 25%. The economic situation of Maribor after the mid-1990s crisis worsened again with the onset of global economic crisis combined with the European sovereign-debt crisis , which was one of the causes for the beginning of 2012–13 Maribor protests which spread into 2012–2013 Slovenian protests . In 2012, Maribor was one of the two European Capitals of Culture , and the following year, Maribor was the European Youth Capital . The oldest known remnants of settlement in the Maribor area date back to the 5th millennium BC, at the time of the Chalcolithic . With the construction of Maribor's western bypass, larger settlements were discovered dating from the 44th to 42nd century BC. Another settlement from around the same period was also discovered in Spodnje Hoče , a town right next to Maribor and another below Melje Hill near Malečnik . Another settlement below Melje Hill was also found dating to the 4th millennium BC. A more intense period of settlement of the Maribor area occurred in the 3rd millennium BC with the advent of the Bronze Age . In the 13th to 12th century BC, in the age of the Urnfield culture , new settlements were found in Pekel . Around 1000 BC, new settlers moved to the Maribor area. An urnfield cemetery was found from that period in today's Mladinska ulica and another necropolis was also found in Pobrežje . With the Iron Age and the Hallstatt Culture , new settlements began to appear on hills. One of them was Poštela in the Pohorje Mountains. Poštela was an old town that was abandoned in the 6th century BC and inhabited again in the 2nd century BC. During Roman times , the area where Maribor later developed was part of the province of Noricum , right on the border with Pannonia . During that period, Roman agricultural estates known as villae rusticae filled the area around Radvanje , Betnava , Bohova , and Hoče. The best-known of them was in today's Borova Vas neighborhood of Maribor. An important trade route was also established in the area, connecting Celeia and Flavia Solva in one direction with Poetovio and central Noricum on the other. After the fall of the Roman Empire, the Maribor area was settled by the Slavs . A Slavic cemetery was found in Radvanje dating to the 10th century AD. The area of what later became Maribor was first part of Samo's Empire and later the area stood on the border between Carantania and Lower Pannonia . In 843 the area was absorbed into the Frankish Empire . In the Frankish Empire, the area again stood on the border, this time between the Frankish Empire and the Principality of Hungary . To protect the Frankish Empire from Hungarian raids, a castle was built on Pyramid Hill . The castle was mentioned for the first time on 20 October 1164 as Castrum Marchburch . A settlement soon began to grow below the castle. Maribor was first mentioned as a market near the castle in 1204, and it received town privileges in 1254. It is likely that the castle stood before 1164 because Bernard of Trixien , the count of the region, already used the title Bernhard von Marchpurg 'Bernard of Maribor' in 1124. The town began to grow rapidly after the victory of Rudolf I of the Habsburg dynasty over King Otakar II of Bohemia in 1278. The town built fortifications, and trade, viticulture, and crafts started to grow. The town had a monopoly over the entire region and also controlled the viticulture trade with Carinthia . The first churches were built, and also around this time the first Jews arrived. The Jews built their own ghetto in the southeastern part of town, where they also built the Maribor Synagogue . Most Slovenians lived in the northwestern part of town on what is now Slovenian Street ( Slovenska ulica ). In 1478, a second castle was built on the northeastern side of the town, today known as Maribor Castle . In 1480 and in 1481, Matthias Corvinus besieged the town but failed to conquer it on both occasions. In 1496, Maximilian I issued a decree to expel all Jews from Maribor and Styria . In 1515, the Maribor Town Hall was built and a few years later, in 1532, Maribor again came under siege, this time by the Ottoman Empire . In the battle that became known as the Siege of Maribor , a 100,000-strong Ottoman army under the leadership of Suleiman the Magnificent attacked the town, which was defended only by the local garrison and its citizens. Despite all the odds, Maribor was defended and the legend of the Maribor shoemaker who raised the sluice gates and flooded the Ottoman army is still popular today. In the 17th century, numerous fires razed the town. The biggest ones occurred in 1601, 1645, 1648, and 1700. As a consequence, the town was rebuilt numerous times. In addition to fires, the plague decimated the town's population. The largest plague epidemics occurred in 1646, 1664, and 1680. Due to the plague, the town lost 35 percent of its population. In gratitude for the end of the plague, a plague column was built in 1681, with the original being replaced in 1743. In 1846, the Southern Railway was built through the town, which resulted in great economic growth and territorial expansion. In 1859, Anton Martin Slomšek , a bishop of the Diocese of Lavant , transferred the seat of the diocese to Maribor, and he further encouraged the use of Slovene. With the transfer, Maribor also received its first higher school. Four years later, Maribor was connected with Carinthia with the construction of the railway from Maribor to Prevalje . The first daily Slovenian newspaper, called Slovenski narod , was established in 1868 on today's Slomšek Square ( Slomškov trg ). On 4 April 1883, the first electric light in Slovene ethnic territory was installed on Castle Square ( Grajski trg ). The renowned electrical engineer Nikola Tesla lived in Maribor from 1878 to 1879, where he received his first job. Maribor National Hall was built in 1899, and it became a political, cultural, and economic centre for all Styrian Slovenes. In 1900, the city itself had a population that was 82.3% Austrian German (19,298 people) and 17.3% Slovene (4,062 people; based on the language spoken at home); : 4 most of the city's capital and public life was in Austrian German hands. However, the county excluding the city had only 10,199 Austrian Germans and 78,888 Slovene inhabitants, meaning the city was completely surrounded by majority-Slovene ethnic territory. : 210, 300 Some former independent settlements that later became part of the city had more ethnic Slovenes than Austrian Germans (e.g., Krčevina, Radvanje, Tezno), whereas others had more Austrian Germans than ethnic Slovenes (e.g., Pobrežje and Studenci). : 202–206 In 1913, a new bridge was opened over the Drava River, today known as the Old Bridge . In World War I , the 47th Infantry Regiment of the Austro-Hungarian Army was based in the city and also fought on the Isonzo front . During the First World War many Slovenes in Carinthia and Styria were detained on suspicion of being enemies of the Austrian Empire. This led to distrust between Austrian Germans and Slovenes. After the collapse of the Austrian-Hungarian Empire in 1918, Maribor was claimed by both the State of Slovenes, Croats and Serbs and German Austria . On 1 November 1918, a meeting was held by Colonel Anton Holik in the Melje barracks, where it was decided that the city would be part of German Austria. Ethnic Slovene Major Rudolf Maister , who was present at the meeting, denounced the decision and organised Slovenian military units that were able to seize control of the city. All Austrian officers and soldiers were disarmed and demobilised to the new state of German Austria. The German city council then held a secret meeting, where it was decided to do whatever possible to regain Maribor for German Austria. They organised a military unit called the Green Guard ( Schutzwehr ), and approximately 400 well-armed soldiers of this unit opposed the pro-Slovenian and pro- Yugoslav Major Maister. Slovenian troops surprised and disarmed the Green Guard early on the morning of 23 November. Thereafter, the city remained in Slovenian hands. On 27 January 1919, Austrian Germans gathered to await the United States peace delegation at the city's marketplace were fired upon by Slovenian troops. Nine citizens were killed and eighteen were seriously wounded; : 142 who had actually ordered the shooting has never been unequivocally established. German sources accused Maister's troops of shooting without cause. In turn Slovene witnesses such as Maks Pohar claimed that the Austrian Germans attacked the Slovenian soldiers guarding the town hall, one even discharging a revolver and hitting one Slovenian soldier in the bayonet. : 141 The German-language media called the incident Marburg's Bloody Sunday . As Maribor was now firmly in the hands of the Slovenian forces and surrounded completely by Slovenian territory; the city had been recognised as part of the Kingdom of Serbs, Croats and Slovenes without a plebiscite in the Treaty of Saint-Germain of 10 September 1919 between the victors and German Austria. For his actions in Maribor and later in the Austro-Slovene conflict in Carinthia , Rudolf Maister is today considered a Slovenian national hero. After 1918, most of Maribor's Austrian Germans left the Kingdom of Serbs, Croats and Slovenes for Austria . A policy of cultural assimilation was pursued in Yugoslavia against the Austrian German minority similar to the Germanization policy followed by Austria against its Slovene minority in Carinthia . From 1922 to 1929, Maribor was the seat of the Maribor Oblast , a subdivision within Yugoslavia and was later part of the Drava Banovina . Up until World War II , Maribor was considered the fastest-developing city in the country. In 1941 Lower Styria , the predominantly Slovene part of Styria, was annexed by Nazi Germany. German troops marched into the town at 9 pm on 8 April 1941. On 26 April Adolf Hitler , who encouraged his followers to "make this land German again", visited Maribor and a grand reception was organised in the city castle by the local Germans. Immediately after the occupation, Nazi Germany began mass expulsions of Slovenes to the Independent State of Croatia , Serbia , and later to the concentration and work camps in Germany. The Nazi goal was to Germanize the population of Lower Styria after the war. Slovene patriots were taken hostage and many were later shot in the prisons of Maribor and Graz. This led to organised resistance by Slovene partisans . The first act of resistance in Maribor and occupied Slovenia occurred only three days after Hitler's visit, when Slovene communists and SKOJ members burned two German cars. Maribor was the site of a German prisoner-of-war camp from 1941 to 1945 for many British, Australian, and New Zealand troops who had been captured in Crete in 1941 . In 1944, the largest mass rescue of POWs of the war in Europe took place when 105 Allied prisoners from the camp were freed by Slovene partisans in the Raid at Ožbalt . The city, a major industrial centre with an extensive armament industry, was systematically bombed by the Allies in the closing years of World War II . A total of 29 bombing raids devastated some 47% of the city area, killing 483 civilians and leaving over 4,200 people homeless. Over 2,600 people died in Maribor during the war. By the end of the war, Maribor was the most war-damaged major town of Yugoslavia. The remaining German-speaking population, except those who had actively supported the resistance during the war, was summarily expelled at the end of the war in May 1945. At the same time Croatian Home Guard members and their relatives who tried to escape from Yugoslavia were executed by the Yugoslav Army . The existence of nine mass graves in and near Maribor was revealed after Slovenia's independence. After the Second World War, Maribor became part of SR Slovenia , within SFR Yugoslavia . A major process of renewal and reconstruction began in the city. Maribor soon after became the industrial centre of Slovenia and the whole of Yugoslavia, hosting many known companies such as the Maribor Automobile Factory among others. The first clash between the Yugoslav People's Army and the Slovenian Territorial Defence in Slovenia's war of independence happened in nearby Pekre and on the streets of Maribor resulting in the conflicts first casualty. After Slovenia seceded from Yugoslavia in 1991, the loss of the Yugoslav market severely strained the city's economy, which was based on heavy industry. The city saw a record unemployment rate of nearly 25%. The economic situation of Maribor after the mid-1990s crisis worsened again with the onset of global economic crisis combined with the European sovereign-debt crisis , which was one of the causes for the beginning of 2012–13 Maribor protests which spread into 2012–2013 Slovenian protests . In 2012, Maribor was one of the two European Capitals of Culture , and the following year, Maribor was the European Youth Capital . On the Drava River lies Maribor Island ( Mariborski otok ). The oldest public bath, still an important and often visited place in Maribor, is located on the island. There are two hills in Maribor: Calvary Hill and Pyramid Hill, both surrounded by vineyards. The latter dominates the northern border of the city. Ruins of the first Maribor castle from the 11th century and a chapel from the 19th century also stand there. The hill offers an easily accessible scenic overlook of Maribor and the countryside to the south over the Drava River. The city of Maribor is divided into 11 districts ( Slovene : mestne četrti ) of the City Municipality of Maribor . The Drava River separates the districts of Center, Koroška Vrata, and Ivan Cankar to the north from other districts south of it. The various city districts are connected by four road bridges, a rail bridge, and a pedestrian bridge . Maribor has a humid continental climate ( Köppen climate classification : Dfb), bordering on oceanic climate (Köppen: Cfb). Average temperatures hover around zero degrees Celsius during the winter. Summers are generally warm. Average temperatures during the city's warmest month (July) exceed 20 degrees Celsius, which is one of the main reasons for the Maribor wine tradition. The city sees on average roughly 900 mm (35.4 in) of precipitation annually and it's one of the sunniest Slovene cities, with an average of 266 sunny days throughout the course of the year. The most recent temperature heatwave record for August is 40.6 °C, measured at the Maribor–Tabor weather station by the Slovenian Environment Agency (ARSO) on 8 August 2013. On the Drava River lies Maribor Island ( Mariborski otok ). The oldest public bath, still an important and often visited place in Maribor, is located on the island. There are two hills in Maribor: Calvary Hill and Pyramid Hill, both surrounded by vineyards. The latter dominates the northern border of the city. Ruins of the first Maribor castle from the 11th century and a chapel from the 19th century also stand there. The hill offers an easily accessible scenic overlook of Maribor and the countryside to the south over the Drava River.The city of Maribor is divided into 11 districts ( Slovene : mestne četrti ) of the City Municipality of Maribor . The Drava River separates the districts of Center, Koroška Vrata, and Ivan Cankar to the north from other districts south of it. The various city districts are connected by four road bridges, a rail bridge, and a pedestrian bridge .Maribor has a humid continental climate ( Köppen climate classification : Dfb), bordering on oceanic climate (Köppen: Cfb). Average temperatures hover around zero degrees Celsius during the winter. Summers are generally warm. Average temperatures during the city's warmest month (July) exceed 20 degrees Celsius, which is one of the main reasons for the Maribor wine tradition. The city sees on average roughly 900 mm (35.4 in) of precipitation annually and it's one of the sunniest Slovene cities, with an average of 266 sunny days throughout the course of the year. The most recent temperature heatwave record for August is 40.6 °C, measured at the Maribor–Tabor weather station by the Slovenian Environment Agency (ARSO) on 8 August 2013. Many historical structures stand in Maribor. Of the remains of city walls surrounding the old downtown, the most prominent are the Judgement Tower , the Water Tower , and the Jewish Tower. Maribor Cathedral was built in the Gothic style in the 13th century. Maribor Synagogue was built in the 14th century, and is the second oldest synagogue of Europe. Today it serves as a centre for cultural activities. Other prominent Medieval buildings are Maribor Castle , Betnava Castle , and the ruins of Upper Maribor Castle on Pyramid Hill. Town Hall was constructed in the Renaissance style , and the Plague Column in the Baroque style . At the start of the 21st century, plans were made for a new modern business, residential and entertainment district, called the Drava Gate ( Dravska vrata ) and nicknamed the Maribor Manhattan . The project includes many new exclusive residential apartments, offices and conference halls, a green and recreational space, and other structures. It also includes a 111 m (364 ft) tall skyscraper that would be the tallest building in Slovenia. Due to lack of finances, the project has been postponed. In 2008, the Studenci Footbridge ( Studenška brv ) was renovated according to the design of the Ponting company. The design was awarded that year at the 3rd International Footbridge Conference in Porto . In 2010, Maribor organised an international architectural competition ECC Maribor 2012 – Drava 2012 to gather proposals for the design and reconstruction of the Drava banks, the construction of a new art gallery, and for a new footbridge. Its jury received about 400 proposals for the three different projects. The footbridge and the river embankments will be built in the near future, but the art gallery was replaced with a cultural center MAKS , which is currently under construction. The construction of a new modern Faculty of Medicine started in 2011 near the Drava River. It was designed by architect Boris Podrecca and was completed in 2013. There are plans to renovate the Maribor Public Library and Town Hall Square ( Rotovški trg ). In addition, the renovation of Maribor Island ( Mariborski otok ) in the Drava River has been planned.The main park of the city is Maribor City Park, with the City Aquarium and Terrarium, and a wide promenade leading to the Three Ponds ( Trije ribniki ), containing over 100 local and foreign species of deciduous and coniferous trees.Maribor, previously in the Catholic Diocese of Graz-Seckau , became part of the Diocese of Lavant on 1 June 1859, and the seat of its Prince-Bishop . The name of the diocese (after a river in Carinthia ) was later changed to the Diocese of Maribor on 5 March 1962. It was elevated to an archdiocese by Pope Benedict XVI on 7 April 2006. Jewish people living in Maribor were first mentioned in 1277. It is suggested that at that time there was already a Jewish quarter in the city. The Jewish ghetto was located in the southeastern part of the city and it comprised, at its peak, several main streets in the city centre including part of the main city square. The ghetto had a synagogue , a Jewish cemetery and also a Talmud school. The Jewish community of Maribor was numerically at its apex around 1410. After 1450 the circumstances changed dramatically: increasing competition that coincided with an economic crisis dealt a severe blow to the economic activities that were crucial to their economic success. According to a decree issued by Emperor Maximilian I in 1496, Jews were forced to leave the city of Maribor. Restrictions on settlement and business for Jews remained in place until 1861. From late spring 1941, after Lower Styria was annexed by the Third Reich, the Jews of Maribor were deported to concentration camps.Maribor, previously in the Catholic Diocese of Graz-Seckau , became part of the Diocese of Lavant on 1 June 1859, and the seat of its Prince-Bishop . The name of the diocese (after a river in Carinthia ) was later changed to the Diocese of Maribor on 5 March 1962. It was elevated to an archdiocese by Pope Benedict XVI on 7 April 2006.Jewish people living in Maribor were first mentioned in 1277. It is suggested that at that time there was already a Jewish quarter in the city. The Jewish ghetto was located in the southeastern part of the city and it comprised, at its peak, several main streets in the city centre including part of the main city square. The ghetto had a synagogue , a Jewish cemetery and also a Talmud school. The Jewish community of Maribor was numerically at its apex around 1410. After 1450 the circumstances changed dramatically: increasing competition that coincided with an economic crisis dealt a severe blow to the economic activities that were crucial to their economic success. According to a decree issued by Emperor Maximilian I in 1496, Jews were forced to leave the city of Maribor. Restrictions on settlement and business for Jews remained in place until 1861. From late spring 1941, after Lower Styria was annexed by the Third Reich, the Jews of Maribor were deported to concentration camps.The city is the location of the University of Maribor , established in 1975, Alma Mater Europaea , and several other higher education institutions. High schools include Maribor High School No. 1 ( Prva gimnazija Maribor ) and Maribor High School No. 2 ( II. gimnazija Maribor ). Every June, the two-week Lent Festival (named after the waterfront district called Lent) is held, with hundreds of musical, theatrical and other events. Every year the festival attracts theatre, opera, ballet performers, classical, modern, and jazz musicians and dancers from all over the world. Maribor is known for wine and culinary specialities of international and Slovene cuisine (mushroom soup with buckwheat mush, tripe, sour soup, sausages with Sauerkraut, cheese dumplings, apple strudel, special cheese cake called gibanica ). There are also many popular restaurants with Serbian cuisine . The Vinag Wine Cellar ( Vinagova vinska klet ), with the area of 20.000 m 2 (215.28 sq ft) and the length of 2 km (1 mi) , keeps 5,5 millions litres of wine. The house of the oldest grapevine in the world ( Hiša stare trte ) at Lent grows the world's oldest grapevine, which was in 2004 recorded in Guinness World Records . The grapevine of Žametovka is over 400 years old. The most listened radio station transmitting from Maribor is the commercial radio station Radio City . Other radio stations broadcasting from Maribor include Radio NET FM, Radio Maribor, Rock Maribor, Radio Brezje, and Maribor Študent Radio (MARŠ). The alternative scene of Maribor is situated in the Pekarna Cultural Centre, located in a former military bakery area in the Magdalena District . Maribor is the hometown of the association football club NK Maribor , playing in the Slovenian top division . NK Maribor has won the domestic title a record 16 times and has participated in the UEFA Champions League group stage on three occasions, in 1999, 2014, and 2017. The club's home ground is Ljudski vrt , located in the Koroška Vrata district. The Maribor Pohorje Ski Resort , situated on the outskirts of the city on the slopes of the Pohorje mountain range, hosted the women's slalom and giant slalom races for the Alpine Skiing World Cup . The competition, known as the Golden Fox ( Slovene : Zlata lisica ), was held for the first time in 1964, and was last held in Maribor in 2019. Since then, due to the lack of snow in the city, the event has been relocated to Kranjska Gora . In November 2012, Maribor hosted the World Youth Chess Championship with Garry Kasparov as the guest of honour. It was presumed that Maribor would also host the 2013 Winter Universiade , but the Government of Slovenia refused any financial support for the project. As a result, in March 2012, the International University Sports Federation decided that it would organise the Universiade elsewhere. In the same year, Maribor also withdrew as one of the host cities of the EuroBasket 2013 due to lack of finances. Maribor's Ljudski vrt stadium was one of the venues for the 2012 UEFA European Under-17 Championship and the 2021 UEFA European Under-21 Championship . In July 2023, Maribor hosted the 17th edition of the European Youth Olympic Festival . Maribor's sports parks include the Pohorje Adrenaline Park ( Adrenalinski park Pohorje ), the Pohorje Bike Park, and the Betnava Adventure Park ( Pustolovski park Betnava ) with ropes courses , zip-lines , and poles. [ clarification needed ]Maribor is the hometown of the association football club NK Maribor , playing in the Slovenian top division . NK Maribor has won the domestic title a record 16 times and has participated in the UEFA Champions League group stage on three occasions, in 1999, 2014, and 2017. The club's home ground is Ljudski vrt , located in the Koroška Vrata district.The Maribor Pohorje Ski Resort , situated on the outskirts of the city on the slopes of the Pohorje mountain range, hosted the women's slalom and giant slalom races for the Alpine Skiing World Cup . The competition, known as the Golden Fox ( Slovene : Zlata lisica ), was held for the first time in 1964, and was last held in Maribor in 2019. Since then, due to the lack of snow in the city, the event has been relocated to Kranjska Gora . In November 2012, Maribor hosted the World Youth Chess Championship with Garry Kasparov as the guest of honour. It was presumed that Maribor would also host the 2013 Winter Universiade , but the Government of Slovenia refused any financial support for the project. As a result, in March 2012, the International University Sports Federation decided that it would organise the Universiade elsewhere. In the same year, Maribor also withdrew as one of the host cities of the EuroBasket 2013 due to lack of finances. Maribor's Ljudski vrt stadium was one of the venues for the 2012 UEFA European Under-17 Championship and the 2021 UEFA European Under-21 Championship . In July 2023, Maribor hosted the 17th edition of the European Youth Olympic Festival . Maribor's sports parks include the Pohorje Adrenaline Park ( Adrenalinski park Pohorje ), the Pohorje Bike Park, and the Betnava Adventure Park ( Pustolovski park Betnava ) with ropes courses , zip-lines , and poles. [ clarification needed ]Maribor is twinned with: Maribor has signed partnerships with: Maribor is twinned with: Maribor has signed partnerships with:
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