atepeq/tico19 huggingface dataset:
COVID-19 affects more elderly individuals than youth and more men than women, and the severity and death rate are also higher in elderly individual than in youth.
Vn COVD-19 k``pv n5 dsx vl7x k` xu0tn5 kvnv wutn5 k` m`n, k` b0cdv kvnv l511 d55tv k` dsx vl7x v /c5 msa xu0tn5.
SARS has higher mortality than COVID-19 (10.91% versus 1.44%).
SARS l`nyv COVID-19 kv n`k nath (10.91% kvnv 1.44%).
COVID-19 patients transmit the virus even when they are symptomless whereas SARS patients do so usually when they are severely ill, which causes much greater difficulty to contain the spread of COVID-19 than SARS.
J5 ju1thn5 COVID-19 la kvn naath vdsp kvv b1yr]th vc`x thivlv kv nyuuthn5, k` j5 ju1thn5 SARS la kvn naath v dsp v c5 juey ksn b0c vl7x, vn nsms cv k`p cu]x d`k` piny COVID-19 jak` bum v l7x k` SARS.
This partially explains why SARS-CoV-2 spread much faster and broader than SARS-CoV.
Vn nvmv nyoothv jv vn h66 v jvn du]]p in th5``x SARS-CoV-2 r7l m5 d55t kv p0th kvjv a l`nyv SARS-CoV.
The regular RNA assay for SARS-CoV-2 can be negative in some COVID-19 patients.
Theem RNAk` SARS-CoV-2 vn wen /caa dee n5 jek k` th11x j5 ju1thn5 COVID-19.
On the other hand, cured patients can be positive for the virus again.
Kv ku5c in d]x, j5 ju1thn5 t5 c5 pu1nykivn gsw d2 b1yr]th n5 jek pu]]nydivn v nysk.
These findings dramatically increase the risk of virus spreading.
Kvn xsaan5 ti caa jek ti reep kvn d`k b1yr]th` piny vl7x.
Given such rapid progress in research on COVID-19, several critical issues remain to be solved, as follows:
C`xn5ms p0th g6r x`c` ms kv ku5c COVID-19, t22 kv xsaan5 t5 xuan t5 /k1n lu`x kv thu]k, cetkv titi:
Where did SARS-CoV-2 come from?
SARS-CoV-2 b22 nik`?
Although 96% genetic homolog was found between SARS-CoV-2 and two bat SARS-like CoVs, we still cannot conclude that SARS-CoV-2 is from bats.
C`x n5ms caa pek m55 96%jek vc``ts k` j55n SARS-CoV-2kvnv SARS in cet kvv CoVn5 d1x rvw min n77x g]thv, xotv /caa jv dee lar5 SARS-CoV-2 n77xv g]th.
What animal was the intermediate species to transmit the virus from the original host, say bats, to humans?
kv ley tin tith te kam kui00n5 ns kv d6p bayr`thk` gu1ndv min nhiam, cet kv xap v we k` raan?
Without knowing answers to #1 and 2, we cannot efficiently cut the transmission, and the outbreak can relapse at any time.
m5 ku5c ksn lus thiec` min, /ca d6pdv b5 lu`x kv xu]k, kacdv fsaa bv tusk nysk ciax.
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?
c`x n5 min c5 msl5kulsr5 kvn bay6k0m5k]l jv nyoth 5 matv rs kvn ACE2, v du]]p in mith cup kv bayr`th dup jsam v bv luex n66x?
Does the virus also bind ACE2-expressing cells in other organs?
Vn bayr`th b` matv cell ACE2 k` cux tin k]x?
Without clear answers to these questions, we cannot achieve fast and accurate diagnosis and effective treatment.
M5 tilv lusc m5 thu]k k` thiec vmv, /canv du]]p jekdv m5 thu]k b5 met nvn kvn tu]mdv.
How long will the epidemic last?
Bv kulv j``ny kv pek m5 n5n d5 vn juey fsaa?
How is the virus genetically evolving during transmission among humans?
La loocv rs 5d5d vn bayr`th kv ksr coth`dv pu]]ny ran?
Will it become a pandemic worldwide, die down like SARS or relapse periodically like the flu?
Jvn bv ku thi`xn5 fsw kvvliw, bv thuuk, cet kv liv bv rs nysk kv gu11th cet piluu?
It is essential but may take some time to search for answers to the above and many other questions.
Lotv rs duxdv f66 bv gu11th nax vn g6r locv thiecnt titi kvn thiecnt k]kivn.
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.
Kuv la f66 kv ms derv nax kvvliws, thilv ksn d]divn m5 banv lvl vn5 f66 banv juey fsaa vmv k1p cu]x kv p0th m5 lotv rs k` banv t2kdan lusc gu1thdv.
Zoonotic origins of human coronaviruses
tukdv k` ley dsaar vn ksrsnabayr`th
Mutation and adaptation have driven the co-evolution of coronaviruses (CoVs) and their hosts, including human beings, for thousands of years.
xutdv kv rs kvn xiecdv v jvn g2r ksrsnabayr`th (CoVs) kvn tin tusskv th5n, t5 te raan th5n kv run t5 k5thn5 t22 c5 we.
Before 2003, two human CoVs (HCoVs) were known to cause mild illness, such as common cold.
v xot 2003, ju1th ran d1x rvw cua kv x1c n77x kvn juey m5 tst, cet kv thony-thony.
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.
tuk kvn d`k fsaa (SARS) nyuuthn5 ju1th l55k` m5 rup-rup kvn juey d`r cu22c fsaa (MERS) ca ciaax m5 ril nyoth kv ji``k luex` HCoV.
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.
vn tuk SARS-CoV-2 rvi d11r Chvyna kv guut 2019 cv jak`jsc nysk k` cv ksn g`y kv d5t d6pdv duxdv f66 kuiy luexdv m5 p11r jv kvn SARS-CoV.
HCoV infection is a zoonosis and understanding the zoonotic origins of HCoVs would serve us well.
luex HCoV v dux leyn5 k` cu]p lsaac kv ley in tusk HCoVs pu]]nydv bv ksn lu`k.
Most HCoVs originated from bats where they are non-pathogenic.
kvn HCoVs t5 xuan tusk kvn k` xap kvn thil kv luex k` jv.
The intermediate reservoir hosts of some HCoVs are also known.
ley tin j``l jv kams kvn th11x HCoV n5 x1c kv kv b`.
Identifying the animal hosts has direct implications in the prevention of human diseases.
x`c l== in tusk k` jv gsayv kv ku5c g1x ju1th k` raan.
Investigating CoV-host interactions in animals might also derive important insight on CoV pathogenesis in humans.
x`c civvx` CoV kvn ley in tusks k` jv derv ksn lu`k b` kv ciaax lue`x k` raan.
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.
Rvi wargak` nvmv, c` ks guec kuex piny kv x`c vn wen kv ju1th d1x b1rsw, kv tiit m5 d55t k` l0x kv jekdivn e nhiam kvvl kv ley tin tusk kv k` kv kvn d6pdivn kamn5 ku00n5 tin g66l.
Importantly, we compare and contrast the different HCoVs from a perspective of virus evolution and genome recombination.
Vl]x, c1 ks p``t kvn gu`c HCoVs ti g66l kv ciaax luc` bayr`th kvn nysak m1t genome l1t.
The current CoV disease 2019 (COVID-19) epidemic is discussed in this context.
Vn juey CoV 201 vmv (COVID-19) v thi``x fswv ca jv lat inv.
In addition, the requirements for successful host switches and the implications of virus evolution on disease severity are also highlighted.
V nysk, min g77rv kv gu11th in cux juey th5n gvrv rs k` d5tdv vn tuk bayr`th` kv d55t ju1th ca kv lat b`.
Coronaviruses (CoVs) belong to the family Coronaviridae, which comprises a group of enveloped, positive-sensed, single-stranded RNA viruses.
Ksrsnabayr`th (CoVs) t22 rvi ju1thn5 t5 csal5 Coronaviridae, bu]n m5 tee kuum, te th5n, kv RNA kvl.
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.
Kvn bayr`thn5 titi civx kvn genome m5 d55t m5 26 v we k` 32 kilobase rvi bayr`thn5 RNA ca jv csl 5 “CoV” kv f66 te kv thac kv thurv piny electron microscope.
Structurally, CoVs have non-segmented genomes that share a similar organization.
T`` pu11nydv CoVs thilv jv genome my jsc cet kv m5 ca cak.
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.
Cet kv 2/3 k` genome te kv rvw t5 m`t kv kuen cu]]xn5 (ORF1a and ORF1b), t5 la lusc kv k` pp1a and pp1ab replicase polyproteins.
The polyproteins are further processed to generate 16 non-structural proteins, designated nsp1~16.
Vn polyproteins we kv kv m5 n66x kv t5 thin n2n d1x 16 ti we k` nsp1~16.
The remaining portion of the genome contains ORFs for the structural proteins, including spike (S), envelope (E), membrane (M) and nucleoprotein (N).
Th11xdv min d]x vn genome t22 kv ORFs kv protein kvvl kv k6m (S), kuum, gu]]p (M) kvn nucleoprotein (N).
A number of lineage-specific accessory proteins are also encoded by different lineages of CoVs.
Pek keer` th5 cux k` protein b` te kv rvikeer5 t5 g66l k` CoVs.
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).
Kv d``kdivn kvn protein kv lu2y, CoVs ca kv d11k k` dh7r xuaan (alpha-CoV, beta-CoV, gamma-CoV and delta-CoV), t5 te dhsr bet` CoV kv HCoVs k` ca d11k k` keer5 xuaan.
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.
Thu]k kv phylogenetic nyoothv jv 5 xapn5 kvnr22l5 kv kvn tin tusk alpha-CoVs kvn beta-CoVs, k` ku diit la kvn f11c gamma-CoVs and delta-CoVs.
For thousands of years, CoVs have constantly crossed species barriers and some have emerged as important human pathogens.
kv run t5 k5thn5 t5 c5 thuuk, CoV, cv ciex j`lv kam5 leeyn5 v c5 th11xkivn lv jssc v la ;u2x k` raan.
To date, seven human CoVs (HCoVs) are known.
Vn walv, b1rsw k` CoVs (HCoVs) ran ca kv x1c.
Among them HCoV-229E and HCoV-NL63 are alpha-CoVs.
Rvidivn kv HCoV-229E kvn HCoV-NL63 kv alpha-CoVs.
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.
Dhieec tin k]x kv k` beta-CoVs kvvl kv HCoV-OC43, HCoV-HKU1, bayr`th in n77x rup-ruup kv p0th k` li``k (SARS-CoV), bayr`th D11r cu22c fsaa in n77x rup-ruup kv p0th k` li``k(MERS-CoV) kv 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 and HCoV-NL63 la malv juey m5 m5 cet kv thony-thony kiv b0c jivc.
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.
V gu1c kv vnv, SARS-CoV, MERS-CoV kv SARS-CoV-2 in pay lv tusk kvn kv luex, n66x kv luex piny l55k` kv j5 ju1th t5 xuan k` th1k f66 bv cop kv luex l55k` min rup-rup(ARDS) kvn r`l lsaac.
The first HCoV-229E strain, B814, was isolated from the nasal discharge of patients with common cold in mid-1960s.
Vn HCoV-229E rivm, B814 k1m jv raar rvi wu]m k` gu1n ju1th m5 cv moc thony-thony kv 1960s.
Since then, more knowledge was accumulated through extensive studies on HCoV-229E and HCoV-OC43, both of which cause self-limiting symptoms.
V ku we ben cu x`c m5 d55 tussk kv jvn gs1r kv HCoV-229E kvn HCoV-OC43 kvn d1x rvw n66x kv nyuuthn5 t5 tst.
Indeed, the concept had been widely accepted that infection with HCoVs is generally harmless until the outbreak of SARS.
V puc, cuv cu cop lssc 5 luex HCoVs 5 thilv jv lustam`n5 m22 c5 SARS ben.
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%.
Vn tuk SARS kv 2003 v kvl rik tin ji`k k` l00x vn walv k` naath t5 8000 t5 c5 li11 kv coc cet kv 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.
Kv ksr run5 d1x w`l, cu juey d11r cueec wec (MERS) tusk rvi r66l Arabiya v we k` w5c mu]]n inn d]x.
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.
kv 2019 cu jvn HCoV (2019-nCoV), ku ben m5 ca nysk kv ci6t SARS CoV-2, v jvn vnv ku toomvv la bayr`th 2019 (COVID-19), min c5 naath t5 b``l 3,120 n`k k` cv naath t5 91,000 luvx kv paydi]k 3, 2020.
The alarm has been ringing and the world has to prepare for the coming pandemic of SARS-CoV-2.
vn jsw cv l6x k` c5 fsw rs jivn kv jvn juey in thi``x fsw n5 SARS-CoV-2.
All seven HCoVs have a zoonotic origin from bats, mice or domestic animals.
Kvn d1x b1rsw kvn HCoVs tusk kvn dial k` leydsaar kvn ley ciex.
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.
keer5 t5 xuan kv min tusk nyooth kvn tuk ju1th kvvl 5 kvn HCoVs dial tusk kvn k` xap, hu11th iv caa kv xic th5n v kvn k` thil kv luex k` jv kuv la f66 nyooth kvn xuandivn.
The COVID-19 epidemic has presented enormous medical, scientific, social and moral challenges to China and the world.
Vn CoV-19 vn thi``x fsw cv ben kv t5 xuan t5 nyin wal, taanytith, wec kvn c1r k` China kvn w5c mu]]n in d]x.
Tracing the zoonotic origins of HCoVs provides a framework to understand the natural history, driving force and restriction factors of species jumping.
Kapdv jssk leyn5 vn tuk ju1th HCoVs nyoothv ciaax in cup kv jv lssc kv l0x, min koot naath kvn g1x ku00n5 tin kac.
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.
Vns derv la b77th b` kv cu]p g6r` x`c` kv gu11th in lvnv ben liep th5n, ran in kap jv kams k` kvn ley tin j`l kv SARS-CoV-2 tin te kv lu1x kv g`xdv kv lvrv k` tin k]x.
In this review we present an overview of the zoonotic origins, interspecies transmission and pathogenesis of HCoVs.
Rvi wargak` nvmv ca guec kv ley tin tusk du]]r pu]nydivn, j1lv kam ku00n5 t5 g66l kvn luex HCoVs.
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.
V civk, c1 ks dup tin thi1k lar k` c1 ks gu11th in dieth kv bayr`th th5n lat5 v HCoVs tin thilv luex k` kv k` cv a luex kv ksr j1lv kamn5 ku00n5 t5 g66l kvn d7pdv.
We also review the trend of HCoV evolution in which the increase in transmissibility often comes with the decrease in pathogenicity.
kvn b` ca min tusk k` HCoV lar kv tukdv min reep d7pdv b22 kvvl kv yuth piny luex`.
The outcome of the ongoing SARS-CoV-2 outbreak is also discussed in this context.
min tusk kv tuk SARS-CoV-2 vmv ca lat inv.
Animal CoVs have been known since late 1930s.
Ley CoVs ca kv x1c n5 kv guut 1930s.
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.
kv gu11th 22 xot /k1n HCoV-229E rivm B814 nvn k` wum mi thiy k` ran tee thony-thony CoVS t5 g66l ca kv x1c k` ley t5 xuan t5 ca luvx, t5 te tukkey th5n, kun yax kundhur nyaaw kvn ji6k.
In the past decades, seven HCoVs have been identified.
kv run t22 c5 we, b1rsw k` HCoVs nvn.
A brief summary of the history of HCoV discovery in chronological order (Table ​1) would be informative and instructive.
l0x m5 thi1k kv ku5c jek` HCoVs kv runkivn tin (Tharb2t1) Bv la l``rk` tiit.
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.
Vn rivm in nhiam cua jv nvn nhial k` li``k ran m5 te kv luex rvi ruun` 1966, k` cua jv dsp k`cuv pith rvi WI-38 k` keer cell pu]]th.
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.
j5 ju1th rin ca luvx v HCoV-229E rin c5 ben kv nyuuthn5 thony-thony`, kvvl kv bak, thi22m kv yiiw r77l, kv l2th pu11ny kv kivl ca kv nvn 10~20% cases.
Later in 1967, HCoV-OC43 was isolated from organ culture and subsequent serial passage in brains of suckling mice.
kv ksrv kv ru]]n HCoV-OC43 cua jv nvn k` cu]]x k` ksrv kvn guur du]]p in cothdv xith` ku]n in math jv.
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.
kvn nyin dueelwal luex` HCoV-OC43 jsc kv v n77x kv HCoV-229E, v la nyuuthn5 t5/ca lu`x kv d``kkvn luexl55k` tin k]xcet kv yinpluvndha Abayr`th kvn raynobayr`th.
Both HCoV-229E and HCoV-OC43 are distributed globally, and they tend to be predominantly transmitted during the season of winter in temperate climate.
Vn HCoV-229E and HCoV-OC43 c5 kv hswt thi`x cet kv kv m5 dsap kv kv kv n5n jsam rvi ks1c fsaa.
Generally, the incubation time of these two viruses is less than one week, followed by an approximately 2-week illness.
kvvliw vn tuk thaak` ju1th bayr`th n5 titi cv jusk nax, ba cu gu]]r juey kv juskn5 rvw.
According to a human volunteer study, healthy individuals infected with HCoV-229E developed mild common cold.
Cet kv m5 ca lar v g6r x`c` kv ku5c ran, naath t5 pusl pu1ntkivn t5 ca k` v bayr`th HCoV-229E laa moocv kv thony-thony m5 tst.
Only a few immunocompromised patients exhibited severe lower respiratory tract infection.
kv naath t5 tst tin cv moc yimuncompromaath la nyuuth luex l55k` piny m5 d55t ts.
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, min csal5 “atyiksl pneumonia” v jvn vn 2 gs1r kv piny kv nhiam min thi``x hsw kv gu11th m5 kuiy kvn yitolsj5ksl SARS-CoV, min la di]]kdivn HCoV in ca jek.
The first case of SARS can be traced back to late 2002 in Guangdong Province of China.
SARS kvl e nhiam cua jv nvn tuskv kv 2002 k` Guangdong k` Chvyna.
The SARS epidemic resulted in 8,096 reported cases with 774 deaths, spreading across many countries and continents.
vn SARS fsaa cv naath t5 8,096 k`p k` cv 774 n`k, cv w55 t5 xuan thi`x w55 mu]]n.
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.
G6l k` d`kdv fsaa, cua jv guic luex kvvl derv r`th k` k`th in rvwdv mi cv tusk kv n5n 4 v we k` 7 kv la copv pek in jsak kv n5n 10 vn d5t ju1th.
Patients infected with SARS-CoV initially present with myalgia, headache, fever, malaise and chills, followed by dyspnea, cough and respiratory distress as late symptoms.
j5 ju1th tin cv k`p kv SARS-CoV kv n5n tin nhiam la mocv kv kv mylagia, bak, leth pu11ny, malaythi kvn k]c, ba kv gu]]r v dithpnea, kivl kvn kuuk l55k` v la nyuuthn5 tin jsak.
Lymphopenia, deranged liver function tests, and elevated creatine kinase are common laboratory abnormalities of SARS.
limpspenia, them gssy` pu1ny kvn kap nhial kinathv kv kvn them SARS tin nhiam k` lab.
Diffuse alveolar damage, epithelial cell proliferation and an increase of macrophages are also observed in SARS patients.
B0c ny11r, nyueeny yipithial cell kvn r2p macrophages b` ca kv nvn k` j5 ju1th SARS.
Approximately 20-30% of patients subsequently require intensive care and mechanical ventilation.
Pek m5 cet kv 20-30% k` j5 ju1th g77r kvn yoop m5 d55t kvn c1p jsam m5 gsaa.
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.
V nysk kv kssr piny l55k`, cu]]x t5 xuan t5 te ji1c th5n, cu`ny kvn rok la luvvxv kv b` min cv d5t, la b22 kvvl kvn xuan thaytskin mi dee leth n66x rvi j5 ju1th t5 c5 bu]m rs ri1t.
The virus was first isolated from the open lung biopsy of a relative of the index patient who travelled to Hong Kong from Guangzhou.
vn bayr`th ca jv nvn kv nhiam k` pu]th t5 ca lvp k` gu1n ju1th m5 c5 we j1l k` Hong Kong kuv lv jivvn k` k` Guangzhou.
Since then, tremendous efforts have been dedicated to HCoV research.
N5 vn c`xs , cu lu1x cu k1n kv ku5c g7r` x`c` kv HCoV.
HCoV-NL63 was isolated from a 7-month-old child from the Netherlands during late 2004.
HCoV-NL63 cua jv nvn k` gat m5 te kv run 7 k` Netherlands kv guut 2004.
It was initially found to be prevalent in young children, the elderly and immunocompromised patients with respiratory illnesses.
cua jv guic kv tukdv 5 la lvmv k` gaat, d5t kvn j5 ju1th tin bu]m pu11nydivn immunocompromised ku00 kv juey l55k`.
Presentation of coryza, conjunctivitis, fever, and bronchiolitis is common in the disease caused by HCoV-NL63.
ben kv ksrydha, k77k c]wn5, leth pu11ny, kvn bronchiolitis la malv jekv rvi ju1th HCoV-NL63.
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.
g6r x`c` d]divn cv jek bayr`th` m5 cet kv jv lar m5 nvn kv rvi wu]m gat` m5 te kv p`th 8 m5 cuc kv pneumonia k` Netherlands.
Although it was identified in Netherlands, it is actually distributed globally.
c`x me c``tv kvn dux Netherlands, cuv fsw thi`x vl]x.
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.
cv jv nvn 5 HCoV-NL63 v jvn n77x ju1th l55k` t5 4.7%, k` la d55tv vl]x kv t]t, jism kvn ruel.
HCoV-NL63 is associated with obstructive laryngitis, also known as croup.
HCoV-NL63 cetv kv b0c tax r66l in csal kv b` 5 kiruup.
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.
kv jvn ru]]m vns, cua HCoV-HKU1 nvn k` wut m5 te kv run t5 71 m5 ca ts11c k` Hong Kong.
Besides community-acquired pneumonia and bronchiolitis, HCoV-HKU1 was reported to be associated with acute asthmatic exacerbation.
kssr pneumonia in la k``p raan kvn, bronchiolitis, HCoV-HKU1 cua jv lar 5 thieekv kv asthmatic yyiw` min rup-rup.
Similar to HCoV-NL63, HCoV-229E and HCoV-OC43, HCoV-HKU1 was found worldwide, causing mild respiratory diseases.
M5 c``t HCoV-NL63, HCoV-229E and HCoV-OC43, HCoV-HKU1, cua jv jek w55 mu]]n kvvliw, n77xv juey l55k` m5 tst.
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.
kvn d1x xuaan dial kvn tin k``p raan, HCoVs ca jv xic v pu]ny ran v kuiy luex in jekv th5n, c`xn5 min c5 rik tusk b` kv dup /caa x`c tin n77x bayrulvn HCoV-NL63 kv, tin ca pay lar thi`k` 5 n77x kvn luex piny l55k` m5 d55t k` 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.
kvvliw, m5 c5 vn HCoVs vmv jv jek 5 bv bu]m v bv naath dsp, k` bv li`p kv ciaax rvi ran, lv jvn cu11 m5 thil bayrulvn m5 d55t kiv luex.
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.
MERS-CoV n0n jv nhiam kv ru]]n 2012 k` pu]th gu1n ju1th m5 run kv 60 m5 cv moc pneumonia m5 rup-rup kvn thil l1t rokn5 rvi 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.
Min ku kvn them dial jv lar vn f66 pek in jekv tusskv d``r cu22c fsaa, th11x pekn5 tin n66x kv gu1thn5 tin k]x b` ca kv lar tin jekv kv r6m kam` nath rvi w55n5 Yursp t5 xuankvn Tunicia.
Another secondary outbreak occurred in South Korea in 2015 with 186 confirmed cases.
tuk kvn d`kdv fsaa d]divn k` jsk Korea kv ru]]n 2015 kv pek m5 186.
Clinical manifestations of MERS resemble those of SARS, characterized by progressive acute pneumonia.
Nyuuthn5 tin xivc jv vn MERS c``t kv kv nyin SARS, te kvn dial kv pneumonia m5 rup-rup.
Unlike SARS, many patients with MERS also developed acute renal failure, which is thus far unique for MERS among HCoV-caused diseases.
V gu1c kv SARS, MERS t5 xuan b` n77x kvn thil l1t rokn5, m5 la duxdv k`rsa rvi ju1thn5 tin n77x HCoV kv.
More than 30% of patients present with gastrointestinal symptoms, such as diarrhea and vomiting.
pek m5 b``l 30% k` j5 ju1th, la bekv kv nyuuuthn5 jivc, cet kv c5th kvn x6k.
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.
kv pay rvw 14, 2020, pek m5 b``l 2500 t5 ca thvm k` lab cua kv lark v li11 m5 34.4%, nyoothv MERS-CoV 5 gula bayr`th m5 rivk k` gat ran.
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.
kv n5n d11r pay w`lrvw 2019, cu j5 ju1th pneumonia th11x m5 c5 rs thi22k kv luex SARS-CoV-2 cua jv jek k` Wuhan, wec 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.
cu srganaydhvcin pusl` pu11nt wec mu]]c jv lar 5 vn mv l``t rs mv v la luex piny l55k` n77xv SARS-CoV-2 ca dux wecmu]]n kvvliw kv ku5c pusl` pu11ny k` cua jv csal 5 COVID-19.
As of March 3, 2020, 90,053 cases have been confirmed worldwide, with a crude case fatality of 3.4%.
kv pay di]k 3, 2020, cua pek m5 90,053 x`thw55 mu]]n kvvliw, kv l511 m5 3.4%.
Notably, the case fatality in Hubei, China is 4.2%, whereas the one outside of it is 1.2%.
V g5m, pek lieth k` Hubei, China v 4.2%, raarv v 1.2%.
SARS-CoV-2 causes severe respiratory infection like SARS-CoV and MERS-CoV, presented as fever, cough and dyspnea.
SARS-CoV-2 n77xv luex l55k` m5 d55t cet kv SARS-CoV kvn MERS-CoV, tin n77x leth pu11ny, kivl kvn dithpnia.
Diarrhea is also seen in some patients.
c5th b` ca nvnk` th11x j5 ju1th.
Pneumonia is one of the most severe symptoms and can progress rapidly to acute respiratory distress syndrome.
pneumonia v kvl m5 te kv nyuuthn5 t5 d5t k` la reep rs kv p0th v bv b0c l55k` m 5rup-rup n66x.
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.
c`x n5 min SARS-CoV SARS-CoV-2 c``t kv kv f66 nyuaak nucleotide kv c11t m5 82%, cux kvn dh7r5 t5 g66l rvi jiaath c`k`.
SARS-CoV-2 is apparently less pathogenic but more transmissible compared to SARS-CoV and MERS-CoV.
SARS-CoV-2 kuiy lu1xdv duxdv f66 dspv naath v kv p0th m5 p11r kv jv kvn SARS-CoV kvn MERS-CoV.
Asymptomatic subjects infected with SARS-CoV-2 have been reported and might contribute to its rapid spreading around the world.
ca naath t5 cv k`p lar k` th5l nyuuthn5, d]x v jvn laa p0th kv jv ms v bv fsw cu thi`x.
Comparing and contrasting SARS-CoV-2 with the other six HCoVs reveal similarities and differences of great interest.
p``r kvn gu`c SARS-CoV-2 kvn HCoVs b1kvl tin k]x nyoothv jv 5 c11t kvn gu1cdivn kv dup t5 k]x.
First, the incubation period and the duration of the course of HCoV disease are very similar.
kv nhiam, tukdivn kvn j1nydivn kvn ju1th HCoV c``tv.
In this regard, SARS-CoV-2 follows the general trend of the other six HCoVs.
kv ku5c vms, SARS-CoV-2 guur kvn ci6k HCoVs b1kvl tin k]x.
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).
rvwdv, d5t nyuuthn5 COVID-19 cuxv kam kvn SARS-CoV tin k``p naath, v la HCoV-229E, HCoV-OC43, HCoV-HKU1 and 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.
kv ku5c kvl, luex SARS-CoV-2 nyoothv civx t5 tin nvn kv kv n5n luex` j5 HCoVs, kvvl kv ben kv t5 thil du]]p kvl, nyuutn5 t5 kuiy.
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.
kv ku5c in d]x, pek m5 tst k` d5t nyuuthn5 COVID-19 b` cetv kv pek in n0n kv k` luex SARS-CoV c`x min kuiy rvyci77.
Third, the transmission of SARS-CoV-2 also shows interesting patterns characteristic of both community-acquired HCoVs and SARS-CoV.
Di]]kdivn, d7pb` SARS-CoV-2 nyoothv t11 civxn5 HCoVs kvn SARS-CoV tin k``p naath.
On one hand, the transmissibility of SARS-CoV-2 is at least as high as that of community-acquired HCoVs.
kv ku5c kvl, d6p SARS-CoV-2 d5tv cetn5 kv dux HCoVs in k``p naath.
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.
kv ku5v ind]x, xotv ba kulv x1c m5 d6p SARS-CoV-2 xookv rs kv ksr k` min cv cop k` naath cet kv t11 in te kv SARS-CoV kvn MERS-CoV.
Finally, same as the other HCoVs, SARS-CoV-2 can be detected in fecal samples.
Guutdv, cet kv ju1th tin k]x HCoVs, SARS-CoV-2 ca jv jek rvi c1th.
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.
m5 dee dsp k` c`th kv thok vn HCoVs, SARS-CoV-2 cet kv min tusk k` SARS-CoV xotv ba kulv x1c kv g6r x`c` min b5 lv ben.
It is also of particularly great interest to see whether SARS-CoV-2 might exhibit seasonality as in the cases of community-acquired HCoVs.
jvn b` gsaayv vn f66 ba nvn m5 vn SARS-CoV-2 nyoothv civx kv d``kn5 fsaa cet kv min tusk k` HCoVs in k``p naath.
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.
c`x v jvn 5ns, civx SARS-CoV-2 kvvl kv d6pdv kv naath, luexdv, kvn thi1xdv kv fsw min cv ku tusk ba jv guic kv jvn tuk COVID-19 vmv.
All four community-acquired HCoVs causing mild symptoms have been well adapted to humans.
kvn ju1th HCoVs d1x xuaan tin k``p naath n77x nyuuthn5 t5 tst ca kv xic v raan.
From another perspective, it might also be true that humans have been well adapted to these four HCoVs.
kv du]]p d]divn, derv a thu]k 5 raan cv kvn ju1th HCoVs titi xic.
In other words, both could be the survivors of ancient HCoV pandemics.
kv ri`t in d]x, kvn d1x rvw dee kvn v j5 k`n` ju1th HCoV 2 c5 ksx tusk kv gu11th 2 wal.
HCoVs that cause severe diseases in humans and humans who developed severe HCoV diseases have been eliminated.
n77xv juey m5 d55t k` raan k` ram 2 took HCoV cv thuuk.
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.
Ɛn ɣöö bi̱ mɛmɛ tuɔk, bi̱ HCoVs rɔ luɔc puɔ̱ny ran kɛ ta̱a̱ mi̱ röŋ mi jak tin kɔ̱ŋ kä dɔap kɛ ta̱a̱ mi̱ gɛɛr min gaŋ tin kɔ̱ŋ.
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.
Kɛ thuɔ̱k, ja̱ny in jäny kɛ SARS-COV-2 bɛ ŋuot te puɔ̱ny nɛɛni̱ ti̱ ŋuan tin cɛ käp, bɛ cu ŋuot kɛ mi̱ dap jɛ ɛ naath.
If it adapts well, its transmission in humans would be difficult to stop by quarantine or other infection control measures.
Mi̱ ca dɔp ɛ lɔ̱ŋ, kɛ rep dɛ kɛ rɔ kä naath, bi̱ käp dɛ cuɔ̱ŋ buɔ̱m ɛ cäŋ lɛ̈y kɛ naath kiɛ dup tin kɔ̱ŋ tin de dɔp kɛ jɛ.
For many years, the four community-acquired CoVs circulate in human populations, triggering common cold in immunocompetent subjects.
Kɛ run ni̱ ti̱ ŋuan, kɛn jua̱th da̱ŋ ŋuaan ti̱ti̱ COVs jäl kɛ puɔ̱ny nath, nööŋ kɛ thonythony mi̱ bi̱ la tuk juäth.
These viruses do not need an animal reservoir.
Ɛn juey ɛmɛ /cɛ jɛ go̱r ɛn ɣöö bi̱ kuak tin la nyin lëëni̱ te kut nath.
In contrast, highly pathogenic SARS-CoV and MERS-CoV have not adapted to humans well and their transmission within humans cannot be sustained.
Min la dääk diɛn, di̱t dɛɛni̱ jua̱thni̱ SARS-CoV and MERS-CoV /ci̱ kɛn naath dɛp ɛ lɔ̱ŋ, kä rep diɛn kɛ rɔ̱ puɔ̱th nath ca jaa ka̱p kɛ cuɔ̱ŋ.
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.
Bi̱ kɛnɛ go̱r ɛn ɣöö bi̱ kɛ rɔ̱ moc gua̱th ciɛŋä mi̱ te kɛ thi̱n gua̱th kɛl in ciëŋ kɛ thi̱n kä bi̱ kɛn gua̱th cu go̱rni̱ kä nɛy tin cuc, dɔ̱ŋ bɛ tok kɛ kɛl kiɛ ti̱ ŋuan ti̱ ba rɔ̱ cu rëp kɛ no̱o̱ŋ kä tin kɔ̱ŋ.
SARS-CoV-2 has features that are similar to both SARS-CoV/MERS-CoV and the four community-acquired HCoVs.
Jvn SARS-CoV-2 t22 kv t22 kv rvw t5 c``t kv SARS-CoV/MERS-CoV k` w55 d1x xuan g6r kv HCOVs.
It is highly transmissible like community-acquired HCoVs, at least for the time being.
Jvn d22 mal dsp kiv d22 j2k kv dup t5 nyin xuan c2t kv min j2kv jv k` HCoVs, kv jv gu1th v tst vms.
However, it is more pathogenic than community-acquired HCoVs and less pathogenic than SARS-CoV or MERS-CoV.
Dux dv f66 jvn t22 kv dvy ju1thn5 t5 xuan t5 l1ny kv nyin w2c kiv HCoVs k` t22 kv dvy ju1thn5 ti tst t5 kuiy n5 kvn k` SARS-CoV kiv 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.
Jvn bv t2 th5n v la m5 baa guic bv w2 kv t11 ran k` bv rsdv wil rvy ran v th2lv l2y d]divn m5 b5 t2 kams.
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.
V /k`n ksn n5 ruac k` t11 in b` l2y kv jv k` HCoVs, jvn bv t2 th5n vla m5 b5 lust dv, t11 in caa cak n5 jv, kiv t11dv kvnv t11 in d22 jv jak` th51k kv t11 HCoVs.
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.
Ɛn lëy puɔ̱ny dɛ te jueyni̱ HCoV ɛmɛ puɔ̱ɔ̱ny dɛ, mi thia̱k duɔ̱p in derɛ rɔ mat kä ta̱a̱ ee wal mi̱ cäät kɛ ta̱a̱ in ci̱ tuɔk.
The ancestral virus is usually well adapted and non-pathogenic in this host.
Juëy mi̱ të rɛy kari̱ raan la jɛ mal ɛ dɔap kɛ ɛ lɔ̱ŋ, kä /ci̱ dɛy kɛ a tëë rɛy jua̱th ɛmɛ.
Likewise, a reservoir host harbours HCoV continuously and for long term.
Kä i̱nɔ bi̱ min ci̱ jak juey HCoV kä të wa̱nɔ cu ŋot kɛ pëk mi̱ bäär.
In both cases, the hosts are naturally infected and are the natural hosts of HCoV or its parental virus.
Kɛ kɛn dup da̱ŋ rɛw ɛ tɔ̱, bi̱ jua̱th tin te thi̱n ni̱ wën cu te kɛ riɛk kä ta̱a̱ in wën kä HCoV kiɛ juey in të rɛy kari.
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.
Kɛ min dɔ̱ŋ, mi̱ ci̱ HCoV mi̱ pay ben rɔ cuɔt kä min të däär kiɛ mi̱ te thin ɛ /kënɛ ni̱ wä kä naath, /cɛ rɔ dɛ a matɛ kä min pay ben, kä ba juey bä.
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.
Ɛn Juey ɛ të däärɔ bɛ cu të wanɔ ala ɣöö bɛ jua̱th dial cu tok kä naath, bɛ la̱t mi̱ di̱t cu la̱t kɛ no̱o̱ŋ dɛ kɛ jua̱th tin kɔ̱ŋ kɛ pɛ̈th kä bɛ kɛ cu jakä wä puɔ̱ɔ̱ny nath ba naath cu käp.
An HCoV can undergo a dead-end infection if it cannot sustain its transmission within the intermediate host.
Kvn HCoVs dial d22 kv j5`k m5 /k1n kv m5 cv rsdv lu`x vb f66 bv tin nhiam jak` w2 kv w2 rvc.
On the contrary, HCoVs can also adapt to the intermediate host and even establish long-term endemicity.
K` min gu1c kv nvmv, Jvn HCoVs jvn b` d2rv l`t kvnv tin nhiam kv f66 d2rv kulv w` nhiam.
In this case, the intermediate host becomes a natural reservoir host.
Kv gu1th m5 cv jssc vn f66 c5 min nhiam m5 cv w` b2n v la min nhiam kiv min d22 kv c52x kv jsk dv.
Epidemiological data revealed retrospectively that the index case of SARS had a contact history with game animals.
Jvn t11 in k1p kv n5 ju2y cu]x caa b2n nyoth vl``r5 t22 caa g\1r piny kv ku5 ju1thin csal5 SARS vn f66 k`pv naath k` l2y k` tukdv.
Subsequent seroprevalence investigations indicated that animal traders had a higher prevalence of anti-SARS-CoV IgG compared with that of the general population.
Jvn caa t11 m,5 c2t kv ns b2n th52c vl7x k` caa j2k vn f66 kvn l2y tin j`l d22 ju2y vms mal j2k k` kv min csal5 SARS-CoV IgG m5 c11t kv jv kv nvy dial tin t2 th5n.
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.
Jvn lvy v csal5 - masked palm covet (Paguma larvata) kiv j57k tin t2k k` thuk caa kv j2k vn f66 jvn c``t kv kv ju2y in caa n66x in csal5 SARS CoV.
This was indirectly supported by the fact that no further SARS was reported after killing all civets in the markets.
Jvn nvmv caa b2n lat v thu]k vn f66 jvn jvn Ju2y v csal5 SARS caa rspust vn f66 n`kv naath rvy thukn5.
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.
Duxdv f66 caa jv b2n rspust vn f66 l`th raan kuum wu]m kvnv thok m5 d]x k1n l1t vgsa jvn bvcv k` d2rv raan jak` j2kv ju2y in csal5 SARS-CoV, m5 lot n5 f66 caa jv b2n car vn f66 jvn kuum wu]m b` d2rv raan gax kv ksr gu1th m5 tst v c5 mua f66 d2rv raan tit v r]x k` ju2y in csal5 SAR-CoV.
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.
Jvn caa x1c kv p2k m5 cop 80% k` l2y t5 g66l rvy thu]]k rvy Guangzhou kvnv tin l6kv r] kv SARS-CoV tin gax kv pu]ny kv ju1th, jvn b` v du]]p m5 l2y t5 g66l l2y tin caa lat 5 SARS-CoV jvn /caa kv d22 mat th5n.
All of these appear to be dead-end hosts of SARS-CoV.
Kvn ti dial vt5 w2 kvn p`l k` tin c5 l5w k` SARS-CoV.
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.
T11 in c5 tusk min g6r kv lvy t5n b22k` SARS-CoV jvn th52kv kv kvc CoV, jvn b` lark v jv csalv SARs m5 maar kvnv Rhinolophus kvc COV HKU3 (SARSr-Rh-BatCoV HKU3), Jvn t22 k` w11r5 chayna tin l1t kv kv k7l mu]l tu]ru]k.
These bats are positive for anti-SARS-CoV antibodies and genome sequence of SARSr-Rh-BatCoV HKU3.
Kvn kvc v ti gsw kv kv SARS-CoV kvnv tin gax pu]ny kv dvy ju1thn5 kvnv t11 in bvc min d22 j2k k` SARS-CoV.
This and other bat CoVs share 88-92% nucleotide sequence homology with SARS-CoV.
Kvn kvc v ti COVs kvn mat 88-92% Kv t11 in t2kvkv kvSARS-CoV.
These studies have laid the foundation for the new concept that bats host emerging human pathogens.
Jvn mv caa g]rv cv x`c m5 r]x jak` t2 th5n kv t11 in j2kv dvy ju1thn5 v raan.
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.
Tha̱a̱ŋ Jua̱th ni̱ ti̱ ŋuan cet kɛ SARS kɛ CoV (SL-CoVs) ca kɛ jëk ɛn ɣöö jek kɛ kɛ kä ŋaprɔkɛdhɔ̱t, duŋ dɛ ɣöö / thiɛlɛ kɛl mi ca kuany go̱lä kä WIV1 ala juey mi tek kärɔa.
Human angiotensin converting enzyme 2 (ACE2) is known to be the receptor of SARS-CoV.
Bi̱ rät riɛm ran rɔ ri̱t kä 2 (ACE2) ba cu ŋa̱c ɛn ɣöö ɛ jɛn no̱o̱ŋ SARS –CoV.
WIV1 derived from fecal sample of bats was demonstrated to use bat, civet and human ACE2 as receptor for cell entry.
WIV1 ca thɛm jek jɛ kä ŋaprɔkɛdhɔ̱t cɛ jɛ nyuoth ɛn ɣöö bɛ te kä ŋaprɔkɛdhɔ̱tni̱ kɛnɛ li̱kli̱kni̱ kɛ naath ɛ jɛn bi̱ ACE2 ku lɛ lor kɛ wä dɛ rɛy räät.
Intriguingly, sera of convalescent SARS patients were capable of neutralizing WIV1.
Ni gɔaa, de nɛy tin cɛ käp kɛ SARS dë kɔn jak ni̱ WIV1 kä gɔaa.
Thus far, WIV1 represents the most closely related ancestor of SARS-CoV in bats, sharing 95% nucleotide sequence homology.
Kä inɔ pa̱ny, ɛn WIV1 nyuothɛ ta̱a̱ mi̱ thia̱k ɛ lɔ̱ŋ kɛ tuk SARS-CoV min jek kɛ kä li̱li̱kni̱, te kɛ pëk mi̱ 95% kä ta̱a̱ in lät kɛ jɛ puɔ̱ny ran.
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.
Cäŋ ɛ jɛn i̱nɔ bä, ta̱a̱ cäätä min te kam jua̱thni̱ da̱ŋ rɛw ɛ ti̱, ŋa̱th kɛ jɛ ɛn ɣöö WIV1 /ciɛ jɛn tuk jua̱th in cɔali SARS-CoV kä li̱kli̱kni̱ /ciɛ kɛn jek kɛ SARS-CoV kä kɛ tɔ̱.
Phylogenetic analysis clusters MERS-CoV to the same group as bat CoV-HKU4 and bat CoV-HKU5.
Kä mat ki̱mni̱ ca MERS-CoV te kä buɔ̱n cät kɛ li̱kli̱k CoV-HKU4 kɛnɛ li̱li̱k CoV-HKU5.
Bat CoV-HKU4 and MERS-CoV utilize the same host receptor, dipeptidyl peptidase 4 (DPP4), for virus entry.
Kä li̱kli̱k CoV-HKU4 kɛnɛ MERS-CoV lät kɛ kɛɛl kɛ käp jɔam cuɔ̱ŋ kɛnɛ nɛŋ dɛ rɛc (DPP4), kɛ naŋ jua̱th rɛc.
RNA-dependent RNA polymerase sequences of MERS-CoV are phylogenetically closer to counterparts in bat beta-CoVs identified from Europe and Africa.
Ɛn RNA in /thiɛl lua̱ŋ, ɛ jɛn RNA in lät kɛ jek dɛ kɛ MERS-CoV ti̱ ŋuan kɛ kɛn tin thiëk kɛ li̱kli̱k beta-CoVs cua ŋic kä Europe kɛnɛ Api̱ri̱ka.
Up to now, no live MERS-CoV can be found in wild bats.
Amäni̱ tämɛ, /thiɛlɛ MERS-CoV mi̱ te thi̱n canyɔk kɛ jek kä Li̱kli̱kni̱ dɔar.
MERS-CoV and its closest relative bat CoV-HKU25 share only 87% nucleotide sequence homology.
MERS-CoV kɛnɛ gua̱n thiëëkä dɛ ni̱ CoV-HKU25 mat kɛni̱ 87% kä ciaaŋ tëëkä min të kɛ.
Thus, bats might not be the immediate reservoir host of MERS-CoV.
Cäŋ ɛ jɛn i̱nɔ ba̱, li̱kli̱kni̱ /ciɛ kɛn tin kua juey MERS-CoV jek kä kɛ kɛ pɛ̈th.
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.
Kɛ ta̱a̱ in dɔ̱ŋ, ca thɛm Kui̱c Känyä Ca̱ŋ ɛn ɣöö Jamɛli̱ tin ciëŋ kɛ naath kɛɛl ca kɛ jëk te kɛ MERS-CoV mi̱ të puɔ̱ny diɛn, cät kɛ nɔ bä, Jamɛli̱ tin te kui̱c Känyä Ca̱ŋ tukdiɛn kɛ nyin wi̱i̱ni̱ ti̱ ŋuan kä Api̱ri̱ka.
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 ta̱a̱ dɛ thi̱n cua jɛ ŋic kɛ ram te juey cua la̱th gölä kɛ thuny ti̱ ca ka̱m raar wumni̱ jamɛli̱ tin te kɛ naath kɛɛl, ɛ wëë wa̱ i̱nɔ cuɛ cu nyuoth ɛn ɣöö te MERS-CoV puɔ̱ɔ̱ny jamɛli̱.
It is also noteworthy that generally mild symptoms but massive virus shedding were observed in camels experimentally infected with MERS-CoV.
Cua cu ŋa̱c ni̱ gɛaa ɛn ɣöö te ti̱ ŋuan ti̱ nyuoth jɛ, duŋ dɛ ɣöö cua jua̱th ti̱ ŋuan tit pua̱nyni̱ jamɛli̱ tin cɛ käp kɛ 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.
Kɛ thuɔ̱k bä, jamɛli̱ tin te kɛ jɔk /ci̱ kɛn juey ɛmɛ jek kɛ jiɔm kä rɔa, jek jɛ bä kɛ tin bee raar thokdiɛn, mi̱ lot ni̱ ɣöö ɛ jɛn duɔ̱p in waa jek ni̱ juey ɛmɛ kɛ jɛ ɛ Li̱kli̱kni̱.
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.
Kä i̱nɔ bä, ŋuot thiëc bä ɛn ɣöö gua̱th tin ca jek thin ɛn MERS /thiɛlɛ kɛ ta̱a̱ mi̱ nyuoth jɛ ɛn ɣöö ci kɛ wä gua̱th mi̱ te jamli̱ thi̱n mi̱ kua kɛ pa̱a̱r kɛ ta̱a̱ in ca nyuoth, kɛ thuɔ̱k ca ŋa̱c ɛn dɔp ramɔ jɛ kä ramɔ, kiɛ te duɔp dɔdiɛn mi dɔap kɛ jɛ kä lëy tin te kɛ MERS-CoV.
SARS-CoV-2 shares 96.2% nucleotide homology with a bat CoV RaTG13 isolated from Rhinolophus affinis bats.
SARS-CoV-2 te nyuak kɛ pek mi̱ 96.2% kɛnɛ CoV RaTG13 li̱kli̱kä kɛ ta̱a̱ in te kɛ jɛ, ca jɛ da̱a̱k kɛ ta̱a̱ li̱kli̱kni̱ tin te kɛ Kil kɛɛl.
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.
Cet kɛ ta̱a̱ in tek kɛ SARS-CoV kɛnɛ MERS-CoV, ci̱ ta̱a̱ rɛ wä gɛ̈r kam SARS-CoV-2 kɛnɛ RaTG13 ci̱ dääk diɛn kɛ ta̱a̱ diɛn kɛɛl cu buɔ̱m ɛ lɔ̱ŋ.
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.
Ɛ jɛn mi̱ lar kɛ jɛ ɛn ɣöö li̱kli̱kni̱ /ciɛ kɛn tin te kɛ SARS-CoV-2 Ɛni̱ mi̱ waa ŋic ɛn ɣöö CoVs ba wä jëk nhiam kɛ guath in bi̱ ben.
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.
Kɛ diɛw, ɛ thuɔ̱k lëy tin të kɛ juey ni̱ SARS-CoV-2 bi̱ kɛ te rɛy lëëni̱ dɔaar tin laa na̱k kɛ kɛnɛ lëy tin la nööŋ kɛ yiëër kä ba kɔak kä thuk in la gual kɛ ŋɔak thi̱n kä Ɣuɣan min te kɛ tuk jua̱thni̱ COVID-19 ɛ jɛn gua̱th in nyuoth jɛ ɛn ɣöö jiɛnɛ kä lëy cuɛ wä kä naath kɛ tukdɛ.
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.
Kɛ gör ŋäcä min pay tuɔɔk kɛ gua̱th ti̱ ŋuan kɛ jɛn ja̱a̱l in kɛ juey ɛmɛ kɛ pɛ̈th ci kɛnɛ diw ɛn ɣöö te kɛ ley tin lëth ti̱ bɛ̈cbɛ̈ɛ̈c tin dap kɛ gaat ti ŋuan cet kɛ (Kuɔ̱ɔ̱n) de kɛn te juey beta-CoVs ni kä dieeth kiɛn mi cäät kɛ SARS-CoV-2.
These novel pangolin CoV genomes share 85-92% nucleotide sequence homology with SARS-CoV-2.
Ɛn juey ɛ pay tuɔkɛ ca jek rɛy CoV mat kɛn pek mi̱ 85-92% kɛnɛ SARS-CoV-2 kɛ ta̱a̱ in të kɛ kɛ puɔ̱ny ran.
However, they are equally closely related to RaTG13 with about 90% identity at the level of nucleotide sequence.
Kä i̱nɔ bä, cäät kɛ kɛ ta̱a̱ RaTG13 min te kɛ pëk mi̱ 90% ŋuiɛc kɛ jɛ kɛ ta̱a̱ in lät kɛ jɛ puɔ̱ɔ̱ny ran.
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.
Ca rɔ̱ duol kɛ gua̱th rɛw kä SARS-CoV-2 mi̱ cet kɛ juey in la jek kɛ puɔ̱ny jiath, kɛl in nyuak ti̱ ŋuan kɛ no̱o̱ŋ diɛn kɛ (RBD) ti̱ cäät kɛ SARS-CoV-2, kɛ 97.4% ti̱ ca ŋic kɛ ta̱a̱ in te kɛ pi̱ riɛm ran.
In stark contrast, the RBDs of SARS-CoV-2 and RaTG13 are more divergent, albeit a higher degree of sequence homology genome-wide.
Kɛ ta̱a̱ in dɔ̱ŋ, RBDs in te kä SARS-CoV-2 kɛnɛ RaTG13 gua̱c kɛ lɔ̱ŋ, cäŋni̱ min ci̱ ta̱a̱ diɛn wä nhial ɛ lɔ̱ŋ rɛy ɣɔaa.
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.
Kɛ gör ŋäcä min nhiam kɛ kui̱ jua̱th lëëni̱ tin lëth cua jɛ nyuoth ɛn ɣöö cɛ te juey mi ca jek kä cuäny, mi̱ cu jɛ nyuoth ɛn ɣöö dëë kɛn ca̱a̱t kɛnɛ 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.
Cua gör ŋäcä nɛmɛ nhɔk kɛ dup ti kɛnɛ buɔkni̱ ti̱ gööl ti̱ ŋuot kɛ mi̱ gör kɛ tha̱ŋ ŋäcä nɛmɛ ɛ mat kɛ ta̱a̱ in tekɛ juey in te kɛ 86.3% thi̱n ɛ lɔŋ.
We cannot exclude the possibility that pangolin is one of the intermediate animal hosts of SARS-CoV-2.
Ci̱ kɔn ley tin leth bä de ba̱ny raar ɛn ɣöö tekɛ rɛy lëëni̱ tin të kɛ SARS-CoV-2.
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.
K` 5ns b`, vn t`mv /thivlv x`c m5 thu]k vn f66 l2y dsaar tin leth tin tivn5 5 kvn tin jek kv SARS-CoV-2 kv ku5 d``k` min te kam SARS-CoV-2 kvnv SARS-CoV-2 min c``t kv 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.
Kv min d]x, SARS-CoV-2 kam divn kvnv RaTG13 civk v l]x v l2nyv kam SARS-CoV-2 kvnv SARS-CoV-2 min te k` l2y tin l2th kvnv beta-CoVs min c``t kv.
The evolutionary pathway of SARS-CoV-2 in bats, pangolins and other mammals remains to be established.
T11 du]p in te kv SARS-CoV-2 in te k` l5kl5kn5 kv l2y tin l2th tin tivn5 kvnv l2y tin k]x tin l2th ba jv dhil x1c.