atepeq/tico19 huggingface dataset:
For the general public in affected or potentially affected areas, it is highly suggested that everybody wash their hands with disinfectant soaps more often than usual, try to stay indoors for self-quarantine and limit contact with potentially infected individuals.
Ha ummatore fu ha nder wakereji je ɗon memmi mala je footi nyau man memmi, lati kanduɗum je ko moy fu lalitta juɗe mada be sabuluji ha wakati fu, ngaɗa dabare bana ko wowa ngam wondugo ha saare mum e usta kawtirol be yimɓe je footi ɗon ronda nyau man
Three feet is considered an appropriate distance for people to stay away from a patient.
Meeta be reeta sey wonda ha cakka ummatore ngam dayugo be nyauɗo.
These actions are effective methods to lower the risk of infection as well as prevent the spread of the virus.
Kuɗe ndu lati dabareji kanduɗum ngam ustugo raɓɓol nyau be darnugo yajjol viriis fu.
Although SARS-CoV-2 came as a new virus to the human world, its high homology to SARS-CoV as reported on 7 January 2020 should have caused high alert to China based on her deep memory of the SARS outbreak in 2003.
Ko to SARS-CoV-2 yotti bana viriis keese ha lesdi neɗɗo bo'o, nandugo maajum be SARS-CoV bana ɗon limti ha 7 Zaanviye 2020 maɓɓitan no hakkilo Cayna ngam ko salli be nyau SARS 2003.
However, not until 19 January 2020 did the director of the Center of Disease Control of Wuhan comfort the citizens by saying that the novel virus has low contagiousness and limited reproductivity from human to human and that it is not a problem to prevent and contain the disease.
Amma, na hidekko 19 Zaanviye 2020 je ɗowuwo Ɗowirde Aynol Nyau Wuhan ɗon no sembintina ummatore gal wi'ugo yo'o viriis je keese raɓɓata jur e tusnata jur diga neɗɗo ha neɗɗo e latay larula aynugo e natinugo nyau ndu.
This message remarkably relaxed the alarm of the public, especially when the entire country was preparing for the Spring Festival, and the critical time was missed to contain the disease at its minimal scale in Wuhan.
Matinol ndu memmi hakkilo ummatore, ɓurna bo'o be lesdi man fu ɗon no nder taskugo Spring Festival, e wakati je be mbiy nyau man timman ndu wonnay bana be hasdi no ha Wuhan.
The disease control agencies in China may take this hard lesson and make critical improvements in the future.
Ɗowirdeji je suklata do aynol nyau ha lesdi Cayna footi hakila hoore mako e laritan dabareji maɓɓe ha yeeso.
For example, these agencies should be (1) more careful when making public announcements as every word counts to citizens and can change their attitude and decisions; (2) more sensitive and reactive to unusual information from clinics rather than waiting for formal reports from doctors or officials; (3) more restrictive to contain a potential epidemic at its early stage rather than attempting to comfort the public; and (4) more often to issue targeted and effective drills to increase the public's awareness about epidemic diseases and to test and improve the response system of the society periodically.
Bana sappinol, ɗowirdeji ndu sey (1) hakkila jur to be ɗon ngaɗa matinolji ha ummatore ngam kala wolde fu ɗon mari daraja ha gite ɓi'i lesdi e footi sanja hakkilo maɓɓe be hasduji maɓɓe; (2) wonda larnama e jabbina law ha matinolji je yahay be lawol je suudi lekki do ndenugo batakeji ngomna ha lekkitaɓe mala arduɓe; (3) heɓɓa dabare darnugo nyau ha fuɗɗam man to wodi do sembintugo ummatore; e wurtuna dabareji kanduɗum ngam taskinugo hakkiloji ummatore do nyau je raɓɓatta e larta e mo'ittina jabbuji ummatore be wakati man.
The outbreak of COVID-19 caused by the novel virus SARS-CoV-2 started in the end of December 2019.
Nyau COOVID-19 je viriis keese je mbiyotto SARS-CoV-2 fuɗɗi no ha ragare Desambre 2019.
In less than two months, it has spread all over China and near 50 other countries globally at the time of this writing.
Ha hidekko leebi ɗiɗi, sankitti fu ha do lesdi Cayna e badi lesde 50 ha nder duniyaru fu ha wakati bindi ndu.
Since the virus is very similar to SARS-CoV and the symptoms are also similar between COVID-19 and SARS, the outbreak of COVID-19 has created a sense of SARS recurring.
Ngam viriis ndu ɗon naandi SARS-CoV e mandolji nyau woni bana je COVID-19 be SARS, nyau COVID-19 lati bana umminki SARS fahin.
However, there are some remarkable differences between COVID-19 and SARS, which are essential for containing the epidemic and treating the patients.
Amma, wodi feeretirolji ɗuɗɗum ha kunde COVID-19 be SARS, je lati kanduɗum ngam darnugo nyau ndu be hurgugo nyauɓe.
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.
COVID-19 ɗon memma ɓurna ndotti'en do sukkaɓe e ɓurna worɓe do rewɓe, e nyaɗugo be limtol mayde ɓuri ha ndotti'en do sukkaɓe.
SARS has higher mortality than COVID-19 (10.91% versus 1.44%).
SARS ɗon mbarda jur ɓuri COVID-19 (10.91% do 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.
Nyauɓe COVID-19 ɗo sallina viriis ko to ɓe sappinay mandolji nyau man tawon, amma nyauɓe SARS ɗon ngaɗa bana ni sey to ɓe ɗon walli timmi, ko ɗon wartira natinugo COVID-19 caɗɗungel do SARS.
This partially explains why SARS-CoV-2 spread much faster and broader than SARS-CoV.
Ndu ɗon sappina ha yakke feere koni SARS-CoV-2 ɗon dogga e ɗon sankitta ɓuri SARS-CoV.
The regular RNA assay for SARS-CoV-2 can be negative in some COVID-19 patients.
Lartol do RNA je tumtum do SARS-CoV-2 footi tawatakke ha nyauɓe COVID-19 feere.
On the other hand, cured patients can be positive for the virus again.
Ha wakere feere bo'o, nyauɓe je ɗon nyambitti footi mara viriis man fahin.
These findings dramatically increase the risk of virus spreading.
Sappinolji ndu besdi sankitol viriis ndu jur.
Given such rapid progress in research on COVID-19, several critical issues remain to be solved, as follows:
Ngam irin yahde nde ha nder teffol COVID-19, emmolji ɗuɗɗum sey heɓɓa jabbuji, bana:
Where did SARS-CoV-2 come from?
SARS-CoV-2 wangi gal toy?
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.
Ko to nandu ha 96 nder 100 tawama ha kunde SARS-CoV-2 be bilwili SARS- ɗiɗi je ɗon naandi COV, footay en yeeca yo'o SARS-CoV-2 wurti ha bilwili.
What animal was the intermediate species to transmit the virus from the original host, say bats, to humans?
Daaba toy woni suudu cakkare ha kunde daabaji je sallini viriis man diga aranol suudu, mbiyotto bilwili, ha neɗɗo na?
Without knowing answers to #1 and 2, we cannot efficiently cut the transmission, and the outbreak can relapse at any time.
Bila aandugo jabbuji ha #1 be 2, footay en ta'a raɓɓol, e footi nyau man fuɗɗita fahin ha wakati fu.
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?
Ko to teffolji mbiyotto molecular modeling be biochemical sappini yo'o SARS-CoV-2 ɗon naandi be ACE2, noy be fakatre viriis man nasti ha nder cellji lawol pofɗe e saanji mandolji nyau mada?
Does the virus also bind ACE2-expressing cells in other organs?
Viriis man bo'o naandi sappinol cellji ACE2 ha nder kujeji ɓaandu feere na?
Without clear answers to these questions, we cannot achieve fast and accurate diagnosis and effective treatment.
To wala jabbuji laɓɗɓum ha do emmolji ndu, footay e larta law e heɓɓa hurgol je fakatre sam.
How long will the epidemic last?
Nyau man neeɓan noy?
How is the virus genetically evolving during transmission among humans?
Noy viriis man yahdi diga fuɗɗam ha yakke raɓɓol neɗɗo?
Will it become a pandemic worldwide, die down like SARS or relapse periodically like the flu?
Latan no nyau je memmatta duniyaru fu na, majjitan bana SARS na mala ummitan be wakati bana ndamba na?
It is essential but may take some time to search for answers to the above and many other questions.
Lati kanduɗum ama footi hoosa wakati seeɗa ngam jaɓɓugo do emmolji je dow ndu be emmolji feere.
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.
Amma, be ko footi hoosatta, en wala dabare feere, sna darnugo nyau man bana ko en wawi be wakati e wartira jonde amin bana nane.
Zoonotic origins of human coronaviruses
Wangol koronaviriis neɗɗo gal daabaji
Mutation and adaptation have driven the co-evolution of coronaviruses (CoVs) and their hosts, including human beings, for thousands of years.
Sanjol be lautugo wadi yahidugo koronaviriis (CoV) be ko be ɗon jaɓɓa ndu, be ɓi adama, ha nder duɓɓi ujinere do ujinere.
Before 2003, two human CoVs (HCoVs) were known to cause mild illness, such as common cold.
Hideko 2003, CoV ji neɗɗo (HCoVs) ɗiɗi tawotto je ɗon aandin ɗon hokka nyau je nyaɗay jur, bana ndamba meere.
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.
Nyauji je larni larulaji nder pofɗe (SARS) be nyau pofɗe Cakkare Funaange (MERS) saanji hoore mum e sappini noy kuje man ɗon halli masitin.
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.
Wangol SARS-CoV-2 ha cakkare Cayna ha ragare hittande 2019 yarɓi CoV ji ngam jayna fahin e hilni amin be raɓɓol maajum je ɗon nyaɗi amma ɓuray mbardugo do miko mako SARS-CoV.
HCoV infection is a zoonosis and understanding the zoonotic origins of HCoVs would serve us well.
Nyau HCoV ɗon wanga gal daabaji e fammugo fuɗorde ko wangi gal daabaji HCoVs footi naffa amin bo'o.
Most HCoVs originated from bats where they are non-pathogenic.
Ɓurna HCoV ji wurti ha bilwili e ɓe wonay no nyaɗum tawon.
The intermediate reservoir hosts of some HCoVs are also known.
Cuuɗi je cakkare HCoV ji feere aandotto bo'o.
Identifying the animal hosts has direct implications in the prevention of human diseases.
Maandugo daabaji je lati bana cuuɗi ɗon mari naffuda ngam aandugo heɓɓa neɗɗo famma noy o aynatta hoore maɗa.
Investigating CoV-host interactions in animals might also derive important insight on CoV pathogenesis in humans.
Lartugo gikkuji CoV ha nder daabaji ɗon aandina noy fuɗɗam CoV ndu ɗon yahda ha neɗɗo bo'o.
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.
Ha nder lartol ndu, min ɗon sappina ekkitol do ko en aandi do HCoV ji joowey e ɗiɗi je en aandi, e en ngewtan do tariyaji maɓɓe be daabaji je be wurti ha ton e raɓɓol ha kunde maɓɓe.
Importantly, we compare and contrast the different HCoVs from a perspective of virus evolution and genome recombination.
Kanduɗum bo'o, min ɗon foonda e larta feeretirolji ha kunde HCoV ji do yahde viriis be hawtirde genome.
The current CoV disease 2019 (COVID-19) epidemic is discussed in this context.
Nyau CoV 2019 (COVID-19)je jonta ndu lartama ha nder ekkitol ndu.
In addition, the requirements for successful host switches and the implications of virus evolution on disease severity are also highlighted.
Ha ɓesdugo, en ɗon limta do ko ɗon waɗa viriisji ndu ɗon saanja ɓaandu ha nder suudu feere-feere e nyaɗugo maɓɓe nder yahde nyau maɓɓe.
Coronaviruses (CoVs) belong to the family Coronaviridae, which comprises a group of enveloped, positive-sensed, single-stranded RNA viruses.
Koronaviriis (CoV) ɗon nder limgal Coronaviridae, je ɗon larni geeɓe viriisji je ɗon sudi, je ɗon positive, be RNA be kosngal gooto.
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.
Irin viriisji je ɗon jaɓɓita genome je ɓuri maunugo je mari kilobase 26 ha 32 ha kunde viriis RNA mbiyottoo "CoV" ngam ɓe ɗon naandi maateleewol to be wati ɗum ha nder mikroskop.
Structurally, CoVs have non-segmented genomes that share a similar organization.
Gal larugo tagle ndu, CoV ji maray genomeji je ɗon ta'i je ɗon mari tagle gooto.
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.
Deydey ɗiɗi ha nder genome tati ɗon mari ɓaandu ɗiɗi je maungel e ɗon yajji ngam jaangugo (ORF1a be ORF1b), je ɗon lorni do pp1a be pp1ab replicase polyproteinji.
The polyproteins are further processed to generate 16 non-structural proteins, designated nsp1~16.
Polyproteinji latan huwidotto fahin ngam heɓɓugo proteinji je wala tagle 16, je mbiyotto nsp1~16.
The remaining portion of the genome contains ORFs for the structural proteins, including spike (S), envelope (E), membrane (M) and nucleoprotein (N).
Luttuɗum ta'irde genome ɗon mari ORF ji ngam tagle proteinji, be hoore (S), laaral (E), ɓaandu (M) be nucleoprotein (N).
A number of lineage-specific accessory proteins are also encoded by different lineages of CoVs.
Wodi lambaji protein je ɗon yahida be asli man ɗon mari bo'o lamba asli CoV ji feere-feere.
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).
Do feeretirol ha ta'irdeji protein, CoV ji footi nasta nder geeɓeji nay (alpha-CoV, beta-CoV, gamma-CoV be delta-CoV), ha kunde man geeɓe beta-CoV ɗon mari ɓurna CoV ji e kanjum bo'o ɗon mari ta'irdeji asngol nay (A, B, C be 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.
Sappinolji phylogenetic hollini yo'o bilwili be nyaamoobe lati bana aranol ɓurna suudu CoV ji-alpha be CoV ji-beta, e coolli lati aranol suudu CoV ji-gamma be CoV ji-delta.
For thousands of years, CoVs have constantly crossed species barriers and some have emerged as important human pathogens.
Duɓɓi ujeneji nay, CoV ji salli diga daaba gooto ha feere-feere e feere'en bo'o lati gilɗi je ɗon nyawa ɓaandu neɗɗo.
To date, seven human CoVs (HCoVs) are known.
Ha wakati nde, wodi CoV ji neɗɗo (HCoV ji) joowey eɗiɗi je aandotto.
Among them HCoV-229E and HCoV-NL63 are alpha-CoVs.
Ha kunde maɓɓe HCoV-229E be HCoV-NL63 woni alpha-CoV ji.
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.
Luttudum beta-CoV ji je joowey feere lati HCoV-OC43, HCoV-HKU1, koronaviriis je ɗon hokka nyau ɓernde je nyaɗum (SARS-CoV), nyau koronaviriis pofɗe Cakkare Funaange (MERS-CoV) be 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 be HCoV-NL63 ɓurna ɗon ndokka mandolji nyau deydey bana peewol je tumtum e/mala caarol.
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.
Amma, SARS-CoV, MERS-CoV be SARS-CoV-2 je keese je be tawi ɗon nyawa yimɓe masin, e ɗon ndokka nyau lawol pofɗe je les ha ɓurna nyauɓe je ɗon mari sa'a maungel ngam naangugo nyau pofɗe je ɗon nyaɗi masitin (ARDS) be mandoolji je larnay fuffu tan.
The first HCoV-229E strain, B814, was isolated from the nasal discharge of patients with common cold in mid-1960s.
Aranol gilɗi HCoV-229E, B814, tawama ha nder ndamba nyauɓe je ɗon no mari ndamba je en aandi ɗo gal hittande 1960.
Since then, more knowledge was accumulated through extensive studies on HCoV-229E and HCoV-OC43, both of which cause self-limiting symptoms.
Diga nden, aandalji jur mofti gal jaangirdeji ɗuɗɗum do HCoV-229E be HCoV-OC43, ɗiɗi fu ɗon sappina matinolji nyau je ɗon dara feere mum.
Indeed, the concept had been widely accepted that infection with HCoVs is generally harmless until the outbreak of SARS.
Fakat, wolde ndu yimɓe jaɓɓi yo'o nyau be HCoV wonay nyadungel hideko fuɗɗam nyau 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%.
Nyau SARS wangi ha 2003 e lati gooto cakka nyauji je ɓuri torrugo ha tariya duniyaru, je raɓɓi yimɓe 8 000 be limtol mayde je ɗon ha fatude 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.
Duɓɓi sappo ha bawo man, nyau pofɗe Cakkare Funaange (MERS) lati bana nyau je timmatakke ha do Cakkare lesdi Arabiya be raɓɓol ndego-ndego ha luttuɗum duniyaru.
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.
HCoV 2019 je keese (2019-nCoV), je innde majum saanjotto do SARS-CoV-2, on lati gilɗi nyau koronaviriis 2019 (COVID-19), je mbardi yimɓe waɗan 3 100 e raɓɓi yimɓe ɓuri 91 000 ha 3 Maars 2020.
The alarm has been ringing and the world has to prepare for the coming pandemic of SARS-CoV-2.
Wodi matinol maungel e duniyaru sey taska ngam nyau SARS-CoV-2 je warata yeeso.
All seven HCoVs have a zoonotic origin from bats, mice or domestic animals.
HCoV fu ummi fu maɓɓe ha bilwili, doombi be daabaji saare.
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.
Sappinolji jur ɗon mballa fammugo yo'o HCoV ummi gal bilwili, ha ton viriis saanji ɓaandu maɓɓe e hallay sam amma ɗon sappina ɗaadolji feere-feere.
The COVID-19 epidemic has presented enormous medical, scientific, social and moral challenges to China and the world.
Nyau COVID-19 sappini saɗirmaji jur ha lekkitoɓe, teffoɓe, ummatore, ngaandi ha Cayna be duniyaru fu.
Tracing the zoonotic origins of HCoVs provides a framework to understand the natural history, driving force and restriction factors of species jumping.
Lartugo asngol gilɗi HCoV ɗon ndokka mandirɗum fammugo tariya ndu, ko ngaɗi ɗum be ko footi waɗa saanja ɓaandu maɗa.
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.
Ndu footi sappina lawol mala lattina teffol suudu aranool, ɗiɗaɓool gilɗi ndu be daaba je lati bana suudu (cuuɗi) SARS-CoV-2 kooyeɗum be dabare aynol nyau je footi raɓɓa yimɓe.
In this review we present an overview of the zoonotic origins, interspecies transmission and pathogenesis of HCoVs.
Ha nder batakewol ndu lartol je wangol gal daabaji, raɓɓol ha kunde geeɓeji be fuɗɗam gilɗi HCoV.
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.
Ɓurna fu, min ɗon sappina e ɗon ngewta do wolde je baabiraɓe viriisji HCoV lati bana footay nyawina ha nder cuuɗi maɓɓe je aranol amma nyawan goɗɗo to salli gal daabaji feere ha suudu keese.
We also review the trend of HCoV evolution in which the increase in transmissibility often comes with the decrease in pathogenicity.
Min ɗon larta bo'o yahde HCoV je raɓɓol nyau ndu ɗon wanga be lessugo ɗaaɗol gilɗi ndi.
The outcome of the ongoing SARS-CoV-2 outbreak is also discussed in this context.
Ɓe tawi yo'o nyau SARS-CoV je ɗon yahida ndu wonan lartama ha do.
Animal CoVs have been known since late 1930s.
CoV daabaji tawotta diga hittande 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.
Hidekko aranol wurtinugo gilɗi HCoV-29E B814 ha seera nder ndamba nyauɓe je raɓɓi ndamba je en aandi, CoV ji feere-feere ha nder daabaji ɗuɗɗum je ɗon no mari nyau bana paula, doomru, naagge, gaduuru, patuuru be raawandu.
In the past decades, seven HCoVs have been identified.
Ha nder duɓɓi sappo do sappo je sallingo, ɓe tawi HCoV ji joowey e ɗiɗi.
A brief summary of the history of HCoV discovery in chronological order (Table ​1) would be informative and instructive.
Wodi tariya tawol HCoV ji ɗon limti be wakati e hittande man (Tabaal 1) je footi naffa be matinolji e ekkitolji.
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.
Aranol gilɗi HCoV-229 tawama ha aranol nder lawol pofde nyauɓe je ɗon no mari nyau lawol pofɗe maɓɓe je dow ha hittande 1966, e saanji ɓaandu mako e mawni ha nder didol cell fuffu WI-38.
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.
Nyauɓe je ɗon mari HCoV-229E ɗon no mari sappinolji nyau je ɗon naandi je ndamba, be paabooje, ɗislol, bilare, daande jorɗum, be wulol ɓaandu e sondaru ha kunde nyauɓe 10 ha 20%.
Later in 1967, HCoV-OC43 was isolated from organ culture and subsequent serial passage in brains of suckling mice.
Ha ɓawo man gal 1967, be wurtini HCoV-OC43 ha seera lartol kujeji ndu be lamba sallugo ngu ha nder ngaandi doombi je ɗon musina.
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.
Maandolji nyau HCoV-OC43 lati bana ɗon naandi be je feere'en je wangi gal HCoV-229E, je mandolji man don naandi be viriisji nyau lawol pofɗe feere bana viriisji A influenza be viriisji ndamba.
Both HCoV-229E and HCoV-OC43 are distributed globally, and they tend to be predominantly transmitted during the season of winter in temperate climate.
Ɗidi fu HCoV-229E be HCoV-OC43 ɗon sankitti ha duniyaru fu, e ɓe ɗon bana ɗon raɓɓa gal dabunde winter ha wakere je wakati ɗon boɗɗe.
Generally, the incubation time of these two viruses is less than one week, followed by an approximately 2-week illness.
Ɓurna fu, wakati wangugo viriisji yottata asawere woore, tokkiti ba nyau ha nder asaweji 2.
According to a human volunteer study, healthy individuals infected with HCoV-229E developed mild common cold.
Bana ekkitol yimɓe feere holli, yimɓe je ɗon jam je jaɓɓi hoosugo HCoV-229E ha nder ɓaandu maɓɓe nangi ndamba je meere.
Only a few immunocompromised patients exhibited severe lower respiratory tract infection.
Sna nyauɓe seeɗa je fadooɓe ɓaandu maɓɓe sattay sappini nyau lawol pofɗe je les je nyaɗungel.
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, je ewnotto bo'o "atypical pneumonia", lati aranool nyau je HCoV on hokki ha nder tariya ummatore e gilɗi etiologic ndu woni SARS-CoV, tataabre HCov je tawama.
The first case of SARS can be traced back to late 2002 in Guangdong Province of China.
Aranol nyau SARS footi lorotto ha 2002 ha Lamorde Guangdong ha Cayna.
The SARS epidemic resulted in 8,096 reported cases with 774 deaths, spreading across many countries and continents.
Nyau SARS raɓɓi mbiyotto nyimɓe 8 096 be 774 maynama, je ɗon sankitti ha nder lesɗe e duniyaru fu.
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.
Ha ɓawo ko ɗon sankitta law, ɗon sappini yo'o kala nyauɗo footi wurtina nyauji feere je seera ɗiɗi, be wakati wangugo ha kunde balɗe 4 be 7 e limgal viriisji je ɓuri maunugo wangan ha ɓawo balɗe 10 nyau ndu.
Patients infected with SARS-CoV initially present with myalgia, headache, fever, malaise and chills, followed by dyspnea, cough and respiratory distress as late symptoms.
Nyauɓe je naangi SARS-CoV ɗon sappina tawon, nawnol daande, paaɓooje, wullugo ɓaandu, diwuunol be peewol, tokkiti be larula be fuffugo, sondaru, saɗirma nder pofɗe bana ragare mandolji.
Lymphopenia, deranged liver function tests, and elevated creatine kinase are common laboratory abnormalities of SARS.
Lymphopeniya, sargi lartolji kugal hengre, e creatine kinase lati bana ko ɗon sarga lartolji SARS ha nder suudu lartol.
Diffuse alveolar damage, epithelial cell proliferation and an increase of macrophages are also observed in SARS patients.
Huudure feere nder alveolji, dimbol cell epitheliya be ɓesdol macrophageji tawama ha nyauɓe SARS.
Approximately 20-30% of patients subsequently require intensive care and mechanical ventilation.
Ɓadi 20 ha 30% nyauɓe ɗon mari haaje suklare do maɓɓe jur e sey fuffu be ordooji feere.
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.
Ɓesdugo ha lawol pofɗe je don usti, labbi ɓaandu feere bana tetekki, fufu be hengre footi wona raɓɓanga to nyau man ɓesdi, tokkiti ha wakati feere be duluru citokin, je footi mbara nyauɓe je ɓaandu maɓɓe maray sembe.
The virus was first isolated from the open lung biopsy of a relative of the index patient who travelled to Hong Kong from Guangzhou.
Viriis lati sigowo ha seera aranool man ha biopsy fuffu baabirawo nyauɗo feere je waɗi jaahangal ha Hong Kong Guangzhou.
Since then, tremendous efforts have been dedicated to HCoV research.
Diga nden, dabareji duɗɗum ngaɗama ngam teffol HCoV.
HCoV-NL63 was isolated from a 7-month-old child from the Netherlands during late 2004.
HCoV-NL63 lati sigowo ha seera ha ɓingel duɓɓi 7 feere je ummi Netherland ha ragare hittande 2004.
It was initially found to be prevalent in young children, the elderly and immunocompromised patients with respiratory illnesses.
Ha aranool man tawama yo'o bana ɓuri wangugo ha ɓikkon pamarron, ndotti'en be nyauɓe be nyauji pofɗe je fadooɓe ɓaandu maɓɓe maray sembe.
Presentation of coryza, conjunctivitis, fever, and bronchiolitis is common in the disease caused by HCoV-NL63.
Sappinol coryza, nawol gite, wullugo ɓaandu, be bronchiolitis ɗon woni tum ha nder nyau je 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.
Wodi jaangirde feere ɗon sappina wurtinol irin viriis man ha seera gal leekku kine ha ɓingel gorgel pamarron lebbi 8 je ɗon no mari pneumoniya ha Netherland.
Although it was identified in Netherlands, it is actually distributed globally.
Ko to tawama no ha Netherland ma, jonta kam ɗon sankitti ha nder duniyaru fu.
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.
Ɗon sappini yo'o HCoV-NL63 ɗon limma ɓadi 4.7% nyauji pofɗe je aanduɗo, e raɓɓol man je ɓuri nyaɗugo ndi ɗon salla ha summer, spring be winter.
HCoV-NL63 is associated with obstructive laryngitis, also known as croup.
HCoV-NL63 ɗon hawti be ngeldaande je ɗon maɓɓa daande, je mbiyotto croup.
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.
Ha hittande ndu, HCoV-HKU1 watotto ha seera ha ndotti feere je ɗon no mari duɓɓi 71 je nasti no ha suudu lekki ngam pneumoniya be bronchiolitis ha Hong Kong.
Besides community-acquired pneumonia and bronchiolitis, HCoV-HKU1 was reported to be associated with acute asthmatic exacerbation.
Ɓesdugo ha nyau peewol be sondaru, HCoV-HKU1 mbiyotto ɗon yahida be nyau dule je ɗon halli.
Similar to HCoV-NL63, HCoV-229E and HCoV-OC43, HCoV-HKU1 was found worldwide, causing mild respiratory diseases.
Kalkal be HCoV-NL63, HCoV-229E be HCoV-OC43, HCoV-HKU1 tawamma ha nder duniyaru fu, e ɗon hokka nyauji pofɗe.
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.
HCoV ji je raɓɓatta ha kunde ummatore ndu ɗon yahida timmi be ɓaandu neɗɗo e ɓurna fu saanjata ngam ha hokka nyauji feere je ɗon nyaɗungel, ko to wodi larulaji salli e en aandi bo'o ujaji ndu bana ha nder geeɓe HCoV-NL63 feere je caadum wanga, je be mbiy neeɓay ɗo ɗon hokka nyau lawol pofɓe je les ha Cayna.
Generally, when these HCoVs acquire the abilities to transmit efficiently and to maintain themselves continuously within humans, they also become less virulent or pathogenic.
Ɓurna fu, to irin HCoV ji hebti dabareji sallinugo boɗɗum e jogga hoore maɓɓe ha nder ɓaandu neɗɗo, be latan fu nyaɗungel mala sappina mandolji nyau.
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 watotto ha seera aranool man ha 2012 ha fuffu nyau feere je ɗon no mari duɓɓi 60 e je heɓɓi no pneumoniya je nyaɗungel be nyau ɓooye ha Lesdi Arabiya.
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.
Nyauɓe je suudu lartol wi'i be fakatre woni kanjuum ummi ha Cakkare Funaange, nyauɓe je ummi ha lesdi feere be raɓɓol seera ha wondugo ha baabal gooto matinama ha lesɗe Erop be Tunisiya.
Another secondary outbreak occurred in South Korea in 2015 with 186 confirmed cases.
Raɓɓol feere je ɗiɗabre wangi ha Korea je Fombina ha 2015 be nyauɓe 186.
Clinical manifestations of MERS resemble those of SARS, characterized by progressive acute pneumonia.
Mandolji nyau MERS ɗon naandi je SARS, je ɗon yahida be pneumoniya nyaɗungel je ɗon besda tum.
Unlike SARS, many patients with MERS also developed acute renal failure, which is thus far unique for MERS among HCoV-caused diseases.
Feere be SARS, nyauɓe ɗuɗɗum je ɗon mari MERS bo'o ɗon sappina nyau ɓooye je nyaɗum, je lati feerejo ha MERS ha cakka nyauji je HCoV ɗon hokka.
More than 30% of patients present with gastrointestinal symptoms, such as diarrhea and vomiting.
Ɓuri 30% nyauɓe ɗon sappina mandolji nyau reedu be tettekki, bana caarol be tuttol.
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.
Diga 14 Feviiriye 2020, ɓuri nyauɓe 2500 je cuddi teffol aandititti je ɗon no mari limtol mayde ha gaɗɗa 34.4%, ndu latini MERS-CoV gotto cakka viriisji je ɓuri nyaɗugo ha nder tatiya neɗɗo.
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.
Diga cakkare ha ragare lewru Desambre, sammere pneumoniya ha nyauɓe to bana lortotto ɗon aandin bana yahidatta be nyau SARS-CoV-2 tawama ha Wuhan, Lamorde Hubei, Cayna.
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.
Geeɓe Duniyaru do Jam Ɓaandu matini yo'o nyau je ɗon torra lawol pofɗe je les ngu je SARS-CoV-2 wadi lati bana Jaawal Jam Ɓaandu Ummatore ha do Lesdi e ewni nyau man COVID-19.
As of March 3, 2020, 90,053 cases have been confirmed worldwide, with a crude case fatality of 3.4%.
Diga nyalade 3 lewru Maars 2020, nyauɓe 90 053 tawama ha nder duniyaru fu, be limtol mayde 3.4 nder 100.
Notably, the case fatality in Hubei, China is 4.2%, whereas the one outside of it is 1.2%.
Ɓurna fu, limtol mayde ha Hubei, Cayna woni 4.2%, amma je yaasi man woni 1.2%.
SARS-CoV-2 causes severe respiratory infection like SARS-CoV and MERS-CoV, presented as fever, cough and dyspnea.
SARS-CoV-2 ɗon hokka nyau pofɗe je nyadungel bana SARS-CoV be MERS-CoV, sappine wullol ɓaandu, sondaru be saɗirma ngam fuffugo.
Diarrhea is also seen in some patients.
Caarol bo'o ɗon matittiri ha nyauɓe feere.
Pneumonia is one of the most severe symptoms and can progress rapidly to acute respiratory distress syndrome.
Pneumoniya woni bana matinolji nyau je ɓuri nyaɗugo e footi lata law bana nyau pofɗe je nyaɗungel.
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.
Ko to SARS-CoV be SARS-CoV-2 ɗon naandi ngam ta'irde nucleotide maɓɓe naandotto ha 82%, ɓe samman ha asli feere-feere ha nder ɗaaɗol maɓɓe.
SARS-CoV-2 is apparently less pathogenic but more transmissible compared to SARS-CoV and MERS-CoV.
SARS-CoV-2 lati bana nyaday jur amma ɓuri raɓɓugo do SARS-CoV be MERS-CoV.
Asymptomatic subjects infected with SARS-CoV-2 have been reported and might contribute to its rapid spreading around the world.
Yimɓe je ɗon mari SARS-CoV-2 amma sappinay mandolji nyau tawotto e footi wonda kaanjum on waɗi nyau man ɗon dogga ha nder duniyaru.
Comparing and contrasting SARS-CoV-2 with the other six HCoVs reveal similarities and differences of great interest.
Foondugo e lartugo SARS-CoV-2 be HCoV ji joowey e go'o feere ɗon sappina naandooje be feeretirolje je ɗon ewna hakkilo.
First, the incubation period and the duration of the course of HCoV disease are very similar.
Aranol, wakati wangol be neɓɓugo nyau HCoV ɗon naandi fu.
In this regard, SARS-CoV-2 follows the general trend of the other six HCoVs.
Nden kadi, SARS-CoV-2 ɗon tokkita yahde HCoV ji fu.
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).
Ɗiɗaɓool, nyaɗugo mandolji nyau COVID-19 ɗon joɗɗi ha kunde SARS-CoV be HCoV ji nay je ɗon raɓɓa ummatore (bana HCoV-229E, HCoV-OC43, HCoV-HKU1 be 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.
Ha wakere feere, nyau SARS-CoV-2 ɗon sappina mandolji je tawama ɓurna ha yakke nyau HCoV je raɓɓotto gal HCoV be sappinol mandolji je feere, deydey mala woda sam.
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.
Ha wakkere feere bo'o, wodi geeɗe pamarron nyauɓe COVID-19 footi bo'o tawama bana ha nder nyau SARS-CoV, ko to limtol ɗon lessi seeɗa bo'o.
Third, the transmission of SARS-CoV-2 also shows interesting patterns characteristic of both community-acquired HCoVs and SARS-CoV.
Tataɓool, raɓɓol SARS-CoV-2 ɗon sappina mandolji boɗɗe je larni raɓɓol HCoV ji be SARS-CoV gal ummatore.
On one hand, the transmissibility of SARS-CoV-2 is at least as high as that of community-acquired HCoVs.
Ha yakke feere bo'o, raɓɓol SARS-CoV-2 footan be raɓɓol HCoV ji HCoV ji ha cakka ummatore.
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.
Ha yakke feere, sey lartotto fahin to raɓɓol SARS-CoV-2 ɗon lessina ha ɓawo to sallo ha neɗɗo bana ko larni SARS-CoV be MERS-CoV.
Finally, same as the other HCoVs, SARS-CoV-2 can be detected in fecal samples.
Ha ragare man, kalkal bana HCoV ji feere, SARS-CoV-2 footi tawama ha nder leekuji buuwe.
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.
To raɓɓol SARS-CoV-2 diga buuwe ha hunduko lati kanduɗum bana ko larni SARS-CoV bana wi'ugo sey larta ndu fahin ha nder jaangirdeji je warango.
It is also of particularly great interest to see whether SARS-CoV-2 might exhibit seasonality as in the cases of community-acquired HCoVs.
To SARS-CoV-2 footi wanga be wakati man bana ko larni HCoV ji je raɓɓatta ummatore feere.
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.
Be man fu, mandolji SARS-CoV-2 be raɓɓol ngu, mandolji ndu, be sankitol man ha je o salli ha nder ɓaandu neɗɗo naffan ngam famtugo ko footi salla be nyau COVID-19 je jonta.
All four community-acquired HCoVs causing mild symptoms have been well adapted to humans.
HCoV ji nay fu je ɗon raɓɓa gal ummatore je ɗon wurtina mandolji je ɗon yahida boɗɗum be ɓaandu neɗɗo.
From another perspective, it might also be true that humans have been well adapted to these four HCoVs.
Gal wakkere feere bo'o, footi wona gonga yo'o ɓaali neɗɗo wawi timmi be HCoV ji ndu fu.
In other words, both could be the survivors of ancient HCoV pandemics.
Bana wi'ugo yo'o, ɗiɗi fu footi wonda kisooɓe nyau HCoV je aran.
HCoVs that cause severe diseases in humans and humans who developed severe HCoV diseases have been eliminated.
HCoV ji je ɗon hokka nyauji je nyaɗungel ha neɗɗo be yimɓe je mari no nyauji HCoV aran nastay nder limgal.
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.
Ha ndu salla, HCoV ji sey fufta ha nder neɗɗo ngam deydey sey jarfa hawtirde saanjolji je yahidata sam be ujaji ustol.
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.
Bana ni, to nyau SARS-CoV-2 neɓɓi e bana ni yimɓe je ɗon raɓɓi, sa'a je nyau man yahidatan be ɓaandu neɗɗo.
If it adapts well, its transmission in humans would be difficult to stop by quarantine or other infection control measures.
To yahidi boɗɗum, raɓɓol ngol ha neɓɓo footi wona caɗɗum ngam darnugo wondugo seera mala dabareji aynol nyau feere.
For many years, the four community-acquired CoVs circulate in human populations, triggering common cold in immunocompetent subjects.
Wadi duɓɓi jur, CoV ji je raɓɓatta ummatore ɗon tara ha cakka ummatore, e ɗon hokka ndamba meere ha be'en je ɓaandu maɓɓe ɗon mari fadooɓe je ɗon be sembe.
These viruses do not need an animal reservoir.
Viriisji ndu maray haaje suudu ha daaba.
In contrast, highly pathogenic SARS-CoV and MERS-CoV have not adapted to humans well and their transmission within humans cannot be sustained.
Sna, SARS-CoV be MERS-CoV je ɗon nyaɗungel masitin yahiday boɗɗum be ɓaandu neɗɗo tawon e raɓɓol maɓɓe ha cakka ummatore footay neeɓa.
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.
Ɓe mari haaje joggugo e sankittugo ha nder cuuɗi daabaji maɓɓe e teffa dabare yahugo ha gaɗɗa neɗɗo, temma gal suudu mala cuuɗi ha mo je sendatta nyau ndu.
SARS-CoV-2 has features that are similar to both SARS-CoV/MERS-CoV and the four community-acquired HCoVs.
SARS-CoV-2 ɗon mari mandolji je ɗon naandi je SARS-CoV/MERS-CoV be HCoV ji je nay je raɓɓatta ummatore.
It is highly transmissible like community-acquired HCoVs, at least for the time being.
Ɗon raɓɓa jur bana HCoV ji je raɓɓata ummatore, ha wakati nde tawon bana wi'ugo.
However, it is more pathogenic than community-acquired HCoVs and less pathogenic than SARS-CoV or MERS-CoV.
Amma, ɓuri nyaɗugo do HCoV ji je rabbatta ha nder ummatore e lessi nyaɗugo do SARS-CoV mala 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.
Sey larta fahin to footi yahida be boɗɗum ha neɗɗo e tara ha kunde ummatore bila keɓɓugo suudu mala daaba je footi siga ndu ha nder ɓaandu mada.
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.
Hidekko en ngewta do wangugo HCoV ji gal daabaji, naffan amin masin ngewtugo do ko woni HCoV ji, cuuɗi maɓɓe je aranool, je cakkare e je raɓɓugo.
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.
Daaba lati bana suudu yahde HCoV to o ɗon sigga irin gildi je footi maama mako ɗon naandi masin ha wakere ta'irde nucleotide ha nder ɓaandu mako.
The ancestral virus is usually well adapted and non-pathogenic in this host.
Maama viriis ɓurna ɗon yahida boɗɗum e nyaɗay sam ha nder suudu daada man.
Likewise, a reservoir host harbours HCoV continuously and for long term.
Bana ni bo'o, suudu siggoowo ɗon jogga HCoV ha tokkita e ha neɓɓa.
In both cases, the hosts are naturally infected and are the natural hosts of HCoV or its parental virus.
Ɗiɗi fu, daabaji je siggotto ndu ɗon mari gilɗi ndu ha nder ɓaandu maɓɓe e woni aranool cuuɗi HCoV ji mala maama maɓɓe.
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.
Amma, to HCoV nasti keese ha nder suudu je cakkare hidekko mala ha yakke nastirde ha neɗɗo, yahidatta boɗɗum be suudu je keese e ɓurna fu ɗon nyaɗi.
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.
Suudu je cakkare ndu footi wona bana ɗaaɗol raɓɓol diga daaba ha neɗɗo e ɗon huwa bana suudu raɓɓungel gal accugo viriisji ndu nufta nden sallina dum ha neɗɗo ngam yajjinugo raɓɓol ngel.
An HCoV can undergo a dead-end infection if it cannot sustain its transmission within the intermediate host.
HCoV footi timma feere mako to footay salla gal dabaji hideko yotta ha nder ɓaandu neɗɗo.
On the contrary, HCoVs can also adapt to the intermediate host and even establish long-term endemicity.
Nden bo'o, HCoV ji footi yahida be suudu je cakkare e footi raɓɓa be wakati ha nder duɓɓiji ɗuɗɗum.
In this case, the intermediate host becomes a natural reservoir host.
Nden kadi, suudu je cakkare latan daaba siggoorde je aranool.
Epidemiological data revealed retrospectively that the index case of SARS had a contact history with game animals.
Matinolji do nyau ndu sappini yo'o wodi kuje feere pamarron ha SARS je footitiri be daabaji ladde.
Subsequent seroprevalence investigations indicated that animal traders had a higher prevalence of anti-SARS-CoV IgG compared with that of the general population.
Teffolji do yonki viriis je tokkiti holli yo'o sippoɓe daabaji ɗon no mari limtol anti-SARS-CoV IgG to en foondi be je ummatore fu.
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.
Daabaji feere bana patuuru (Paguma larvata) be rawaandu feere bana doomruweela ha nder lumo daabaji lati aranool je rondi irin viriis SARS-CoV je ɗon naandi be SARS-CoV.
This was indirectly supported by the fact that no further SARS was reported after killing all civets in the markets.
Ndu ngam ɗon fadi ha seera gal ngewte je wi'atta yo'o wala SARS feere je ɓe matini ha ɓawo mbardol irin daabaji ndu fu da nder lumo.
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.
Amma, ɓe matini yo'o daabaji bana patuuru go'o je ladde mala ngeesaji je nastay lumo daabaji be gite rondaay no SARS-CoV man sam, ko ɗon holla yo'o footi irin patuuji man lati bana suudu cakkare je rondi gilɗi amma wonay suudu aranool SARS-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.
Bana wi'ugo, nde 80% daabaji feere-feere ha nder lumoji Guangzhou ɗon mari fadooɓe ɓaandu anti-SARS-CoV, footi bo'o daabaji pamarron feere lata bana cuɗɗi je cakkare raɓɓol SARS-CoV.
All of these appear to be dead-end hosts of SARS-CoV.
Ndu fu woni bana ragare cuɗɗi ha 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.
Teffol je tokki daaba je lati bana suudu aranool SARS-CoV sappini CoV je ɗon ɓadi be je bilwili feere, je mbiyotto bilwili CoV HKU3 (SARSr-Rh-BatCoV HKU3) je naandi be Rhinolophus, je tawama ha cakka bilwili feere ha lesdi Cayna.
These bats are positive for anti-SARS-CoV antibodies and genome sequence of SARSr-Rh-BatCoV HKU3.
Bilwili ndu ɗon mari fadooɓe ɓaandu je anti-SARS-CoV be ta'irde genome SARSr-Rh-BatCoV HKU3.
This and other bat CoVs share 88-92% nucleotide sequence homology with SARS-CoV.
CoV ji bilwili ndu be feere ɗon mari 88-92% naandu ta'irde nucleotide be SARS-CoV.
These studies have laid the foundation for the new concept that bats host emerging human pathogens.
Jaangirdeji lati mahol ngewte keese je bilwili ɗon mari mandolji je ummi ha neɗɗo.
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.
CoV ji duɗɗum je ɗon naandi SARS (SL-CoVs) manditto ha bilwili, amma wala gooto sna je mbiyotoo WIV1 footi siggotto ha seera ba viriis je ɗon nyeeɗa.
Human angiotensin converting enzyme 2 (ACE2) is known to be the receptor of SARS-CoV.
Neebam latinugo angiotensin 2 (ACE2) lati bana jabbowo SARS-CoV.
WIV1 derived from fecal sample of bats was demonstrated to use bat, civet and human ACE2 as receptor for cell entry.
WIV1 je wurti ha leeku buuwe bilwili ɗon holla bilwili, patuuru be ACE2 neɗɗo bana jaɓɓowo nastirde cell.
Intriguingly, sera of convalescent SARS patients were capable of neutralizing WIV1.
Fahin bo'o, iyamji nyauɓe SARS je ɗon be daama footi no natina WIV1.
Thus far, WIV1 represents the most closely related ancestor of SARS-CoV in bats, sharing 95% nucleotide sequence homology.
Nden kadi, WIV1 ɗon holla maama SARS-CoV je ɓuri ɓadugo ha nder bilwili, ɓe ɗon senda 95% ta'irde naandu nucleotide.
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.
Ko to naandu lati ɗuɗɗum ha kunde viriisji didi ndu, yimɓe ɓurni tammugo yo'o WIV1 wonnay maama cakkare viriis SARS-CoV e bilwili wonnay siggorde cakkare SARS-CoV.
Phylogenetic analysis clusters MERS-CoV to the same group as bat CoV-HKU4 and bat CoV-HKU5.
Lartol phylogenetic sammere MERS-CoV be irin geeɓe be bilwili CoV-HKU4 be bilwili CoV-HKU5.
Bat CoV-HKU4 and MERS-CoV utilize the same host receptor, dipeptidyl peptidase 4 (DPP4), for virus entry.
Bilwili CoV-HKU4 be MERS-CoV ɗon mari jaɓɓowo gooto, dipeptidyl peptidase 4 (DPP4), ngam nastirde viriis.
RNA-dependent RNA polymerase sequences of MERS-CoV are phylogenetically closer to counterparts in bat beta-CoVs identified from Europe and Africa.
Ta'irdeji polymerase RNA je RNA-dependent MERS-CoV ɗon naandi gal ɗaaɗol maɓɓe be ko ɓe tawi ha nder beta-CoV ji bilwili je maandi ha Erop be Afirika.
Up to now, no live MERS-CoV can be found in wild bats.
Ha jonta, wala MERS-CoV je ɗon nyeeɗa footi tawama ha nder bilwili.
MERS-CoV and its closest relative bat CoV-HKU25 share only 87% nucleotide sequence homology.
MERS-CoV be bilwili baabirawo maɗa CoV-HKU25 don mari 87% naandu ta'irde nucleotide maɓɓe.
Thus, bats might not be the immediate reservoir host of MERS-CoV.
Nden kadi, bilwili footay wona suudu cakkare ha MERS-CoV.