atepeq/tico19 huggingface dataset:
Without knowing answers to #1 and 2, we cannot efficiently cut the transmission, and the outbreak can relapse at any time.
Ku na cïn te dhuk ok kïït thiëc #1 ku 2 nhïïm, ka cïn te lɛ̈u bï ok tuany gɛ̈l thïn bï rɔt cï tek piny, ku tuany abï lɔ̈k la tueŋ juak rɔt.
Although molecular modeling and biochemical assays have demonstrated that SARS-CoV-2 binds to ACE2, how exactly does the virus enter the airway cells and cause subsequent pathological changes?
Cɔk alɔn cï käk lui guopic yen nyuɔth lɔn ye SARS-CoV-2 rot mat ke ACE2, yekede ye köm la kɔc ŋum ku war köm rɔt?
Does the virus also bind ACE2-expressing cells in other organs?
Ye köm rɔt mat kek ACE2 ku bïk käk guop kök pïïc?
Without clear answers to these questions, we cannot achieve fast and accurate diagnosis and effective treatment.
Te cïn yen kën kïït thiëc kä dhuk nhïïm, ka cïn te lɛ̈u bï ok tuany ŋiɛc thïn ku jɔl a elacde.
How long will the epidemic last?
Ye kam yïnde yen bï tuɛny kën nɔk?
How is the virus genetically evolving during transmission among humans?
Ye köm la tueŋ ke diɛ̈t kede te le yen ran guop?
Will it become a pandemic worldwide, die down like SARS or relapse periodically like the flu?
Bï ya tuany dït pinynhom, bï thou piny path cïmen SARS wula bï la piny amäth cïmen juäi?
It is essential but may take some time to search for answers to the above and many other questions.
Eke path ku abï kam dït nyai ku bï kïït thiëc tɔ̈u nhial dhuk nhïïm ku kïït thiëc kök.
However, with whatever expense it may demand, we have no other choice but to stop the epidemic as soon as possible and bring our life back to normal.
Cɔk ke yïnde ben nyai, ka buk dhiɛl them ku buk tuany kën cɔl akääc ku buk dhuk pïïrdan thɛɛr ic.
Zoonotic origins of human coronaviruses
Lääi ye käm corona kɔc dom thïn
Mutation and adaptation have driven the co-evolution of coronaviruses (CoVs) and their hosts, including human beings, for thousands of years.
Awɛ̈r rɔt yen kuat (CoV) ku ɣɔ̈ɔ̈n ye kek yɔ̈k, la iic kɔc, run juëc apɛi cɔl ale tueŋ.
Before 2003, two human CoVs (HCoVs) were known to cause mild illness, such as common cold.
Ke ruon 2003 kïc guɔ bën, tuɛnytuuɛny kuat (HCoVs) kärɔu aake cï ŋic lɔn ye kek kɔc yiɛ̈n tuany thiin kor, cïmen juän wum.
The outbreaks of severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) have flipped the coin to reveal how devastating and life-threatening an HCoV infection could be.
Jɔ̈k cök cï (SARS) jɔk ku tuany pan Middle East (MERS) acï rɛ̈ɛ̈c tuany nyuɔth ku të ye HCoV pïïr riäc thïn
The emergence of SARS-CoV-2 in central China at the end of 2019 has thrusted CoVs into the spotlight again and surprised us with its high transmissibility but reduced pathogenicity compared to its sister SARS-CoV.
Bɛ̈n cï SARS-CoV-2 bɛ̈n pan China ciɛlic thɔ̈k 2019 acï kuat CoV nyuɔth kɔc ku acï ok gɔ̈i tekde rɔt piny ku dhuŋde piny te thɔ̈ɔ̈ŋ kek ke SARS-CoV.
HCoV infection is a zoonosis and understanding the zoonotic origins of HCoVs would serve us well.
HCoV e tuɛny lääi ku buk te ye yen ben lääi gup thïn detic kuat HCoVs abï ok kony apɛi.
Most HCoVs originated from bats where they are non-pathogenic.
Kuat HCoV juec aaye yɔ̈k aliɛ̈k gup ku aace gup la tuany.
The intermediate reservoir hosts of some HCoVs are also known.
Te ye käm kuat HCoV rɛ̈ɛ̈r thïn aa ŋic kek aya.
Identifying the animal hosts has direct implications in the prevention of human diseases.
Wɛ̈tden ku bï län muk köm ŋic ka bï kɔc kony ku bï tuɛnytuɛny kɔc ya gɛ̈l.
Investigating CoV-host interactions in animals might also derive important insight on CoV pathogenesis in humans.
Wɛ̈tden bï te ye CoV yɔ̈k thïn buɔth cɔk lääi iic alɛ̈u bï te ye CoV bën thïn kɔc gup detic.
In this review, we present an overview of the existing knowledge about the seven HCoVs, with a focus on the history of their discovery as well as their zoonotic origins and interspecies transmission.
Ke cuk tïŋ kën ic, ok aacï ke ŋicku alɔŋ käm kä dhorɔu kuat HCoV, ku ke cï cuk täu o nhïïm anyïköl te ye kek yɔ̈k thïn lääi gup ku te ye kek jiɛ̈l thïn bï la kɔc gup.
Importantly, we compare and contrast the different HCoVs from a perspective of virus evolution and genome recombination.
Kuat HCoV aaye ku thɔ̈ɔ̈ŋ kɔ̈ɔ̈th ku wɛ̈ɛ̈c ku kek tecït te yeku tiɛ̈ŋ köm thïn ke diɛ̈t ku mɛ̈n ic käk guop.
The current CoV disease 2019 (COVID-19) epidemic is discussed in this context.
Tuany CoV 2019 (COVID-19) acï jääm ic tecït te ŋïc yen.
In addition, the requirements for successful host switches and the implications of virus evolution on disease severity are also highlighted.
Te bï te ye köm yɔ̈k ŋic ku käk rɔ̈t looi te cï köm rɔt juak ku rɛ̈ɛ̈c aacï kek jaam iic tën.
Coronaviruses (CoVs) belong to the family Coronaviridae, which comprises a group of enveloped, positive-sensed, single-stranded RNA viruses.
Käm coronavirus kuat (CoV) aa kuat Coronaviridae, ku aala iic akut kum, kïn ye nyuɔth lɔ̈n tɔ̈u yen, ku käm RNA kek cï gäk guop ic.
These viruses harbouring the largest genome of 26 to 32 kilobases amongst RNA viruses were termed “CoVs” because of their crown-like morphology under electron microscope.
Käm la kilo 26 le 32 kam käm ye yɔ̈k RNA aacï kek cɔl kuat "CoV" rin gɛlgɛl ye tïŋ microscope ic wɛnh ye kɔc caath gup tuany.
Structurally, CoVs have non-segmented genomes that share a similar organization.
Tecït te cï cäk kek, kuat CoV aala käk guop la tecït te cï kek guir thïn thɔ̈ɔ̈ŋ.
Approximately two thirds of the genome contain two large overlapping open reading frames (ORF1a and ORF1b), which are translated into the pp1a and pp1ab replicase polyproteins.
Rɔ̈u diäk ic aala iic käŋ kärɔu ŋaany (ORF1a ku ORF1b), ku aye ben tet ic ku bïk aa pp1a ku pp1ab miök protin.
The polyproteins are further processed to generate 16 non-structural proteins, designated nsp1~16.
Miök guop protin aaye miöök juëc guir ku bïk protin 16, ku aacï yiɛ̈k nsp1-16.
The remaining portion of the genome contains ORFs for the structural proteins, including spike (S), envelope (E), membrane (M) and nucleoprotein (N).
Kuat akut käk guop dɔ̈ɔ̈ŋ aala iic ORFs ku bi mioo;k rɔ̈t cɔ̈k piny, cïmen Juɛ̈ŋ rɔt miök (), akum (E), dɛ̈l (M) ku ɣɔ̈n miök (N).
A number of lineage-specific accessory proteins are also encoded by different lineages of CoVs.
Kuat Miöök protin guop juëc apɛi aa käk rɔt looi kuat CoV juëc iic.
Based on the difference in protein sequences, CoVs are classified into four genera (alpha-CoV, beta-CoV, gamma-CoV and delta-CoV), among which the beta-CoV genera contains most HCoVs and is subdivided into four lineages (A, B, C and D).
Tecït te cï yɔ̈k ke wääc protin ic, kuat CoVs aacï kek tek iic ŋuan (alpha-CoV, beta-CoV, gamma-CoV ku delta-CoV), ku e beta-CoV yen ala ic kuat HCoVs ku acï tek ic dhiɛ̈th kä ŋuan (A,B,C, ku D).
Phylogenetic evidence has shown that bats and rodents serve as the gene source of most alpha-CoVs and beta-CoVs, while birds are the main reservoir of gamma-CoVs and delta-CoVs.
Acï phylogentic nyuɔth lɔn ye aliɛ̈k ku luɔk kuat lääi e tuany alpha-CoVs ku beta-CoVs kök bɛ̈i, ku diɛt aa kek gamma-CoVs ku delta-CoVs bɛ̈i.
For thousands of years, CoVs have constantly crossed species barriers and some have emerged as important human pathogens.
Run juëc, kuat CoV aacï ya käm kamken ku aacï bën ya käm ye guop ran wïc.
To date, seven human CoVs (HCoVs) are known.
Gut yaköl, kuat CoVs kadhorou raan dɔm (HCoVs) aa ŋic kek.
Among them HCoV-229E and HCoV-NL63 are alpha-CoVs.
Ku kamken e HCoV-229E ku jɔl a HCoV-NL63 ku aa kuan alpha-CoV tööŋ.
The other five beta-CoVs include HCoV-OC43, HCoV-HKU1, severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and SARS-CoV-2.
Käm kok kadhiic beta-CoV ala iic HCoV-OC43, HCoV-HKU1, tuany puou ye ran kuɔ̈c wɛ̈i (SARS-CoV), Tuɛny Middle East (MERS-CoV) ku SARS-CoV-2
HCoV-229E, HCoV-OC43, HCoV-HKU1 and HCoV-NL63 usually cause mild symptoms, like common cold and/or diarrhea.
HCoV-229E, HCoV-OC43, HCoV_HKU1 ku HCoV-NL63 aa kɔc yiɛ̈k kïït thïï kor, cïmen juän wum ku/wula yäc.
In contrast, SARS-CoV, MERS-CoV and the newly-identified SARS-CoV-2 are highly pathogenic, causing severe lower respiratory tract infection in relatively more patients with a higher chance to develop acute respiratory distress syndrome (ARDS) and extrapulmonary manifestations.
Ku bï kek wäc, SARS-CoV, MERS-CoV ku SARS-CoV-2 yam ken aa käm rɛc, aa wɛ̈i cɔl aril ic ku e kɔc juëc yiɛ̈n kɔ̈ɔ̈c puou ku cïk ŋiɛ̈c wɛ̈i (ARDS) ku käjuëc kök jɔ̈ɔ̈r puou ic.
The first HCoV-229E strain, B814, was isolated from the nasal discharge of patients with common cold in mid-1960s.
Kïït tuany HCoV-229E, B814, ecï lel thok kam kɔc ke ci tuany juäi ruon 1960 ciɛlic.
Since then, more knowledge was accumulated through extensive studies on HCoV-229E and HCoV-OC43, both of which cause self-limiting symptoms.
HCoV-229E ku HcoV-OC43 aacï kek kuen ku käjuëc aacï kek ŋic thïn, ku kek akïït ken puöl.
Indeed, the concept had been widely accepted that infection with HCoVs is generally harmless until the outbreak of SARS.
Etɔ̈u kɔc nhïïm ebën lɔn ade ka kuat HCoV acïn keye kä looi kɔc gup ɣet jɔ̈k cɔ̈k SARS.
The SARS outbreak occurred in 2003 is one of the most devastating in current history, infecting over 8,000 people with a crude case fatality of approximately 10%.
Tuɛny SARS cï rɔt looi ruon 2003 e tuany rac apɛi anyïköl ic, ecï ran 8,000 dɔm ku thuou aye 10%.
Ten years later, the Middle East respiratory syndrome (MERS) outbreak resulted in a persistent epidemic in the Arabian Peninsula with sporadic spreading to the rest of the world.
Ruon thiäär cï la, tuany pan Middle East (MERS) ecï rɔt wɛr piny bï ya tuany bɛ̈i Arab iic ku ecï rɔt diɛ̈t tɛk pinynhom.
The 2019 novel HCoV (2019-nCoV), which has subsequently been renamed SARS-CoV-2, is the causative agent of the ongoing epidemic of coronavirus disease 2019 (COVID-19), which has claimed more than 3,120 lives and infected more than 91,000 people as of March 3, 2020.
Tuany 2019 kuat HCoV (2019-nCoV), cï cak ke cɔl SARS-CoV-2 e yen acï tuany cɔl coronavirus 2019 (COVID-19), acï ran 3,120 cɔl a thou ku ran 91,000 le tueŋ aacï luaŋ pɛi Diäk aköl nïïn 3, ruon 2020.
The alarm has been ringing and the world has to prepare for the coming pandemic of SARS-CoV-2.
Lɔ̈ɔ̈th eye cɔl dhiau ku pinynhom adhil rɔt guir rin tuany cɔl SARS-CoV-2 bɔ.
All seven HCoVs have a zoonotic origin from bats, mice or domestic animals.
Kuat HCoV kädhorou aaye yɔ̈k lääi gup cïmen aliɛ̈k, luɔk wula lääi ye mac bai.
Multiple lines of evidence support an evolutionary origin of all HCoVs from bats, where viruses are well adapted and non-pathogenic but show great genetic diversity.
Ala kajuëc ye nyuɔth lɔn ade ka kuat HCoV e bën alɔŋ aliɛ̈k, teye käm juëc yɔ̈k thïn ku käm ce kɔc nɔ̈k ku e kuat juëc nyuɔth.
The COVID-19 epidemic has presented enormous medical, scientific, social and moral challenges to China and the world.
COVID-19 e tuany cï pinynhom jɔ̈ɔ̈r käjuëc ic apɛi cïmen panakïm, kɔc ŋic käŋ pinynhom, ciɛŋ ku dhɔ̈l ye kɔc ke pïïr pan China ku pinynhom ebën.
Tracing the zoonotic origins of HCoVs provides a framework to understand the natural history, driving force and restriction factors of species jumping.
Yäp ye tuɛnytuɛny lääi kuat HCoV yɔ̈p cɔk e kɔc kony ku bï tuany thïn ŋic, käk yen cɔl a jɔk rɔt ku käk lɛ̈u bï kek looi ku bï ke yen cɔl acï kɛc wei.
This might also guide or facilitate the search for the reservoir, intermediate and amplifying animal host(s) of SARS-CoV-2, with important implications in the prevention of future spillovers.
Kën alɛ̈u bï kɔc kony yäp, län ye yɔ̈k ye guop ku lää(i) yen tɛk piny yen SARS-CoV-2, ku piathde te bï tuany gɛ̈l thïn bï cï wer piny akölciɛ̈n.
In this review we present an overview of the zoonotic origins, interspecies transmission and pathogenesis of HCoVs.
Athɔ̈rkën ic, ok aacï te tuɛnytuɛny lääi bën thïn jaam ic, te ye yen cuɔt tueŋ thïn ten kɔc kök ku käm kuatHCoV.
Particularly, we highlight and discuss the common theme that parental viruses of HCoVs are typically non-pathogenic in their natural reservoir hosts but become pathogenic after interspecies transmission to a new host.
Acuk nyuɔth ku jiɛ̈m ku ic lɔn kɔc ke dhiɛ̈th kuat HCoV aacïn gup käm tecït tën acï cäk kek ku aacï jal ben la käm wën cï kek jal kök kɔc kök gup.
We also review the trend of HCoV evolution in which the increase in transmissibility often comes with the decrease in pathogenicity.
Ok aacï tecït te ye HCoV dït thïn tïŋ ku juek rɔtde bï kɔc kök dɔm e bën kek dhuŋ piny köm.
The outcome of the ongoing SARS-CoV-2 outbreak is also discussed in this context.
Ke cï yɔ̈k alɔŋ tuɛny SARS-CoV-2 acï jaam ic tecït te ŋïc yen.
Animal CoVs have been known since late 1930s.
Kuat CoV tɔ̈u lääi gup aa ŋic kek mɛ̈n ruon 1930.
Before the first isolation of HCoV-229E strain B814 from the nasal discharge of patients who had contracted common cold, different CoVs had been isolated in various infected animals, including turkey, mouse, cow, pig, cat and dog.
Ke kɔc cï tuany HCoV-229E B814 tën kɔc ic ŋuɛ̈n juän wum, kuat CoV juëc aacï kek lel thook lääi cï luaŋ gup, cïmen din cɔl turkey, lok, weŋ, aŋau ku jɔ̈ŋ.
In the past decades, seven HCoVs have been identified.
Run juëc cï jäl, HCoV kä dhorou aacï kek yɔ̈k.
A brief summary of the history of HCoV discovery in chronological order (Table ​1) would be informative and instructive.
Anyïköl HCoV cï looi ke cɛk ic tecït tën cï yen yɔ̈k thïn (Agït 1) abï kɔc ya lɛ̈k ku ye kɔc piɔ̈ɔ̈c.
The first HCoV-229E strain was isolated from the respiratory tract of patients with upper respiratory tract infection in the year of 1966, and was subsequently adapted to grow in WI-38 lung cell lines.
HCoV-229E tueŋ ecï lel thok tën kɔc la tuany ke puoth nhial ruon 1966, ku ecï dït alɔŋ yɔ̈kyɔ̈k WI-38 ic.
Patients infected with HCoV-229E presented with common cold symptoms, including headache, sneezing, malaise and sore-throat, with fever and cough seen in 10~20% cases.
Kɔc cï HCoV-229E dɔm aake cï yɔ̈k kela kïït juän wum, ku ala ic aɣar nhom, thïïm, riäk puou ku arɛm rɔ̈l, atuöc/juäi ku ɣɔl cï yɔ̈k ran 10-20%.
Later in 1967, HCoV-OC43 was isolated from organ culture and subsequent serial passage in brains of suckling mice.
Ruon 1967, HCoV-OC43 ecï lel thok alɔŋ ciɛŋ ku te ye tɛ̈k nyiith luɔk iic.
The clinical features of HCoV-OC43 infection appear to be similar to those caused by HCoV-229E, which are symptomatically indistinguishable from infection with other respiratory tract pathogens such as influenza A viruses and rhinoviruses.
Te ye HCoV-OC43 döm kɔc athɔ̈ɔ̈ŋ kek te ye HCoV-229E döm kɔc, ku kïït ken yeke ŋic aace rɔt puoc ten käm kɔc yiɛ̈k tuany puou cïm käm juäi A ku akut käm kɔc yiɛ̈ juän wum.
Both HCoV-229E and HCoV-OC43 are distributed globally, and they tend to be predominantly transmitted during the season of winter in temperate climate.
HCoV -229E ku HCoV-OC43 aacï wer pinynhom, ku aa kɔc dom dhamanden ye piny liɛr.
Generally, the incubation time of these two viruses is less than one week, followed by an approximately 2-week illness.
Nïïn yeke nɔ̈k kek käm kä bï kek dhiɛ̈th ace wudhbuɔɔ nɔ̈k, ku aye tuany buɔth cɔk tecït tën wudhbuɔ̈ɔ̈ kä 2.
According to a human volunteer study, healthy individuals infected with HCoV-229E developed mild common cold.
Tëcït tën kɔc cï rɔ̈t juar ku bïk akuën looi, Kɔc puɔl gup cï HCoV-229E ajɔk kek juän wun.
Only a few immunocompromised patients exhibited severe lower respiratory tract infection.
Aa kɔc lik cï tuany lui riɛmden aa kek ye riɛlic wɛ̈i rɔ̈t nyuɔth thïn.
SARS, also known as “atypical pneumonia”, was the first well documented HCoV-caused pandemic in human history and the etiological agent is SARS-CoV, the third HCoV discovered.
SARS, cïmen ŋic yen ke cɔl "pneumonia", e yen acï kaŋ yɔ̈k keye tuɛny HCoV anyiköl raan ic ku kën yen bɛ̈i e SARS-CoV, ku yɔ̈k HCoV.
The first case of SARS can be traced back to late 2002 in Guangdong Province of China.
Raan tööŋ tueŋ acï kaŋ tuany SARS alɛ̈u bï diɛ̈c cɔ̈k thɔ̈k ruon 2002 gen Guangdong pan China.
The SARS epidemic resulted in 8,096 reported cases with 774 deaths, spreading across many countries and continents.
Tuany SARS acï ran 8,096 luaŋ ku ran 774 ke cï thou, acï rɔt tɛk gɛth pinynhom ku bɛ̈ɛ̈idït pinynhom.
Apart from the super-spreaders, it was estimated that each case could give rise to approximately two secondary cases, with an incubation period of 4 to 7 days and the peak of viral load appearing on the 10th day of illness.
Tën käk yen lac tɛk piny, acï thɔ̈ɔ̈ŋ ic lɔn ka tok alɛ̈u bï rɔt juak käŋ kärɔu, ku kam ye yen dhiɛ̈th atɔ̈u kam nïïn kä 4 le nïïn 7 ku köm e jäl tuöl aköl ye nïïn 10 ke ran tuany.
Patients infected with SARS-CoV initially present with myalgia, headache, fever, malaise and chills, followed by dyspnea, cough and respiratory distress as late symptoms.
Kɔc tuany SARS-CoV aala arɛm rïŋ ic, aɣar nhom, atuöc/juäi, riäk puou ku aliɛr kuc të bï yen thïn, ku buɔth riɛlic wɛ̈i, ɣɔl ku diɛr keye kïn ciɛ̈n.
Lymphopenia, deranged liver function tests, and elevated creatine kinase are common laboratory abnormalities of SARS.
Lymphopenia, kam yeke cuɛ̈ny them, athɛ̈m riɛm wula lɛc aa kek ye SARS lac jɔ̈ɔ̈r thïn ɣɔ̈n ye kɔc them gup thïn.
Diffuse alveolar damage, epithelial cell proliferation and an increase of macrophages are also observed in SARS patients.
Abaŋ kë cï riäk cuɛ̈ny ic, gɛm abaŋ rïŋ ku juɛ̈kjuɛ̈k cäth riɛm cï tïŋ kɔc tuany SARS gup.
Approximately 20-30% of patients subsequently require intensive care and mechanical ventilation.
Tecït tën abaŋ 20-30% tën kɔc tuany aawïc kuony dït ku të la ic aliir.
In addition to lower respiratory tract, multiple organs including gastrointestinal tract, liver and kidney can also be infected in these severe cases, usually accompanied with a cytokine storm, which might be lethal particularly in immunocompromised patients.
Ajuɛ̈kic alɔŋ ye kɔc wɛ̈i piny, käjuëc yɛ̈c ic agut cïïn, cuɛ̈ny ku rok aa lɛ̈u bï tuɛnytuɛny ka. ke dom, ku aa rɔ̈t mat kek kä guop cɔl alɔc dït, ku e thuou bɛ̈i ten kɔc ci tuany cï riɛmden ril.
The virus was first isolated from the open lung biopsy of a relative of the index patient who travelled to Hong Kong from Guangzhou.
Köm ecï tek thok tën raan acï yakyak la ret ku ecï keny gen Hong Kong ke jäl Guangzhou.
Since then, tremendous efforts have been dedicated to HCoV research.
Mɛ̈ne dhamanɛ̈, luɔi dïttet acï täu ku bï HCoV kuen.
HCoV-NL63 was isolated from a 7-month-old child from the Netherlands during late 2004.
HCoV-NL63 ecï tek thok tën manh la pɛ̈i kä 7 pan Netherland thɔ̈k ruon 2004.
It was initially found to be prevalent in young children, the elderly and immunocompromised patients with respiratory illnesses.
Ku acï yɔ̈k ke rɛ̈ɛ̈r mïth kor gup, kɔc dït ku kɔc cï riɛmden lui kek tuɛnytuɛny ye yɔ̈k wɛ̈i ic.
Presentation of coryza, conjunctivitis, fever, and bronchiolitis is common in the disease caused by HCoV-NL63.
Të cï yen acuök wum, thiɛth nyin, atuöc/juäi nyuɔth, ku bronchiolitis aye lac yɔ̈k tuɛny ye HCoV-NL63 ic.
Another independent study described the isolation of the same virus from a nasal specimen from an 8-month-old boy suffering from pneumonia in the Netherlands.
Akuën dɛ̈t loi thok acï tɛ̈ktɛ̈k thok köm tööŋ kan tet ic alɔŋ athuɔ̈r acï nyai tën manh dhɔ̈k la pɛ̈i kä 8 tuany pneumonia pan Netherland.
Although it was identified in Netherlands, it is actually distributed globally.
Cɔk alɔn cï yen yɔ̈k pan Netherland, kä cï tɛk pinynhom ebën.
It has been estimated that HCoV-NL63 accounts for approximately 4.7% of common respiratory diseases, and its peak incidence occurs during early summer, spring and winter.
Acï thɔ̈ɔ̈ŋ ic lɔn le HCoV-NL63 tëcït tën 4.7% tuɛnytuɛny ye yɔ̈k wɛ̈i, ku e jɔk dhaman rut, ruɛ̈l ku kɛ̈r.
HCoV-NL63 is associated with obstructive laryngitis, also known as croup.
HCoV-NL63 a thään thok ke rɔ̈l yɔ̈ɔ̈k ye cɔl akum rɔl piny.
In the same year, HCoV-HKU1 was isolated from a 71-year-old man who had been hospitalized with pneumonia and bronchiolitis in Hong Kong.
E ruon tööŋɛ̈, HCoV-HKU1 acï tek thok tën mony dït la ruon 71 cï tääc rin le yen pneumonia ku bronchiolitith Hong Kong ic.
Besides community-acquired pneumonia and bronchiolitis, HCoV-HKU1 was reported to be associated with acute asthmatic exacerbation.
Päl pneumonia ku bronchiolitith ye yɔ̈k akut ic, HCoV-HKU1 acï luel lɔn thiɛ̈k yen thok tuɛny adhiama.
Similar to HCoV-NL63, HCoV-229E and HCoV-OC43, HCoV-HKU1 was found worldwide, causing mild respiratory diseases.
ke thɔ̈ɔ̈ŋ kek HCoV-NL63, HCoV-229E ku HCoV-OC43, HCoV-HKU1 aacï kek yɔ̈k pinynhom ebën, keye kɔc yiɛ̈k tuɛnytuɛny wɛ̈i ic.
All these four community-acquired HCoVs have been well adapted to humans and are generally less likely to mutate to cause highly pathogenic diseases, though accidents did occur for unknown reasons as in the rare case of a more virulent subtype of HCoV-NL63, which has recently been reported to cause severe lower respiratory tract infection in China.
Kek tuɛnytuɛny kuat HCoV käŋuan ye yɔ̈k akut ic kä aacï kɔc dom ku kek aa rɔ̈t diɛ̈t waar ku bïk ya tuɛnytuɛny käm, ccɔk alɔn le yen kën cï jɔ̈ɔ̈r kë cïn kë ŋic thïn alɔŋ kuat tuany HCoV-NL63, puɔc cal aɣer ku e yen tuɛny wɛ̈ɛ̈i ic cɔl ajɔk rot pan China.
Generally, when these HCoVs acquire the abilities to transmit efficiently and to maintain themselves continuously within humans, they also become less virulent or pathogenic.
Wɛ̈n cï kuat HCoV riɛl yɔ̈ɔ̈p ku bïk rɔ̈t tɛk piny ku muk kë rɔ̈t kɔc iic, go ke thuou jäl juak nyin wula käm kɔc luaŋ.
MERS-CoV was first isolated in 2012 from the lung of a 60-year-old patient who developed acute pneumonia and renal failure in Saudi Arabia.
Tuɛny MERS-CoV ecï kaŋ tek thok ruon 2012 tën cuɛ̈ny ran la ruon 60 cï tuany ku jɔ̈k pneumonia ku kääc ruɔ̈k bïk cï lui pan Saudi Arabia.
Whereas most of the laboratory-confirmed cases originate from the Middle East, imported cases with occasional secondary spreads to close contacts have been reported in various European countries and Tunisia.
Kuat tuɛnytuɛny cï ke yɔ̈k ɣɔ̈n ye kɔc them gup thïn aa bɛ̈n Middle East, tuɛnytuɛny cï kek bɛ̈i bɛ̈ɛ̈i kök iic aacï kek cal gɛth Ɣurupa iic ku Tunisa.
Another secondary outbreak occurred in South Korea in 2015 with 186 confirmed cases.
Kam dɛ̈t ye kek rɔu cï tuany rɔt jɔt ecï rɔt looi pan Korea alɔŋ ciɛ̈n ruon 2015 ku e ran 186 aa kek cï kek yɔ̈k.
Clinical manifestations of MERS resemble those of SARS, characterized by progressive acute pneumonia.
Käk cï gɔ̈t panakim rin MERS aa thɔ̈ɔ̈ŋ kek käk cï kek gɔ̈t alɔŋ SARS, ku aala iic pneumonia.
Unlike SARS, many patients with MERS also developed acute renal failure, which is thus far unique for MERS among HCoV-caused diseases.
Ku ke cï thɔ̈ɔ̈ŋ kek SARS, kɔc juëc tuany MERS aace cuɛ̈ny lui tën kek, ku e yen kën ye MERS thok loi tën kuat tuɛnytuɛny HCoV kök.
More than 30% of patients present with gastrointestinal symptoms, such as diarrhea and vomiting.
Tëcït tën 30% le tueŋ kɔc tuany aala kïït tuany cïïn ic, cïmen yäc ku aŋɔ̈ɔ̈k.
As of February 14, 2020, over 2500 laboratory confirmed cases were reported with a high case fatality of 34.4%, making MERS-CoV one of the most devastating viruses known to humans.
Aköl nïï 14 pɛi Rɔu ruon 2020, ran 2500 le tueŋ kɔc ke cï yɔ̈k ke la tuany aacï yɔ̈k ke thuou dït thïn abaŋ 34.4%, ku e yen MERS-CoV cɔl aye tuany rac kam käm ŋic kɔc.
During middle to late December 2019, clusters of pneumonia patients retrospectively known to be associated with SARS-CoV-2 infection were detected in Wuhan, Hubei Province, China.
Pɛi ciɛl ic ku thökde pɛi thiärkurɔu 2019, akut kɔc tuany pneumonia thɛɛr ke ŋic lɔn le kek SARS-CoV-2 aake cï rɔ̈t nyuɔth gen Wuhan, pan Hubei, China.
World Health Organization declared the ongoing outbreak of lower respiratory tract infection caused by SARS-CoV-2 a Public Health Emergency of International Concern and also named the disease COVID-19.
Manadhama lui käk pial guop acï tuɛny kɔc jɔ̈ɔ̈r wɛ̈i iic ye SARS-CoV-2 bɛ̈i cal aɣer keye tuany cï kɔc ɣɔ̈m wïc kuony pinynhom ku ciɛ̈k ke cɔl COVID-19.
As of March 3, 2020, 90,053 cases have been confirmed worldwide, with a crude case fatality of 3.4%.
Ku na ye pɛi Diäk aköl nïïn 3 ruon 2020, go ran 90,053 yɔ̈k ke cï luaŋ ku thuou ke ye 3.4%.
Notably, the case fatality in Hubei, China is 4.2%, whereas the one outside of it is 1.2%.
Të cï tiɛ̈ŋ yen, thuou pan Hubei, China e 4.2%, ku ke të aɣer Hubei e 1.2%.
SARS-CoV-2 causes severe respiratory infection like SARS-CoV and MERS-CoV, presented as fever, cough and dyspnea.
SARS-CoV-2 e tuɛny wɛ̈i iic bɛ̈i cïmen SARS-CoV ku MERS-CoV, ku e atuöc, ɣɔl ku riɛl ic wëi nyuɔth.
Diarrhea is also seen in some patients.
Yäc acï tïŋ tën kɔc kök tuany.
Pneumonia is one of the most severe symptoms and can progress rapidly to acute respiratory distress syndrome.
Pneumonia e kïn tööŋ rac ku alɛ̈u bï ɣet kïït tuany ye wɛ̈i ic riɛl.
Although SARS-CoV and SARS-CoV-2 are very similar due to high nucleotide sequence homology of 82%, they cluster into different branches in the phylogenetic tree.
Cɔk alɔn thɔ̈ɔ̈ŋ SARS-CoV ku SARS-CoV-2 rin dït të ye kek lui guop ic abaŋ 82%, kek aala akut wäc ic alɔŋ kuat.
SARS-CoV-2 is apparently less pathogenic but more transmissible compared to SARS-CoV and MERS-CoV.
SARS-CoV-2 ace kɔc lac nɔ̈k ku e rɔt lac tɛk piny të thɔ̈ɔ̈ŋ kek ke SARS-CoV ku MERS-CoV.
Asymptomatic subjects infected with SARS-CoV-2 have been reported and might contribute to its rapid spreading around the world.
Liu kïït raan cï SARS-CoV-2 dom guop aci luel ku alɛ̈u bi tuany kony bï rɔt tɛk pinynhom ebën.
Comparing and contrasting SARS-CoV-2 with the other six HCoVs reveal similarities and differences of great interest.
Thɔ̈ɔ̈ŋ ku wääc ic SARS-CoV-2 kek kuat HCoV kök kädetem e kä thɔ̈ɔ̈ŋ ku kä wääc nyuɔth ku bï kek ŋic.
First, the incubation period and the duration of the course of HCoV disease are very similar.
Tueŋ, nïïn ye HCoV dhiɛ̈th ku nïïn ye nɔ̈k kɔc gup aa thɔ̈ɔ̈ŋ.
In this regard, SARS-CoV-2 follows the general trend of the other six HCoVs.
Ku rin kën, SARS-CoV-2 e të ye kuat HCoV kök kädetem lui thïn buɔth ic.
Second, the severity of symptoms of COVID-19 lies between SARS-CoV and the four community-acquired HCoVs (i.e. HCoV-229E, HCoV-OC43, HCoV-HKU1 and HCoV-NL63).
Kën ye kek rɔu, rɛ̈ɛ̈c kïït COVID-19 atɔ̈u kam SARS-CoV ku jɔ̈l a kuat HCoV ye kek yɔ̈k akut ic (ku aa: HCoV-229E, HCoV-OC43, HCoV-HKU1 ku HCoV-NL63).
On one hand, SARS-CoV-2 infection exhibits features that are more commonly seen during infection with community-acquired HCoVs, including the presentation of non-specific, mild or even no symptoms.
Tëdɛ̈t, SARS-CoV-2 e kä cït kä ye tuɛnytuɛny kuat HCoV kök ye yɔ̈k akut ic nyuɔth, ku ala ic kïït rɛc, kïït kor wula acïn kïït.
On the other hand, a small subset of severe cases of COVID-19 can also be seen as in the case of SARS-CoV infection, although the ratio is a bit lower.
Ku tëdɛ̈t, akut tuany COVID-19 alɛ̈u bï kek tïŋ alɔŋ SARS-CoV, cɔk alɔn kor të yen kɔc dam thïn.
Third, the transmission of SARS-CoV-2 also shows interesting patterns characteristic of both community-acquired HCoVs and SARS-CoV.
Diäk, tek piny SARS-CoV-2 anaŋ ke pɛth ye nyuɔth te ye kek lui thïn kek kuat HCoV ku SARS-CoV tuɛnytuɛny ye yɔ̈k akut ic.
On one hand, the transmissibility of SARS-CoV-2 is at least as high as that of community-acquired HCoVs.
Tëdɛ̈t, tek rɔt piny SARS-CoV-2 a tɔ̈u nhial cïmen kuat HCoV ye yɔ̈k akut ic.
On the other hand, it remains to be verified whether the transmissibility of SARS-CoV-2 decreases after passages in humans as in the cases of SARS-CoV and MERS-CoV.
Ku tëdɛ̈t aya, aŋot atɔ̈u ku bï lääth ic lɔn tek rɔt piny SARS-CoV-2 e dhuk piny të cï yen tɛ̈ɛ̈k kɔc gup cïmen SARS-CoV ku MERS-CoV.
Finally, same as the other HCoVs, SARS-CoV-2 can be detected in fecal samples.
Thökde, ke thɔ̈ɔ̈ŋ cïmen kuat HCoV kök, SARS-CoV-2 alëu bï tïŋ ceth cï ke kuany iic.
Whether fecal-oral transmission of SARS-CoV-2 plays an important role as in the case of SARS-CoV at least under some circumstance remains to be clarified by future studies.
Cɔk alɔn ye te SARS-CoV-2 tɛk piny thïn ceth iic le yen kë ye looi alɔŋ SARS-CoV ka kök aabï ke det iic akuën bï looi aköl ciɛ̈n.
It is also of particularly great interest to see whether SARS-CoV-2 might exhibit seasonality as in the cases of community-acquired HCoVs.
E ke path ku bï tïŋ lɔn bï SARS-CoV-2 rɔt ya bɛɛr tëcït të ye tuɛnytuɛny kuat HCoV yɔ̈k akut ic luɔ̈i yen.
Nevertheless, the features of SARS-CoV-2 including its transmissibility, pathogenicity and sustainable spreading after passages in humans will be influential on the ultimate fate of the ongoing outbreak of COVID-19.
Ku na cɔk ya keya, të ye SARS-CoV-2 ŋiɛc thïn ku ala ic të eye tek piny thïn, thuou ku të e yen rɔt muök thïn të cï yen la kɔc gup abï kë kony kɔc e rɛ̈ɛ̈c tuɛny COVID-19 la tueŋ emɛ̈nɛ̈.
All four community-acquired HCoVs causing mild symptoms have been well adapted to humans.
Kek kuat tuɛnytuɛny kuat HCoV ye yɔ̈k akut ic kɔc yiɛ̈k kïït kor tuany aacï kɔc nyai.
From another perspective, it might also be true that humans have been well adapted to these four HCoVs.
Tɛ̈ktɛ̈kdä ic, alɛ̈u bï dhiɛl ya yic lɔn cï kɔc tuɛnytuɛny kuat HCoV kä käŋuan nyai.
In other words, both could be the survivors of ancient HCoV pandemics.
Ku bï ben luel wɛ̈l kök, kek kedhie aa dhil ya abɛ̈k tuɛnytuɛny HCoV thɛɛr.
HCoVs that cause severe diseases in humans and humans who developed severe HCoV diseases have been eliminated.
Kuat HCoV tuɛnytuɛny bɛ̈i kɔc gup ku kɔc cï tuɛnytuɛny HCoV tuöl ke gup aacï kek muör nyïn.
For this to happen, HCoVs have to replicate in humans to sufficient extent to allow the accumulation of adaptive mutations that counteract host restriction factors.
Ku bï kë rɔt looi, HCoV a dhil rɔt juak kɔc iic ku bï dhɔ̈ɔ̈l ye kek rɔ̈t juak ku bï të ye kek rɛ̈ɛ̈r thïn gɛ̈l.
In this sense, the longer the SARS-CoV-2 outbreak persists and the more people that it infects, the greater chance that it will fully adapt to humans.
Ku rin kënë, kam ye SARS-CoV-2 nɔ̈k kela tueŋ ku kɔc juëc ye dom, e yen kënn yen nyuɔth lɔn bï yen dom kɔc gupebën .
If it adapts well, its transmission in humans would be difficult to stop by quarantine or other infection control measures.
Ku na cï ŋiɛc dom apath, ka tekde piny kɔc gup a ril ic ku bï kɔ̈ɔ̈c lɛ̈lɛ̈l thok wula dhɔ̈ɔ̈l kök yeke tuany gɛ̈l.
For many years, the four community-acquired CoVs circulate in human populations, triggering common cold in immunocompetent subjects.
Run juëc, tuɛnytuɛny kuat CoV ye yɔ̈k akut ic aacï rɔ̈t gööt kɔc iic, ku acï juän wum thuör bei kɔc cï riɛmden lui apath gup.
These viruses do not need an animal reservoir.
Käm kä aace wïc län bï kek rɛ̈ɛ̈r ye guop.
In contrast, highly pathogenic SARS-CoV and MERS-CoV have not adapted to humans well and their transmission within humans cannot be sustained.
Ku bï kek wääc, käk kɔc nɔ̈k apɛi cïmen SARS-CoV ku MERS-CoV aa kïc dom kɔc gup apath, ku la den kɔc gup ace rɔt muk.
They need to maintain and propagate in their zoonotic reservoirs and seek the chance to spillover to susceptible human targets, possibly via one or more intermediate and amplifying hosts.
Aa wïc kä ku bïk lääi ken ye kek rɛ̈ɛ̈r ke gup duut ku dït kä thïn ku a wïc dhel bï kek rɔ̈t wɛr piny bïk la kɔc gup, bïk tök luɔ̈i wula käjuëc lɛ̈u bï kek rɔ̈t tɛk piny.
SARS-CoV-2 has features that are similar to both SARS-CoV/MERS-CoV and the four community-acquired HCoVs.
SARS-CoV-2 ala käk thɔ̈ɔ̈ŋ kek SARS-CoV/MERS-CoV ku jɔl aa tuɛnytuɛny kuat HCoV ye yɔ̈k akut ic.
It is highly transmissible like community-acquired HCoVs, at least for the time being.
E rɔt tɛk piny apɛi cïmen tuɛnytuɛny kuat HCoV, ye yɔ̈k akut ic tëcït tën kam thiin kor.
However, it is more pathogenic than community-acquired HCoVs and less pathogenic than SARS-CoV or MERS-CoV.
Ku keya, thuou a dït ka wäär tuɛnytuɛny kuat HCoV ye yɔ̈k akut ic ku thuou a kor thïn tën tuɛnytuɛny SARS-CoV wula MERS-CoV.
It remains to be seen whether it will adapt fully to humans and circulate within humans without a reservoir or intermediate animal host.
Abï ŋuɔt ye tïŋ cɔk dom kɔc gup apath ku tek rɔt piny kɔc iic ke cïn te ye yen rɛ̈ɛ̈r thïn wula län tɔ̈u ciɛl.
Before discussing the animal origins of HCoVs, it will serve us well to discuss the definitions and characteristics of evolutionary, natural, reservoir, intermediate and amplifying hosts of HCoVs.
Të kïc ok të ye kuat HCoV yɔ̈k thïn lɛ̈i guop, apath buk wɛ̈tde ic ku te ye kek lui thïn ŋic, jɔ̈kde, te ye yen rɛ̈ɛ̈r thïn, të ye yen lac yɔ̈k thïn ku ye kuat HCoV rɔ̈t juak thïn.
An animal serves as the evolutionary host of an HCoV if it harbours a closely related ancestor sharing high homology at the level of nucleotide sequence.
E lɛ̈i yen ye HCoV yök ye guop të muk yen raan thiääk ke yen ke ɔm tëcït të ye kek lui thïn guop ic.
The ancestral virus is usually well adapted and non-pathogenic in this host.
Käm thɛɛr e ŋiɛc dom ku acïn ic thuou të ye yen rɛ̈ɛ̈r thïn kën.
Likewise, a reservoir host harbours HCoV continuously and for long term.
Cïmende, kën HCoV ɣääc aye muk kela tueŋ ku kam bärkɔ̈u.
In both cases, the hosts are naturally infected and are the natural hosts of HCoV or its parental virus.
Käkä iic kedhie, käk kek muk aaye luaŋ ku aa kek HCoV muk wula a köm a dhiɛth yen.
In contrast, if the HCoV is newly introduced to an intermediate host right before or around its introduction to humans, it is not well adapted to the new host and is often pathogenic.
Ku wɛ̈ɛ̈cde, të cï HCoV nyuöth teden rɛ̈ɛ̈r yen thïn ke kïc guɔ la kɔc gup, ka kïc dom apath ku thuou e dït.
This intermediate host can serve as the zoonotic source of human infection and play the role of an amplifying host by allowing the virus to replicate transiently and then transmitting it to humans to amplify the scale of human infection.
Të yën lac yɔ̈k thïn alɛ̈u bï ya alɔŋ lääi ye yen raan dom thïn ku e yen te ye yen rɔt juak ku köm alɛ̈u bï dhiɛ̈th ku tek rɔt piny bi la kɔc gup ku tuany raan cɔl a dït nyin.
An HCoV can undergo a dead-end infection if it cannot sustain its transmission within the intermediate host.
HCoV alɛ̈u bï thou piny tëcïn yen te muk yen rɔt nhial tekde rɔt piny tɛ̈ rɛ̈ɛ̈r yen thïn.
On the contrary, HCoVs can also adapt to the intermediate host and even establish long-term endemicity.
Ku ke wääc, kuat HCoV aa lɛ̈u ku bïk rɔ̈t ŋiëc të cïk yɔ̈k bï kek rɛ̈ɛ̈r thïn ku aa rɔ̈t cɔ̈k piny bïk ya tuɛnytuɛny pinynhom.
In this case, the intermediate host becomes a natural reservoir host.
Ku e tën, te ye köm rɛ̈ɛ̈r thïn e yen ya te ye yen jɔk thïn.
Epidemiological data revealed retrospectively that the index case of SARS had a contact history with game animals.
Akuën cï looi ku bä anyïköl dhuɔ̈k cɔk acï nyuɔth lɔn ka adat SARS ala anyïköl kek lääi ye mac adika ic.
Subsequent seroprevalence investigations indicated that animal traders had a higher prevalence of anti-SARS-CoV IgG compared with that of the general population.
Giɛ̈k cï looi ku bï akut käm tɔ̈u guop ic ŋic acï nyuɔth lɔn adë ka kɔc ɣɔɔc wei lääi aala gup käk köm cït SARS-CoV IgG tiɛt wei te thɔ̈ɔ̈ŋ kek akut e kɔc.
Masked palm civets (Paguma larvata) and a racoon dog in live animal markets were first identified to carry SARS-CoV-like viruses that are almost identical to SARS-CoV.
Kuat aŋɔn pan Athia ye cɔl (paguma larvata) ku jɔ̈ŋ rakuun thuŋ ye lääi ɣaac wei thïn aa kek ke cï kaŋ tïŋ lɔn ɣɛ̈ɛ̈c kek köm cït SARS-CoV ku aa thɔ̈ɔ̈ŋ kek SARS-CoV.
This was indirectly supported by the fact that no further SARS was reported after killing all civets in the markets.
Kën ecï gam ke kïc giik ic rin cïn yen SARS dɛ̈t cï bën rɛ̈ɛ̈r thïn wën cï aŋääth nɔ̈k thuɔ̈k iic ebën.
However, it has been reported that masked palm civets from the wild or farms without exposure to the live animal markets were largely negative for SARS-CoV, suggesting that masked palm civets might only serve as the intermediate amplifying host but not the natural reservoir of SARS-CoV.
Ku keya, acï luel lɔn ka kuat aŋɔn pan Athia kam lääi rɔɔr wula lääi rɛ̈ɛ̈r bai/dum iic kïc röm kek lääi rɛ̈ɛ̈r thuɔ̈k iic aacï yɔk ke cïn gup SARS-CoV, ku aye thɔ̈ɔ̈ŋ ic lɔn ka aŋääth Athia ace kek ye SARS-CoV rɛ̈ɛ̈r thïn ku aa lɛ̈u bïk tuany tɛk piny.
Notably, since 80% of the different animals in the markets in Guangzhou have anti-SARS-CoV antibodies, the possibilities that multiple species of small mammals might also serve as intermediate amplifying hosts of SARS-CoV cannot be excluded.
Të cï tiɛ̈ŋ ye, rin le 80% lääi tɔ̈u thuuŋ Guangzhou ic ke la gup käk ke tiɛt gup wei SARS-CoV, kën yen nyuɔth lɔn le lääi kök SARS-CoV a dhil rɛ̈ɛ̈r thïn ku acï lɛ̈u bï nyäŋ wei.
All of these appear to be dead-end hosts of SARS-CoV.
Ku e yen të cï te ye SARS-CoV rɛ̈ɛ̈r thïn tïŋ ke cï thou piny.
Subsequent search for the natural animal host of SARS-CoV unveiled a closely related bat CoV, termed SARS-related Rhinolophus bat CoV HKU3 (SARSr-Rh-BatCoV HKU3), which exists in Chinese horseshoe bats.
Akuën cï looi tën lääi la gup SARS-CoV acï CoV lïk nyuɔth, SARS-thiääk kek kuat alïk ye cɔl Rhinolophath CoV HKU3 (SARSr-Rh-BatCoV HKU3), ku a rɛ̈ɛ̈r aliɛ̈k China ye cɔl horseshoe.
These bats are positive for anti-SARS-CoV antibodies and genome sequence of SARSr-Rh-BatCoV HKU3.
Aliɛ̈k aala gup kën SARS-CoV tiɛt wei ku käk guop akut SARSr-Rh-BatCoV HKU3.
This and other bat CoVs share 88-92% nucleotide sequence homology with SARS-CoV.
Tuany kën ku kuat CoV aliɛ̈k kök aa rɔm 88-92% akut käm tɔ̈u SARS-CoV guop.
These studies have laid the foundation for the new concept that bats host emerging human pathogens.
Akuën nyuɔth lɔn aliɛ̈k aa kek la gup käm kɔc yiɛ̈k tuany.
Several SARS-like CoVs (SL-CoVs) have also been identified from bats, but none except for one designated WIV1 can be isolated as live virus.
SARS cïmen CoV kuat (SL-CoV) aacï kek tïŋ aliɛ̈k ic, acïn kedɛ̈t ku abaŋ töŋ WIV1 alɛ̈u bï lel thok cïmen köm.
Human angiotensin converting enzyme 2 (ACE2) is known to be the receptor of SARS-CoV.
Angiotensin tɔ̈u guop ran ic ye käk riɛm waar ic 2 (ACE2) ku e yen SARS-CoV dom.
WIV1 derived from fecal sample of bats was demonstrated to use bat, civet and human ACE2 as receptor for cell entry.
WIV1 ecï nyai ceth aliɛ̈k ic ku bï lui alïïk nyuɔth, civet ku ACE2 ran keke ye te ye köm rɛ̈ɛ̈r thïn.
Intriguingly, sera of convalescent SARS patients were capable of neutralizing WIV1.
Kɔc la gup SARS aa WIV1 thɔ̈ɔ̈ŋ nyin.
Thus far, WIV1 represents the most closely related ancestor of SARS-CoV in bats, sharing 95% nucleotide sequence homology.
WIV1 amuk nyin te ye SARS-CoV aliɛ̈k ic, ku aa rom 95% akut miök käm.
Albeit the high homology between these two viruses, it is generally believed that WIV1 is not the immediate parental virus of SARS-CoV and bats are not the immediate reservoir host of SARS-CoV.
Na cɔk lɔn thɔ̈ɔ̈ŋ kek, acï gam lɔn ade ka WIV1 ace kek la köm SARS-CoV ku aace kek ye SARS-CoV yɔ̈k thïn tecït te cï kä wääc tën käm kä kärɔu.
Phylogenetic analysis clusters MERS-CoV to the same group as bat CoV-HKU4 and bat CoV-HKU5.
Kë cï Phylogenetic luel alɔŋ MERS-CoV tën akut tɔ̈ɔ̈ŋ cïmen CoV-HKU4 aliɛ̈k ku CoV-HKU5 aliɛ̈k.
Bat CoV-HKU4 and MERS-CoV utilize the same host receptor, dipeptidyl peptidase 4 (DPP4), for virus entry.
Bat CoV-HUK4 ku MERS-CoV aa të tööŋ ye kek rɛ̈ɛ̈r thïn luɔ̈i, dipeptidyl peptidase 4 (DPP4), të ye köm tëk thïn.
RNA-dependent RNA polymerase sequences of MERS-CoV are phylogenetically closer to counterparts in bat beta-CoVs identified from Europe and Africa.
Abaŋ riɛm tɔ̈u guop ic cɔl RNA-dependent ku RNA polymerase dhɔ̈ɔ̈l ye MERS-CoV lui aa thiääk kek beta-CoV alïïk cï ke tïŋ Ɣurupp ku Afrika.
Up to now, no live MERS-CoV can be found in wild bats.
Agut yemɛ̈n, acïn MERS-CoV pïr lɛ̈u bï yɔ̈k aliɛ̈k rɔɔr gup.
MERS-CoV and its closest relative bat CoV-HKU25 share only 87% nucleotide sequence homology.
MERS-CoV ku CoV-HKU25 alïïk thiääk kek yen aa rɔm 87% te ye kek lui thïn guop ic.
Thus, bats might not be the immediate reservoir host of MERS-CoV.
Aace aliɛ̈k kek ye ke MERS-CoV lac yɔ̈k thïn.
On the other hand, studies in Middle East have shown that dromedary camels are seropositive for MERS-CoV-specific neutralizing antibodies, same as camels of Middle East origin in multiple African countries.
Ku tëdɛ̈t, akuën cï kek looi Middle East aacïk nyuɔth lɔn adë ka thɔ̈rɔ̈ɔ̈l aala gup MERS-CoV guop thɔ̈ɔ̈ŋ ic, cïmen thɔ̈rɔ̈ɔ̈l Middle East tɔ̈u bɛ̈ɛ̈i Afrika juëc iic.
Live MERS-CoV identical to the virus found in humans was isolated from the nasal swabs of dromedary camels, further indicating that camels serve as the bona fide reservoir host of MERS-CoV.
MERS-CoV pïr thɔ̈ɔ̈ŋ kek köm cï yɔ̈k kɔc gup ecï tek thok athuɔ̈r acï nyai tën thɔ̈rɔ̈ɔ̈l baai, ku acï nyuɔth lɔn kä thɔ̈rɔ̈ɔ̈l aa MERS-CoV ɣääc.
It is also noteworthy that generally mild symptoms but massive virus shedding were observed in camels experimentally infected with MERS-CoV.
Apath ku bï ŋic lɔn ka kïït aa kor ku juɛ̈ŋ rɔt köm aa ke cï ke tïŋ thɔ̈rɔ̈ɔ̈l ke cï tuany MERS-CoV.
Notably, infected camels shed viruses not only through respiratory route but also through fecal-oral route, which is also the main route for virus shedding from bats.
Të cï tiɛ̈ŋ yen, thɔ̈rɔ̈ɔ̈l cï luaŋ aace rɔ̈t juak të ye kɔc wɛ̈i rot ku e rot juak te ciëth tɛ̈ɛ̈k thïn, ku e yen të ye köm rot juak thïn aliɛ̈k iic aya.
However, questions still remain since many confirmed cases of MERS have no contact history with camels prior to symptom onset, plausibly ascribed to human-to-human transmission or unknown transmission routes involving unrecognized animal species that harbour MERS-CoV.
Ku këya, kïït thiëc aa ŋuɔt ke tɔ̈u mɛ̈nɛ̈ cï kɔc juëc cï luaŋ MERS aacïn anyïköl kek thɔ̈rɔ̈ɔ̈l tëcït tën kïït cï kek yɔ̈k, e raan yen ye ɣäth raan dä guop wula të ye yen rot tɛk piny thïn akuc ku ala ic kuat län kïc det ke ɣɛ̈ɛ̈c MERS-CoV.
SARS-CoV-2 shares 96.2% nucleotide homology with a bat CoV RaTG13 isolated from Rhinolophus affinis bats.
SARS-CoV-2 arɔm 96.2% të ye guop lui thïn kek CoV alïïk RaTG13 cï tek thok tën alïïŋ Rhinolophuth affinis.
As in the cases of SARS-CoV and MERS-CoV, the sequence divergence between SARS-CoV-2 and RaTG13 is too great to assign parental relationship.
Abaŋ SARS-CoV ku MERS-CoV, abaŋ dït kam SARS-CoV-2 ku RaTG13 a dït ku dhiɛ̈ɛ̈th atɔ̈u kamken.
That is to say, bats might not be the immediate reservoir host(s) of SARS-CoV-2 unless almost identical bat CoVs are found in future.
Ku e wɛ̈t bï luel, aliɛ̈k aace kek ye SARS-CoV-2 rɛ̈ɛ̈r (ke) gup ela na yɔ̈k CoV alïïk CoV ke thɔ̈ɔ̈ŋ kek yen aköl ciɛ̈n.
Presumably, the intermediate animal hosts of SARS-CoV-2 should be among the wildlife species sold and killed at the Huanan Seafood Wholesale Market, with which many of the initial cases of COVID-19 were associated, indicative of a probable animal-to-human transmission event.
Të cï yen thɔ̈ɔ̈ŋ ic thïn, lääi ye SARS-CoV-2 rɛ̈ɛ̈r ke gup aa dhil rɛ̈ɛ̈r kam lääi rɔɔr cï ke ɣac wëi ku näk kek gen Huanan thuŋ Seafood ye käŋ guɔl wei thïn, ku e yen tën abï tuany COVID-19 thïn, ye nyuɔth lɔn ye yen jäl lɛ̈i guop ku le raan guop tekde piny.
Several recent studies based on metagenomic sequencing have suggested that a group of endangered small mammals known as pangolins (Manis javanica) could also harbour ancestral beta-CoVs related to SARS-CoV-2.
Akuën apuɔc looi tëcït të ye käm lui thïn kɔc gup acï lɔn ka la akut lääi kök rɛc ye cɔl pangolini (Manith javanica) aalɛ̈u bï wunken beta-CoV thääny thook kek SARS-CoV-2 ɣääc .
These novel pangolin CoV genomes share 85-92% nucleotide sequence homology with SARS-CoV-2.
Kek CoV pangolin kä aa rɔm 85-92% të ye guop lui thïn kek SARS-CoV-2.
However, they are equally closely related to RaTG13 with about 90% identity at the level of nucleotide sequence.
Ku këya, kek aa thiääk kek RaTG13 ku të ye ŋiɛ̈c yen tëcït të yen lui thïn guop ic e 90%.
They cluster into two sub-lineages of SARS-CoV-2-like viruses in the phylogenetic tree, one of which share a more similar receptor binding domain (RBD) with SARS-CoV-2, with 97.4% amino acid sequence identity.
Kek aa löny akuut kärɔu kuat SARS-CoV-2 cït käm e dhiɛ̈nhden pinynhom, ku tök ala kë thɔ̈ɔ̈ŋ kek kën yen rɛ̈ɛ̈r thïn (RBD) kek SARS-CoV-2, ku kek amino acid tëcït tën 97.4%.
In stark contrast, the RBDs of SARS-CoV-2 and RaTG13 are more divergent, albeit a higher degree of sequence homology genome-wide.
Ku bï kek wääc, RBD käk SARS-CoV-2 ku RaTG13 aa kiith iic, abaŋ dït tɔ̈u nhial e të ye guop lui thïn.
An earlier study on diseased pangolins also reported the detection of viral contigs from lung samples, which turn out to be similarly related to SARS-CoV-2.
Alɔŋ kë cï kuen alɔŋ tuany pangoiln acï luel aya lɔn cii köm tïŋ cuɛ̈ny acï nyai bï la them ic, ku acï yɔ̈k ke thɔ̈ɔ̈ŋ kek SARS-CoV-2.
This study adopted different assembly methods and manual curation to generate a partial genome sequence comprising about 86.3% of the full-length viral genome.
Akuën kën acï dhɔ̈ɔ̈l loi thook löm ku dhɔ̈ɔ̈l ye kɔc dem ku bï të ye guop lui thïn tïŋ ku ala ic 86.3% kek käm rɛ̈ɛ̈r thïn ebën guop ic.
We cannot exclude the possibility that pangolin is one of the intermediate animal hosts of SARS-CoV-2.
Acï lɛ̈u bï jai lɔn adë ka pangolin acï SARS-CoV-2 ɣɛ̈ɛ̈c.
However, currently there is no evidence in support of a direct pangolin origin of SARS-CoV-2 due to the sequence divergence between SARS-CoV-2 and pangolin SARS-CoV-2-related beta-CoVs.
Ku yemɛ̈n thiin, acïn kën yen kuɔny cɔ̈k lɔn tɔ̈u SARS-CoV-2 pangolin guop rin käjuëc wääc tɔ̈u kam SARS-CoV-2 ku SARS-CoV-2 pangolin thääny thok kek beta-CoV.
In addition, the distance between SARS-CoV-2 and RaTG13 is even shorter than that between SARS-CoV-2 and pangolin SARS-CoV-2-related beta-CoVs.
Ku kë juɛk thïn, kam tɔ̈u kam SARS-CoV-2 ku RaTG13 acek ic tën kam tɔ̈u kam SARS-CoV-2 ku SARS-CoV-2 pangolin thaäny thok kek beta-CoV.
The evolutionary pathway of SARS-CoV-2 in bats, pangolins and other mammals remains to be established.
Dhɔ̈ɔ̈l ye SARS-CoV-2 jɔk thïn aliɛ̈k iic, pangolin ku lääi kök dhiɛ̈th aŋot ke kïc yɔ̈k.
Whereas the highest sequence homology has been found in the RBDs between SARS-CoV-2 and pangolin, SARS-CoV-2-related beta-CoVs, SARS-CoV-2 and RaTG13 share the highest genome-wide sequence homology.
Ku këya, abaŋ dït ye guop lui thïn acï yɔ̈k RBD ic kam SARS-CoV-2 ku pangolin, SARS-CoV-2 thääny thok kek beta-CoV, SARS-CoV-2 ku RaTG13 aa rɔm abaŋ dït të ye guop lui thïn.
It is highly speculative that the high degree of similarity between the RBDs of pangolin SARS-CoV-2-related beta-CoVs and SARS-CoV-2 is driven by selectivity-mediated convergent evolution.
Acï thɔ̈ɔ̈ŋ ic apɛi lɔn adë ka kä thööŋ kam RBD alɔŋ SARS-CoV-2 pangolin thääny thok kek beta-CoV ku SARS-CoV-2 aye kuɛ̈nykuɛ̈ny rɔm thɔ̈ɔ̈c.
A counter-proposal is in favour of a recombination between a pangolin SARS-CoV-2-related beta-CoV and RaTG13 in the third wild animal species.
Kë dɛ̈t cï kuɔny cɔ̈k aye nuɛ̈t cï SARS-CoV-2 pangolin thääny thok kek beta-CoV ku RaTG13 kek län rɔɔr ye kek diäk.
As a driving force in evolution, recombination is widespread among beta-CoVs.
Këye kën ciɛ̈k thööc cɔ̈k, nuɛ̈tnuɛ̈t acï wer piny kam beta-CoV.
The jury is still out on the immediate zoonotic origin of SARS-CoV-2.
Tëtök aŋuɔt ŋoot lääi ye ke SARS-CoV-2 yɔ̈k ke gup.
Besides the highly pathogenic HCoVs, the zoonotic origin of HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1 have also been studied.
Alɔŋ thuou dït kuat HCoV iic, lääi ye ke HCoV-229E, HCoV-OC43, HCoV-NL63 ku HCoV-HKU1 yɔ̈k thïn aa ŋot ke kuen.
Phylogenetic evidence indicated that both HCoV-NL63 and HCoV-229E might have originated from bat CoVs, while the parental viruses of HCoV-OC43 and HCoV-HKU1 have been found in rodents.
Acï kuën cï looi nyuɔth lɔn adë ka HCoV-NL63 ku HCoV-229E aa dhil bɛ̈n bei kuat CoV aliɛ̈k ic, ku kën adhiɛ̈ɛ̈th käm HCoV-OC43 ku HCoV-HKU1 aacï ke yɔ̈k luɔk gup.
It has been reported that a bat CoV termed ARCoV.2 (Appalachian Ridge CoV) detected in North American tricolored bat displayed close relationship with HCoV-NL63.
Acï luel lɔn ka CoV alïïk ye cɔl ARCoV.2 (Appalachian Ridge CoV) cï tïŋ pan Amerika alɔŋ tueŋ alïïŋ la kïït kä diäk acï nyuɔth lɔn le yen ruäi kek HCoV-NL63.
On the other hand, HCoV-229E was genetically related to another bat CoV, termed Hipposideros/GhanaKwam/19/2008, which was detected in Ghana, while camelids have also been suspected as its intermediate host.
Ku tëdɛ̈t aya, HCoV-229E e thääny thok kek CoV alïïŋ dɛ̈t, ye cɔl Hipposideros/GhanaKwam/19/2008, ecï tïŋ pan Ghana, ku akut thɔ̈rɔ̈ɔ̈l aye täk lɔn ye kek tuany ɣääc aya.
For clarity, the current knowledge on animal origins of known HCoVs is summarized in Figure ​1 and Table 2.
Ku bï det ic apath, kë ŋic alɔŋ lääi la gup kuat HCoV acï tet ke cek ic Thura 1 ku Agït 2.
Phylogenetic analysis has provided evidence for interspecies transmission events of HCoVs in the history.
Akuën acï looi acï yic nyuɔth të ye tuany kuat HCoVs rɔt tɛk piny thïn anyïköl ic.
When HCoV-OC43 crossed species to infect humans from domestic livestock around 1890, a pandemic of respiratory infection was recorded.
Të tɛ̈m HCoV-OC43 bï kɔc luaŋ lääi yeke mac baai tëcït tën ruon 1890, tuany e wɛ̈i ic riɛl ecï gät piny.
The interspecies transmission history of HCoV-229E is less clear.
Anyïköl tek piny tuany kam lääi wäc e HCoV-229E ace det ic apth.