atepeq/tico19 huggingface dataset:
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.
Ha wakere feere bo'o, jaangirdeji ha Lesdi Caakare sappini yo'o ngeeloba ɗon mari gilɗi MERS-CoV je ɗon naatina kujeji jam ɓaandu, kalkal bana ngeeloba Lesdi Caakare je wangi ha nder lesdi Afirika ɗuɗɗum.
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 je ɗon nyeeɗa je ɗon naandi viriis je tawotto ha nder neɗɗo je ɓe wurtini seera ha leekuji ngeeloba, je ɗon sappina fihin yo'o ngeelobaji lati suudu jaɓɓowo MERS-CoV je gonga.
It is also noteworthy that generally mild symptoms but massive virus shedding were observed in camels experimentally infected with MERS-CoV.
Sey famma bo'o ɓurna mandolji nyau deydey ɗon wanga nattinol viriis jur maandama ha ngeelobaji je ɓe tuffini be MERS-CoV ngam lartol.
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.
Ngeelobaji je ɗon mari nyau ɗon wurtina viriisji ndu na gal lawol pofɗe tan amma gal lawol buuwe be hunduko, je lati bo'o lawol aranool ha wurtol viriis bilwili.
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.
Amma, ha jonta wodi emmolji feere ɗon ngam wodi geeɓeji MERS feere je ɗon aandi meeɗay footugo be ngeelobaji hidekko fuɗɗam mandol nyau, bana wi'ugo yo'o neɗɗo on sallini ɗum ha neɗɗo mala labbi raɓɓol aandakke be asngol daaba je ɗon jaɓɓitatta MERS-CoV aandakke.
SARS-CoV-2 shares 96.2% nucleotide homology with a bat CoV RaTG13 isolated from Rhinolophus affinis bats.
SARS-CoV-2 ɗon mari 96.2% naandu nucleotide be bilwili CoV RaTG13 je wurti seera gal bilwili Rhinolophus affinis.
As in the cases of SARS-CoV and MERS-CoV, the sequence divergence between SARS-CoV-2 and RaTG13 is too great to assign parental relationship.
Bana SARS-CoV be MERS-CoV, ta'irde feeretirol ha kunde SARS-CoV-2 be RaTG13 lati maungel ngam hoosugo ndu baabirawo maɗa.
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.
Bana wi'ugo, bilwili footay wona suudu mala cuuɗi aranool je SARS-CoV-2 sna to CoV ji je naandi je bilwili tawama ha yeeso.
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.
En tamman yo'o, daaba je footi wona suudu cakkare SARS-CoV-2 wonan ha kunde daabaji ladde je ɗon sippi mala hiirsi ha Lumo Daabaji Huanan, be ɗume ɓurna arandere nyauɓe COVID-19 ɗon larni, je footi holla yo'o raɓɓol ngu salli diga daaba ha neɗɗo.
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.
Jaangirdeji je keese ɗuɗɗum do ta'irdeji gilɗi ngu sappini yo'o wodi geeɓeji daabaji je pamarron je mbiyotto pangolin (Manis javanica) footi jogga gilɗi beta-CoV je lati bana SARS-CoV-2.
These novel pangolin CoV genomes share 85-92% nucleotide sequence homology with SARS-CoV-2.
CoV genomeji pangolin je keese ɗon mari 85-92% ta'irde nucleotide ɗon naandi be je SARS-CoV-2.
However, they are equally closely related to RaTG13 with about 90% identity at the level of nucleotide sequence.
Amma, ɓe ɗon ɓadi masitin be RaTG13 with be 90% naandu ha ta'irde nucleotide maɓɓe.
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.
Ɓe ɗon samma ha nder asli je ɗon naandi viriisji SARS-CoV-2-didi ha nder asngol maɓɓe, gooto don naandi gal jaɓɓowo kuje hawtirde (RBD) with SARS-CoV-2, be 97.4% ta'irde maandirɗum amino acid.
In stark contrast, the RBDs of SARS-CoV-2 and RaTG13 are more divergent, albeit a higher degree of sequence homology genome-wide.
Ko yahay bo'o, RBD ji SARS-CoV-2 be RaTG13 ɗon ɓuri feeretirigo, ko to ta'irde genome maɓɓe ɗon naandi jur bo'o.
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.
Ha nder jaangirde je arti do pangolinji je mari no nyau sappini contigji viriis ha nder leeku fuffu, je ɗon naandi be 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.
Jaangirde ndu hoosi dabareji kawtal ɗiɗi e yiggugo be jungo ngam wurtinugo ta'irde genome feere je ɗon mari deydey 86.3% juttol genome viriis.
We cannot exclude the possibility that pangolin is one of the intermediate animal hosts of SARS-CoV-2.
Footay en acca bo ekkitol je sappinata pangolin lati gooto ha cakka daabaji je woni suudu cakkare 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.
Amma, jonta kam wala sappinol je ɗon holla yo'o pangolin on woni suudu aranool SARS-CoV-2 ngam wodi feeretirol ta'irde ha kunde SARS-CoV-2 be beta-CoV SARS-CoV-2-pangolin.
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.
Ha ɓesdugo, dayuggo ha kunde SARS-CoV-2 be RaTG13 lati pamarron do je ha kunde SARS-CoV-2 be CoV jipangolin be beta-CoV ji SARS-CoV-2-pangolin.
The evolutionary pathway of SARS-CoV-2 in bats, pangolins and other mammals remains to be established.
Yahde SARS-CoV-2 ha nder bilwili, pangolinji be daabaji feere sey larta ndu fahin.
Whereas the highest sequence homology has been found in the RBDs between SARS-CoV-2 and pangolin, SARS-CoV-2-related beta-CoVs, SARS-CoV-2 and RaTG13 share the highest genome-wide sequence homology.
Bana ta'irde naandu je ɓuri tawama ha nder RBD ji ha kunde SARS-CoV-2 be pangolin, beta-CoV ji SARS-CoV-2, SARS-CoV-2 be RaTG13 ɗon mari naandu maungel ha ta'irde genome maɓɓe.
It is highly speculative that the high degree of similarity between the RBDs of pangolin SARS-CoV-2-related beta-CoVs and SARS-CoV-2 is driven by selectivity-mediated convergent evolution.
Yimɓe jur ɗon wolwa do naandu je ɗon jur ha kunde RBD ji beta-CoV ji pangolin SARS-CoV-2 be SARS-CoV-2 ɗon joɗɗi do suɓɓol ngam yahde hawtirde.
A counter-proposal is in favour of a recombination between a pangolin SARS-CoV-2-related beta-CoV and RaTG13 in the third wild animal species.
Wodi sappinol feere je yiɗi larta hawtirde ha kunde beta-CoV SARS-CoV-2 PANGOLIN be RaTG13 ha nder tataɓool asngol daaba.
As a driving force in evolution, recombination is widespread among beta-CoVs.
Bana sembe yahde, hawtirde ɗo sankitti ha kunde beta-CoV ji.
The jury is still out on the immediate zoonotic origin of SARS-CoV-2.
Wakili'en ɗon larita daaba je wadi SARS-CoV-2 ndu.
Besides the highly pathogenic HCoVs, the zoonotic origin of HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1 have also been studied.
Ha ɓesdare HCoV je ɗon nyaɗi masin, wangol HCoV-229E man gal daabaji, HCoV-OC43, HCoV-NL63 be HCoV-HKU1 lati jaanginama.
Phylogenetic evidence indicated that both HCoV-NL63 and HCoV-229E might have originated from bat CoVs, while the parental viruses of HCoV-OC43 and HCoV-HKU1 have been found in rodents.
Sappinol asngol holli yo'o ɗiɗi fu HCoV-NL63 be HCoV-229E footi wurti ha CoV ji bilwili, amma maama viriisji HCoV-OC43 be HCoV-HKU1 tawama ha nder nyamooɓe.
It has been reported that a bat CoV termed ARCoV.2 (Appalachian Ridge CoV) detected in North American tricolored bat displayed close relationship with HCoV-NL63.
Ɗon sappini yo'o CoV bilwili mbiyotto ARCoV.2 (Appalachian Ridge CoV) je tawama nder bilwili Woila America je ɗon mari didolji tati ɗon mari no naandu HCoV-NL63.
On the other hand, HCoV-229E was genetically related to another bat CoV, termed Hipposideros/GhanaKwam/19/2008, which was detected in Ghana, while camelids have also been suspected as its intermediate host.
Ha wakkere feere, ɗaaɗol HCoV-229E hawtama be CoV bilwili, je mbiyotto Hipposideros/GhanaKwam/19/2008, je tawama ha Ghana, e bo'o ngeelobaji hoccama bana suudu cakkare maɗa.
For clarity, the current knowledge on animal origins of known HCoVs is summarized in Figure ​1 and Table 2.
Ngam laɓɓinugo wolde, aandal je jonta do ɗaaɗol daaba je HCoV ji je ɗon aandin ɗon hawti ha nder Foto 1 be Tabaal 2.
Phylogenetic analysis has provided evidence for interspecies transmission events of HCoVs in the history.
Lartol ɗaadol holli sappinol do kuje je footi sallina HCoV ji ha kunde daaba be neɗɗo ha nder tariya.
When HCoV-OC43 crossed species to infect humans from domestic livestock around 1890, a pandemic of respiratory infection was recorded.
To HCoV-OC43 salli daabaji ha raɓɓa neɗɗo gal daabaji saare gal 1890, wodi no nyau pofɗe je ɗon wangi.
The interspecies transmission history of HCoV-229E is less clear.
Raɓɓol daaba-neɗɗo ha nder tariya HCoV-229E laɓɓay boɗɗum.
Bat alpha-CoVs closely related to HCoV-229E have been found.
Bilwili alpha-CoV ji je ɗon naandi jur be HCoV-229E tawama.
Between them there is an alpaca alpha-CoV.
Ha kunde maɓɓe wodi alpha-CoV alpaka feere.
Several lines of evidence support the transmission of virus from bats to humans directly.
Sappinolji duɗɗum ɗon sembintina ko be wi'i viriis man salli diga bilwili ha neɗɗo ciir.
First, humans but not alpacas might have contact with bats in a shared ecological niche.
Aranool, neɗɗo amma na alpakaji footi hawta be bilwili ha nder wakere jonde gooto.
Instead, humans have close contact with alpacas.
Sna non, yimɓe ɗon foota be alpakaji.
Second, HCoV-229E-related bat alpha-CoVs are diverse and non-pathogenic in bats, whereas alpaca alpha-CoV caused an outbreak of respiratory disease in infected animals.
Ɗiɗaɓool, alpha-CoV ji HCoV-229E ɗon waagi e maray mandolji nyau ha bilwili, amma alpha-CoV alpaka wangini nyau pofɗe ha daabaji je raɓɓi viriis ndu.
Finally, alpaca alpha-CoV has not been found in feral animals.
Timminool, alpha-CoV alpaka tawakke ha nder ɓaandu daabaji ladde.
Thus, the possibility cannot be excluded that alpacas obtain the HCoV-229E-related alpha-CoV from humans.
Nden, dabare footay wata ɗum ha seera je alpakaji keɓɓi alpha-CoV hcOv-229E ha neɗɗo.
In fact, bats are the direct source of human pathogenic viruses including rabies virus, Ebola virus, Nipah virus and Hendra virus.
Mbiyotto, bilwili on woni daarol viriisji je ɗon mari mandolji nyau ha neɗɗo be viriis rabies, viriis Ebola, viriis Nipah be viriis Hendra.
It is therefore not too surprising that bats might transmit HCoV-229E to humans directly.
Hilnatta fahin je bilwili footi wona ɓe'en je sallini HCoV-229e ha neɗɗo bila lawol feere.
Alternatively, whereas bat alpha-CoVs serve as the gene pool of HCoV-229E, alpacas and dromedary camels might serve as intermediate hosts that transmit viruses to humans, exactly as in the case of MERS-CoV.
Mala bo'o, bana alpha-CoV ji bilwili ɗon woni bana ɓundu gene HCoV-229E, alpakaji be ngeelobaji footi lata bana cuudi je cakkare je ɗon sallinaviriisji ha neɗɗo, bana ko don salli be MERS-CoV.
MERS-CoV serves as an excellent example of interspecies transmission from bats to dromedary camels and from dromedary camels to humans.
MERS-CoV lati bana sappinol kanduɗum ngam sallinol nyau diga bilwili ha ngeeloba e diga ngeeloba ha neɗɗo.
The evolutionary origin of MERS-CoV from bats is known at its initial identification and has also been strengthened by subsequent findings.
Ɗaadol yahde MERS-CoV diga bilwili ɗon aandin ha fuɗɗam mandirdum ndu e heɓɓi sembe gal sappinolji je tokkiti.
It is obvious that bats provide a rich pool of virus species for interspecies exchange of genetic fragments and interspecies transmission.
Lati gonga je bilwili lati bana ɓundu viriisji ngam sanjol ta'irdeji geneha kunde daadaji e sallinol ha neɗɗo.
Longevity, densely packed colonies, close social interaction and strong ability to fly are all favourable conditions for bats to be an ideal 'virus spreader'.
Juttol nyonki, hawtirde geeɓeji ha baabe gooto, wondugo ha wakkere yimɓe be dabare fiirugo do hendu lati kujeji je ɗon waɗa bilwili lati bana 'sankittowo viriis'.
On the other hand, MERS-CoV has been introduced to dromedary camels for decades.
Ha wakkere feere, MERS-CoV tuffama ha ɓaandu ngeelobaji ɓuran hittande sappo do sappo.
It is well adapted to these camels that have turned from an intermediate host to a stable and natural reservoir host.
Ɗon yahida boɗɗum be ngeelobaji je waylitti diga cakkere suudu ha siggorde aranool je ɗon joɗɗi.
MERS-CoV causes very mild disease and maintains a relatively low mutation rate in these animals.
MERS-CoV ɗon hokka nyau je nyaɗay jur e ɗon waɗa daabaji ndu wala saanjugo jur sam.
Its sporadic transmission to humans is an accident and humans remain a dead-end host of MERS-CoV as its transmission cannot be sustained.
Raɓɓol ngu je ɗon salla laugel ha neɗɗo woni bana larula e neɗɗo laatan bana ragare cuuɗi MERS-CoV ngam sallinol ndu footay neeɓa.
In contrast to the role of camels in the transmission of MERS-CoV, the role of pangolins, if there is any, in the transmission of SARS-CoV-2 is different.
Na bana kugal ngeelobaji ha nder sallinol MERS-CoV, kugal pangoliji, to wodi, ha nder sallinol SARS-CoV-2 don feerejo.
Particularly, pangolin beta-CoVs are highly pathogenic in pangolins.
Ɓurna, beta-CoV ji pangoljin don nyaɗi masitin be mandolji.
They might be a dead-end host for SARS-CoV-2-related beta-CoVs, similar to civets in the case of SARS-CoV.
Footi ɓe lata ragare cuuɗi ha beta-CoV ji SARS-CoV-2, bana patuuji be nyau SARS-CoV.
Several possibilities for interspecies transmission of SARS-CoV-2 from animals to humans have to be ruled in or ruled out in future studies.
Dabareji ɗuɗɗum ngam sallinol SARS-CoV-2 diga daabaji ha neɗɗo sey larta nder be yaasi ha jaangirdeji je warango.
First, bats could be the reservoir host of a SARS-CoV-2-related virus almost identical to SARS-CoV-2.
Aranol, bilwili footi wona suudu aranool viriis SARS-CoV-2 je ɗon naandi jur be SARS-CoV-2.
Humans might share the ecological niche with bats through butchering or coal mining.
Neɗɗo footi mara wakere jonde gootoo be bilwili gal hirsugo daabaji mala waasugo lesdi.
Second, pangolins could be one of intermediate amplifying host to which a SARS-CoV-2-related virus had been newly introduced.
Ɗidaɓool, pangolji footi wona suudu cakkare jaɓɓitol viriis SARS-CoV-2 je nasti neeɓay nder ekkitol.
Humans contract the virus through butchering and consumption of game meat.
Neɗɗo ɗon raɓɓa viriis gal hirsugo e nyammugo kusel daabaji ladde.
It is possible that many mammals including domestic animals are susceptible to SARS-CoV-2.
Footi yo'o daabaji duɗɗum be daabaji saare footi raɓɓa SARS-CoV-2.
A survey of domestic and wild animals for antibodies is warranted.
Teffol do daabaji saare be je ladde ngam fadooɓe ɓaandu ɗon mari baabal mako.
Third, as mentioned above, recombination and adaptation of SARS-CoV-2 might have occurred in a third species that has contact with both bats and pangolins.
Tataɓool, bana ɗon matini ha dow, hawtirde be lartol SARS-CoV-2 footi salli no ha tataɓool daaba je footitiri be ɗiɗi fu bilwili be pangolinji.
The search for the animal origins of SARS-CoV-2 is still on.
Teffol ɗaaɗol daabaji SARS-CoV-2 ɗon tokkiti.
Apart from different types of the animal hosts, three major factors on the viral side are also important in facilitating CoVs to cross species barriers.
Ha ɓawo dabaji je feere feere je ɗon jogga gilɗi ndu, woodi ujaji maungel tati do ko larni gilɗi lati kanduɗum nder latinugo CoV koyɗum.
First of all, their relatively high mutation rates in RNA replication.
Ama ha fuɗɗam man, ko en aandi kam ɓe ɗon sanja RNA maɓɓe laugel.
In comparison to other single-stranded RNA viruses, the estimated mutation rates of CoVs could be regarded as “moderate” to “high” with an average substitution rate being ~10-4 substitution per year per site 2, depending on the phase of CoV adaptation to novel hosts.
To en foondi be viriisji feere je ɗon mari kosɗe RNA gooto tan, limtol saanjolji CoV ji footi hoccama bana “deydey” ha “duɗɗum” be limtol saanjol je ɗon yaha diga ~10-4 ha nder hittande nder wakkere 2, do yahde lartol saanjol CoV ha cuuɗi keese.
CoVs have a proof-reading exoribonuclease, deletion of which results in exceedingly high mutability and attenuation or even inviability.
CoV ji ɗon mari jaangowo exoribonuclease, je to willi ni ɗon saanja dabajeri ɓesdol e ustol mala bo mayde maɗa.
Interestingly, the nucleotide analogue Remdesivir is known to suppress CoV replication through inhibition of this exoribonuclease and the RNA-dependent RNA polymerase.
Ko wooɗi fahin bo'o, ko mbiyotto nucleotid Remdesivir je ɗon nandi aandama yo'o naffan ngam willugo CoV gal illugo exoribonuclease ndu be RNA je wondi do RNA polymerase.
Remdesivir is one of most promising anti-SARS-CoV-2 agents to be tested in clinical trials.
Remdesivir woni gooto cakka kujeji anti-SARS-CoV-2 je footi larta ha yakke teffolji.
Nevertheless, mutation rates of CoVs are about a million times higher than those of their hosts.
Be man fu, limtol saanjol CoV ji ɓuri ɓe waɗan nde milionji do ɓe'en je cuuɗi maɓɓe.
In addition, mutation rate is often high when CoVs are not well adapted to the host.
Fahin bo'o, limtol sanjol lati maungel to COV wonday boɗɗum be suudu maɗa.
Compared to SARS-CoV with a high mutation rate, the mutation rate of SARS-CoV-2 is apparently lower, suggestive of a higher level of adaptation to humans.
To foondi be SARS-CoV je ɗon mari limtol saanjol je ɗon ɗuɗɗum, limtol saanjol SARS-CoV-2 lati bana lessi, bana wi'ugo footi yahida lau be ɓaandu neɗɗo.
Presumably, it has already been adapted to another host close to humans.
Ɗon tammi yo'o, lati ɗon yahida timmi be jaɓɓowo je ɗon ɓadi be neɗɗo.
In addition to SARS-CoV-2, this also applies to MERS-CoV, which is well adapted to dromedary camels.
Ha ɓesdugo ha SARS-CoV-2, ndu ɗon larni bo'o MERS-CoV, je ɗon yahida boɗɗum be ɓaandu ngeelobaji.
Theoretically, it is unlikely that genetic drift would render vaccines and antivirals against SARS-CoV-2 ineffective quickly.
Ha nder wolde kam, footay saanjol gene wartira baatalji mala lekki SARS-CoV-2 majja sembe mako laugel.
Second, the large RNA genome in CoVs exerts extra plasticity in genome modification for mutations and recombination, thereby increasing the probability for interspecies co-evolution, which is advantageous for the emergence of novel CoVs when the conditions become appropriate.
Ɗiɗaɓool, genome je ɓuri maunugo ha CoV ji ɗon latina genome bana leeda ngam saanjol e hawtirde, ndu gal ɓesdugo yahde gilɗi ndu ha kunde daabaji feere-feere, je mari ribaji ngam wanguɗe CoV je keese to kujeji wartiri bana nane.
This is supported by the copious unique open reading frames and protein functions encoded towards the 3′ end of the genome.
Ndu ɗon fadi gal ɓaandu je ɗon feerejo e maɓɓiti be kude protein je mari lamba gal 3' ɗaaɗol maɗa.
Third, CoVs randomly and frequently switch templates during RNA replication through a unique “copy-choice” mechanism.
Tataɓool, CoV ji ɗon saanja ɓaali ha yakke nufturol RNA gal dabare je mbiyotto "copy-choice".
In a host that serves as the mixing vessel, strand switching occurs frequently during CoV RNA transcription.
Ha nder suudu je ɗon naandi bana tassawo jillugo kujeji, saanjol ɗon salla tum ha yakke windol RNA.
Highly homologous full-length and subgenomic RNAs could recombine to generate new CoVs.
RNA je ɗon jutti masin e ɗon naandi footi hawtira ngam keɓɓugo CoV ji keese.
Phylogenetic evidence of natural recombination has been found in both HCoV-HKU1 and HCoV-OC43, as well as animal CoVs such as bat SL-CoV and batCoV-HKU9.
Sappinol asngol hawtirde aranool tawama ha HCoV-HKU1 be HCoV-OC43 ɗiɗi fu, be CoV ji daabaji bana bilwili SL-CoV be bilwili CoV-HKU9.
Virus-host interaction in relation to transmission
Fiijol suudu viriis be sallinol
Besides three viral factors stated above, viral interaction with host receptor is another key factor influential on interspecies transmission.
Ɓesdugo ha kujeji viriis tati je en limti ha dow ndu, fiijol viriis be jaɓɓowo lati kanduɗum masin nder sallinol ha kunde daabaji be neɗɗo.
Herein, recombination of SARS-CoV is taken as a typical example, which also showed evidence of positive selection during interspecies transmission events.
Ndu, hawtirde SARS-CoV hoccama bana sappinol kanduɗum, je ɗon holla bo'o suɓɓol bodde ha yakke sallinol ha kunde daabaji be neɗɗo.
Based on the comparative analysis between isolates of human and civet SARS-CoVs, SARS-CoV is thought to undergo rapid adaptation in different hosts, particularly with mutations at the RBD of the S protein.
Do lartol do foondol ha cakka SARS-CoV ji neɗɗo be je patuuru je siggotto ha seera, SARS-CoV bana ɗon saanja lau ha nder ɓaandu daabaji mala neɗɗo, ɓurna be saanjolji ha wakere RBD protein S.
Generally, the RBD in the S protein of a CoV interacts with the cellular receptor and is intensely selected by the host antibody response.
Ɓurna fu, RBD ha nder protein S CoV feere fiijidan be jaɓɓowo cell e ɗon suɓɓi be hakkika gal jabbuye fadoowo ɓaandu.
In SARS-CoV, the RBD is in the 318th to 510th amino acids on the S1 fragment, which binds to the human ACE2 as well as its coreceptors for viral entry.
Nder SARS-CoV, RBD ɗon limmi ha cakka amino acid jje 318 ha 510 ha do ta'irde S1, je ɗon hawta ACE2 be ko ɗon jaɓɓa ndu ngam nastirde viriis.
The RBD of SARS-CoV is capable of recognizing the ACE2 receptors of various animals, including bat, civet, mouse and raccoon dog, allowing interspecies transmission of the virus.
RBD je SARS-CoV footi maanda jaɓɓolji ACE2 ha daabaji feere-feere, bana, bilwili, patuuru, doomru be rawandu doomruweela, je ɗon jarfa sallinol viriis ha cakka daabaji be neɗɗo.
In fact, only 6 amino acid residues were observed to be different from human and civet viral isolates in the RBD and 4 of them locate in the receptor-binding motif for interaction with the ACE2 receptor.
Be gonga, sna coolaaje amino acid 6 tawama bana feerejo be viriis je siggoto ha seera neɗɗo be patuuru ha nder RBD e 4 ha cakka maɓɓe ɗon wondi ha nder jaɓɓowo hawtirde ngam fiijol be jaɓɓowo ACE2.
Civet SARS-CoV has K479N and S487T mutations in its RBD, which might increase the affinity of the interaction of spike protein with human ACE2 receptor.
Saanjolji SARS-CoV wodi K479N be S487T ha nder RBD maɗa, je footi ɓesda naandol fiiji hoore protein je jaɓɓowo neɗɗo.
In other words, these two amino acid substitutions might be critical to viral adaption to humans.
Bana wi'ugo, saanjolji amino acid je ɗiɗi ndu footi lata hannay ha saanjol viriis ha neɗɗo.
It is noteworthy that SARS-CoV-2 shares the same cellular receptor with SARS-CoV.
Boɗɗum fammugo yo'o SARS-CoV-2 ɗon mari jaɓɓowo cell gooto be SARS-CoV.
A 30% difference between SARS-CoV-2 and SARS-CoV in the S1 unit of the S protein implicates that the binding affinity of its S protein with human ACE2 might have altered.
Feeretirol 30% ha kunde SARS-CoV-2 be SARS-CoV ha nder toɓe S1 protein S yiɗi wi'ugo yo'o naandol hawtirde protein S maɗa be ACE2 neɗɗo saanji.
Indeed, a cryo-EM study indicates a 10- to 20-fold higher affinity of this binding than that between human ACE2 and SARS-CoV S protein.
Gonga, jaangirde cryo-EM ɗon holla naandol je nde 10 ha 20 je ɓuri do je ha cakka ACE2 neɗɗo be protein S ACE2 be SARS-CoV.
It will also be of interest to determine whether any other coreceptor might be required for SARS-CoV-2 transmission.
Wonan bo'o kanduɗum ngam fammugo to woodi jaɓɓowo feere je footi emmotto ngam sallinol SARS-CoV-2.
Intriguingly, HCoV-NL63 also binds to ACE2 but with a different part of S.
Ko ɗon hilna, HCoV-NL63 ɗon hawta be ACE2 amma be ta'irde S feere.
There exist many other HCoV receptors, such as aminopeptidase N for HCoV-229E, and 9-O-acetylated sialic acid for HCoV-OC43.
Wodi jaɓɓoɓe HCoV feere, bana aminopeptidase N je HCoV-229E, be 9-O-acetylated sialic acid je HCoV-OC43.
They might also account for successful adaptation of these CoVs in humans after interspecies transmission from their animal hosts.
Footi ɓe naffa ngam saanjol CoV ji ha nder ɓaandu neɗɗo ha ɓawo sallinol ha kunde daabaji diga suudu siggorde maɓɓe.
In addition to cellular receptors, the outcome of interspecies transmission of HCoVs is also governed by other host dependency and restriction factors.
Ɓesdugo ha jaɓɓoɓe cellji, sappinol sallinol HCoV ji ha kunde daabaji je kujeji siggorde feere on fadatta ndu.
The divergence of these host proteins between humans and natural reservoir hosts of HCoVs such as bats, dromedary camels and rodents might constitute a barrier to interspecies transmission.
Feeretirol cuuɗi proteinji je ɗon woni ha kunde neɗɗo he cuuɗi siggorde HCoV ji bana bilwili, ngeelobaji, mala nyamooɓe footi wona ko haɗatta sallinol ha kunde daabaji.
HCoVs have to usurp host dependency factors and subvert host restriction factors for a successful interspecies transmission.
HCoV ji sey njaamba wondugo do kujeji fadol e saanja ko haɗatta hadol heɓɓa sallinol ha kunde daabaji salla boɗɗum.
In this regard, molecular determinants in this important area of virus-host interaction remain to be identified and characterized.
Bana ni, sappinooɓe molekulji ha nder wakkere fiiji suudu viriis sey manda ɗum e hokka kugal maɗa.
An unbiased genome-wide screening of host dependency and restriction factors for SARS-CoV-2 using the state-of-the-art technology of CRISPR might be fruitful.
Wodi lartol maungel feere je wala suɓɓol feere do suudu SARS-CoV-2 be kujeji ustugo gal dabare CRISPR footi hokka ɓiɓe.
Emergence of novel HCoVs: back to ground zero
Wangol HCoV ji keese: lortol ha fuɗɗorde
The diversity of bat CoVs provides ample opportunities for the emergence of novel HCoVs.
Waagare CoV ji ɗon hokka dabareji ɗuɗɗum ngam wangol HCoV ji keese.
In this sense, bat CoVs serve as the gene pool of HCoVs.
Nden kadi, CoV ji bilwili lati bana ɓundu gene HCoV ji.
In addition, rapid mutation and genetic recombination also drive HCoV evolution and serve as two important steps in this process.
Ha ɓesdugo, saanjol laugel be hawtirde asngol footi bo'o ngaɗa yahde HCoV e wurtira ta'irdeji ɗiɗi nder laahal ndu.
For example, the acquisition or loss of novel protein-coding genes has the potential to drastically modify viral phenotypes.
Bana sappinol, keɓɓol mala majjol geneji protein je keese footi saanja phenotypeji viriis be boɗɗum.
Among SARS-CoV accessory proteins, ORF8 has been thought to be important in adaptation to humans, as SARS-CoV-related bat viruses were isolated but found to encode divergent ORF8 proteins.
Ha kunde proteinji mballol SARS-CoV, ORF8 lati bana kanduɗum nder saanjol ha nder neɗɗo, bana viriisji bilwili SARS-CoV siggotto ha seera amma lati bana mari lamba proteinji ORF8 feere.
A 29-nucleotide deletion characteristic of SARS-CoVs has been found in strains isolated at the beginning of the human epidemic.
Willugo 29-nucleotide je lati maandirɗum SARS-CoVs tawama ha nder gildiji je siggotto ha seera ha fuɗorde nyau ha neɗɗo.
This deletion splits ORF8 into ORF8a and ORF8b and is thought to be an adaptive mutation that promotes the switch of hosts.
Willol ndu ɗon senda ORF8 ha ORF8a be ORF8b e tammi latugo bana saajonl je ɗon walla saanjol cuuɗi.
Besides, SARS-CoV has a possible recombination history with lineages of alpha- and gamma-CoVs, where a large number of smaller recombinant regions were identified in the RNA-dependent RNA polymerase.
Fahin, SARS-CoV footi mara tariya hawtirol be asli CoV ji alpha- be gamma, e limgal wakkere hawtirooɓe maungel be pamarron tawama ha nder polymerase RNA je joɗɗi do RNA.
Recombination locations were also identified in the nsp9, most of nsp10, and parts of nsp14.
Wakkereji hawtirolji tawama bo'o ha nder nsp9, ɓurna nsp10, e ta'irdeji nsp14.
Likewise, it has been shown that the epidemic MERS-CoV experienced recombination events between different lineages, which occurred in dromedary camels in Saudi Arabia.
Fahin bo'o, be sappini yo'o nyau MERS-CoV hawti kujejiha kunde asli feere-feere, je wangi ha ngeelobaji ha Saudi Arabiya.
Besides SARS-CoV and MERS-CoV, recombination events have also been observed in other HCoVs, in which the HCoVs recombine with other animal CoVs in their non-structural genes.
Ha ɓesdugo SARS-CoV be MERS-CoV, kujeji hawtirde maandama ha HCoV ji feere, nder ton HCoV ji ɗon hawtira be CoV ji daaba feere ha nder geneji maɓɓe je maray ɓaandu je ɗon aandin.
It should also be cautioned that artificial selection can contribute to unintended changes in viral genomes, most likely resulting from relieving viruses from selection pressures exerted, such as by the host immune system.
Sey famma bo'o yo'o suɓɓol feere footi naffa ngam saanjol genomji viriis je tammay sam, ɓurna je ummiki ha viriisji ha suɓɓol jaawalji, bana dabare fadol suudu.
An example of these effects is the loss of a full-length ORF4 in the HCoV-229E prototype strain, owing to a two-nucleotide deletion.
Sappinol kujeji ndu lati majjol ORF4 je juttungel ha nder irin gilɗi HCoV-229E, je ɗon larni willol nucleotideji ɗiɗi.
While intact ORF4 could be observed in bat and camel viruses related to HCoV-229E, the alpaca alpha-CoV displays a single nucleotide insertion, resulting in a frameshift.
Ha wakati je ORF4 je ɗon wondi footi tawama ha nder viriisji bilwili be ngeeloba je larni HCoV-229E, alpha-CoV je alpaka ɗon sappina nastirde nucleotide woore, je ngaɗan saanjol ɓaandu.
Last but not least, the evolution of novel HCoVs is also driven by the selection pressure in their reservoir hosts.
Ragare amma kanduɗum, yahde HCoV ji ngadama gal suɓɓol jaawal ha nder cuuɗi siggorde.
Asymptomatic or only mild symptoms were detected when bats were infected with CoVs, indicating the mutual adaptation between CoVs and bats.
Mandolji nyau je fammatakke mala je deydey tan tawama ha yakke je bilwili raɓɓi CoV ji, je sappinatta saanjol oya be oya ha kunde CoV ji be bilwili.
It appeared that bats are well adapted to CoVs anatomically and physiologically.
Salli bana bilwili ɗon yahida be boɗɗum be CoV ji gal ɓaandu maɓɓe be huwirde maɓɓe fu.
For example, defects in the activation of pro-inflammatory response in bats efficiently reduce the pathology triggered by CoVs.
Bana sappinol, harbuggo nder umminugo jabbuye do ko footi ngaɗa huudure ha nder bilwili ɗon usta be boɗɗum nawnol je CoV ji wadi.
Besides, the natural killer cell activity in bats is suppressed due to upregulation of inhibitory natural killer cell receptor NKG2/CD94 and low expression level of major histocompatibility complex class I molecules.
Ha ɓesdugo, kuje je ɗon mbarda yimɓe ha nder bilwili wilakke ngam wangugo kuje je ɗon mbara go NKG2/CD94 be lessugo ngu
Moreover, the high level of reactive oxygen species (ROS) generated from high metabolic activity of bats could both suppress CoV replication and affects proofreading by exoribonuclease, thus providing the selection pressure for the generation of virus strains highly pathogenic when introduced into a new host.
Fahin bo'o, limtol hendu je ɗon ɗuɗɗum (ROS) wangi gal kuɗe nyamɗe ha bilwili je footi willa nuftol CoV e memma jaangirde gal exoribonuclease, ndu ɗon ngaɗa jaawal do asli bilwili je ɗon nyaɗungel to bana nastidi ha nder suudu keesum.
More pathogenic CoV strains might also evolve by recombination, leading to the acquisition of novel proteins or protein features for host adaptation.
Gilɗi CoV ɗuɗɗum je nyaɗungel footi bo'o yahida gal hawtirde, je ɗon ndokka proteinji keese mala mandolji protein ngam saanjol suudu.
Thus, it is not by chance that three novel HCoVs have emerged in the past two decades.
Nden kadi, latay sa'a je HCoV ji keese tati wangi ha nder duɓɓi cappan ɗiɗi je sallingo.
CoVs are non-pathogenic or cause mild symptoms in their reservoir hosts such as bats and camels.
CoV ji wonay nyaɗungel mala ɗon sappina mandolji nyau deydey ha nder suudu jaɓɓowo bana bilwili be ngeelobaji.
They replicate robustly without eliciting a strong host immune response.
Ɓe ɗon nufta be sembe bila emmugo jabbuye je caɗɗum ha fadooɓe ɓaandu.
Herein lie the secrets of why asymptomatic carriers are seen and what causes the severe cases in human infection.
Ha do on woni siiriji je koni rondooɓe je sappinatta mandolji tawama e ɗumme on ngaɗi nyau je ɗon torra neɗɗo.
The severe symptoms are mainly due to the hyperactivation of immune response and the cytokine storm wherein the stronger the immune response, the more severe the lung damage.
Mandolji nyau je nyaɗungel ɓurna fu ɗon wanga ngam jabbuye fadol ɓaandu be duluru cytokine je ɗon woni jur, ngam to bana jabbuye fadol ɓaandu ɗon wa'a, bana ni bo'o nawne fuffu ɗon ɓesda.
In contrast, in asymptomatic carriers, the immune response has been de-coupled from CoV replication.
Be man fu, ha nder rondooɓe je nyaday ndu, jabbuye fadol lati sendirama be nuftol CoV.
The same strategy of delinking the immune response might have beneficial effects in anti-SARS-CoV-2 therapy.
Irin dabare sendirugo jabbuye fadol footi woni kanduɗum ha nder hurgol anti-SARS-CoV-2.
The interferon response is particularly strong in bats.
Jabbuye interferon lati bana mari sembe jur ha bilwili.
Thus, administration of type I interferon at least in the early phase of SARS-CoV-2 infection in humans should be beneficial.
Bana ni, hokkugo interferon type I pettum man ha fuɗɗam yahde nyau SARS-CoV-2 ha neɗɗo wonan kanduɗum.
In addition, NLRP3 inflammasome activation in bats is defective.
Fahin bo'o, je be wi'i bilwili ɗon ndokka nyau NLRP3 yahay be lawol.
By this reasoning, inhibition of NLRP3 inflammasome with MCC950 might be useful in the treatment of COVID-19.
Gal irin nummolji, illol NLRP3 inflammasome be MCC950 footi naffa ha nder hurgol COVID-19.
The emergence of SARS-CoV-2 follows the general theme by which SARS-CoV and MERS-CoV arose.
Jaawal SARS-CoV-2 ɗon tokkita hoore ngewte laungel gal nden SARS-CoV be MERS-CoV wangi.
Whereas a bat beta-CoV sharing 95% nucleotide homology with SARS-CoV has been found, there also exists a bat-CoV sharing 96% nucleotide homology with SARS-CoV-2.
Ha yakke je sendol 95% naandol nucleotide be SARS-CoV tawama, wodi bo'o sendol CoV bilwili 96% naandol nucleotide be SARS-CoV-2.
Whereas civets and other animals in the markets have been found to harbour viruses identical to SARS-CoV, immediate intermediate hosts for SARS-CoV-2 have not been identified.
Ha wakati je pattuji be daabaji feere ha nder lumo tawama bana siggotto viriisji je ɗon naandi SARS-CoV ha nder ɓaandu maɓɓe, suudu siggorde je aranol SARS-CoV-2 tawakke tawon.
Pangolin beta-CoVs strikingly homologous to SARS-CoV-2 have been found, indicating that pangolins might serve as one of intermediate hosts or pangolin beta-CoVs could contribute gene fragments to the final version of SARS-CoV-2.
Beta-CoV ji pangolin je ɗon naandi masitin be SARS-CoV-2 tawama, ko hollatta yo'o pangoliji footi wona bana suudu siggorde cakkare mala beta-CoV ji footi walla ta'irdeji gene nder ragare SARS-CoV-2.
Although questions remain, there is no evidence that SARS-CoV-2 is man-made either deliberately or accidentally.
Ko to emmolji wondan, ɗon aandin yo'o SARS-CoV-2 neɗɗo on wadi ndu be aniyaa mala yotti bana ni tan.
CoVs have returned to the limelight due to the recent outbreak of SARS-CoV-2.
CoV ji lorti fahin ngam yottol nyau SARS-CoV-2 je keese.
The study of CoVs in bats and other animals has drastically changed our perception of the importance of zoonotic origins and animal reservoirs of HCoVs in human transmission.
Jaangirde CoV ji ha nder bilwili be daabaji feere saanji nummolji amin fu do ko larni naffuda wangol gal daabaji be cuuɗi siggorde HCoV ji ha do sallinol nder ɓaandu neɗɗo.
Pervasive evidence has shown that SARS-CoV, MERS-CoV and SARS-CoV-2 have a bat origin and are transmitted to humans via intermediate hosts.
Sappinol je ɗon lara be gite holli yo'o SARS-CoV, MERS-CoV be SARS-CoV-2 ummi ha bilwili e sallini ha neɗɗo gal daabaji feere.
Given that SARS-CoV infection originates from the contact between humans and civets in the markets, closing wet markets and killing civets therein could have effectively ended the SARS epidemic.
Nde nyau SARS-CoV ummi gal kawtirde neɗɗo be patuuji ha nder lumo, maɓɓol lumo je sippata daabaji je ɗon nyeeɓa be hirsugo patuuji ha ton footi darni no nyau SARS.
By the same reasoning, pangolins should be removed from wet markets to prevent zoonotic transmission, in view of the discovery of multiple lineages of pangolin beta-CoVs closely related to SARS-CoV-2.
Gal irin nummolji ndu, pangolinji sey wona wurtama ha lumoji ngam haɗɗugo ta raɓɓol salla gal daabaji, bana sappinol je ɗon holla naandolji beta-CoV ji paangolin be SARS-CoV-2.
However, whether and how SARS-CoV-2 is transmitted to humans through pangolins and other mammals remain to be clarified in future investigations.
Amma, to SARS-CoV-2 ɗon sallini ha neɗɗo gal pangolinji be daabaji feere e noy sey laɓɓina ɗum ha nder teffolji je warango.
On the other hand, MERS-CoV has existed in dromedary camels for a long time.
Ha yakke feere, MERS-CoV woni no ha nder ngeelobaji diga naane ma.
These camels serve as an important tool for transportation as well as a main source of meat, milk, leather and wool products for the local people.
Ngeelobaji ndu lati bana kuje je naffata ngam jaahangal e hoorugo kujeji e ɗon hokka kuusel, kossam, laaral be gaasa ha ummatore.
They are widely distributed across the Middle East and Africa.
Ɓe ɗon sendama ko to fu ha Cakkare Funaange be Afirika.
It is therefore impossible to sacrifice all camels for the control of MERS, as what was done in wild animal markets in China to prevent the spreading of SARS-CoV and SARS-CoV-2.
Footay bo'o en mbarda ngeelobaji fu ngam natinugo MERS, be ko ɓe waɗi ha lumo daabaji ha Cayna ngam aynol sankittol SARS-CoV be SARS-CoV-2.
To stop the recurrent outbreaks of MERS, a comprehensive approach should be taken to develop effective vaccines against MERS-CoV for camels, in combination with other infection control measures.
Ngam darnugo lortolji nyau MERS, wodi dabare feere wangi ngam wurtinugo baatalji MERS-CoV je ngeelobaji, hawti be dabareji aynugo nyauji feere.
As we are not able to eliminate these viruses, new genotypes might emerge to cause outbreaks.
Ngam footay en natina viriisji ndu, genotypeji feere footi wanga e hokka nyauji feere fahin.
A variety of zoonotic CoVs are circulating in the wild.
Waagare CoV ji je wangi gal daabaji ɗon tara ha nder ladde.
Particularly, bat CoVs with zoonotic potential are so diverse.
Ɓurna bo'o, CoV ji bilwili je footi wangi gal daabaji ɗon waagi.
There are plenty of opportunities that these zoonotic CoVs evolve and recombine, resulting in the emergence of new CoVs that are more transmissible and/or deadly in humans in future.
Wodi dabareji ɓuɗɗum je CoV ji je sallata gal daabaji ndu yahida e hawtida, je ndokatta CoV ji keesum je latan ɓuri raɓɓugo e/mala mbardan yimɓe ha yeeso.
The culture of eating wild animals in some places of China should be abandoned to reduce unnecessary contact between humans and animals.
Nyamugo daabaji ladde ha wakkereji feere ha Cayna sey acca ɗum ngam ustugo hawtirol ha kunde neɗɗo be daabaji.
With the ordeals of SARS, MERS and COVID-19, a better preparedness and response plan should be in place.
Be larulaji SARS, MERS be COVID-19, sey taska boɗɗum e heɓɓa jaahargal jabbuye kanduɗum wonda.
In fact, many viruses have existed in the planet for a very long time.
Be gonga, viriisji ɗuɗɗum woni no ha do lesdi meɗen diga aran.
They stay in their own natural reservoirs until there is a chance for spillover.
Ɓe ɗon woni ha nder cuuɗi siggorde maɓɓe ha wakati sankittol maɓɓe.
Although bats have many features that favours the spreading of viruses, the chance for humans to be in contact with bats and other wildlife species can be minimized if people are educated to stay away from them.
Ko to bilwili ɗon mari dabareji ɗuɗɗum ngam sankittugo viriisji, sa'a ha neɗɗo hawtira be bilwili be daabaji feere footi ustotto to yimɓe emmotto ta be wonda be maɓɓe sam.
Continuous surveillance in mammals is necessary for better understanding of the ecology of CoVs and their natural hosts, which will prove useful in preventing animal-to-human transmission and future outbreaks.
Tokkitol aynol ha daabaji naffan ngam fammugo baabal jonde CoV be wakkere jonde maɓɓe je gonga, je sappinan noy haddugo nyau diga daabaji ha neɗɗo be nyau je footi wara ha yeeso.
To conclude, the most effective way to prevent viral zoonosis is for humans to stay away from the ecological niches of the natural reservoirs of the zoonotic viruses.
Ngam timminugo, dabare kanduɗum ngam aynugo raɓɓol viriis diga daabaji sey neɗɗo daaya be wakere cuuɗi siggordeji viriisji ndu.
Several pieces in the puzzle of the zoonotic origin of SARS-CoV-2 are still missing.
Kujeji jur ha nder nukkure je wangol SARS-CoV-2 gal daabaji wala ɗon.
First, if bats transmit an ancestral virus of SARS-CoV-2 to pangolins, it will be of interest to see under what circumstances bats and pangolins could share the same ecological niche.
Aranool, to bilwili ɗon sallina maama viriis SARS-CoV-2 ha pangolji, naffan masin to en teffi noy bilwili be pangolin maran wakkere jonde gooto.
Second, if bats play a more direct role in human transmission, how humans get into contact with bats should be determined.
Ɗiɗaɓool, to bilwili lati sallinowo ha neɗɗo, noy neɗɗo hawtidi be bilwili sey aanda ɗum bo'o.
Third, if a third mammal acts as the true intermediate host, how it interacts with the different species including humans, bats and pangolins has to be clarified.
Tataɓool, to wodi tataɓool daaba je lati bana siggorde je cakkare, sey laɓɓina noy fiijira be daabaji feere e larni bo'o neɗɗo, bilwili be pangolinji.
Finally, since many mammals including domestic animals might be susceptible to SARS-CoV-2, both surveillance and experimental infection should be conducted.
Timminool, nde dabaaji ɗuɗɗum be daabaji saare footi mara SARS-CoV-2, ɗiɗi fu aynol be teffol nyau sey wonotto.
Should it be a bat, a pangolin or another mammal, it is expected that SARS-CoV-2 or its parental viruses that are almost identical will be identified in its natural hosts in future.
Ko to woni bilwili, pangolin mala daaba feere, min yidi fammugo yo'o viriisji SARS-CoV-2 mala maama maɗa je ɗon naandi masitin ha nder suudu siggorde aranool.
Continued investigations in this area will elucidate the evolutionary pathway of SARS-CoV-2 in animals, with important implications in the prevention and control of COVID-19 in humans.
Teffol je tokkitata ha nder wakkere nde laɓɓinan yahde SARS-CoV-2 ha nder daabaji, be dabareji ɗuɗɗum nder aynol e lartol COVID-19 ha nder ɓaandu neɗɗo.
Preliminary Estimates of the Prevalence of Selected Underlying Health Conditions Among Patients with Coronavirus Disease 2019 — United States, February 12–March 28, 2020
Preliminary Estimates of the Prevalence of Selected Underlying Health Conditions Among Patients with Coronavirus Disease 2019 — United States, 12 Feviriye –28 Maars 2020
On March 11, 2020, the World Health Organization declared Coronavirus Disease 2019 (COVID-19) a pandemic.
Ha 11 Maars 2020, Ɗowirde Duniyaru do Jam Ɓaandu holli yo'o Nyau Koronaviriis 2019 (COVID-19) lati nyau duniyaru fu.
As of March 28, 2020, a total of 571,678 confirmed COVID-19 cases and 26,494 deaths have been reported worldwide.
Diga 28 Maars 2020, hawti nyauɓe COVID-19 571 678 tawama be yimɓe 26 494 maynama ha nder duniyaru fu.
Reports from China and Italy suggest that risk factors for severe disease include older age and the presence of at least one of several underlying health conditions.
Kuubaruji gal Cayna be Italy ɗon hollina yo'o kujeji je ɗon saɗɗina nyau man larni duɗɗi be wondugo nyau feere-feere ha nder ɓaandu.
U.S. older adults, including those aged ≥65 years and particularly those aged ≥85 years, also appear to be at higher risk for severe COVID-19–associated outcomes; however, data describing underlying health conditions among U.S. COVID-19 patients have not yet been reported.
Mauɓe ha Lesdi America, be ɓe'en je mari duɓɓi ≥65 e ɓurna be'en je ɗon mari duɓɓi ≥85, ɗon sappini bana mari sa'a jur raɓɓugo nyau COVID-19–je nyaɗungel; amma, matinolji je ɗon sappina nyauji ha kunde nyau COVID-19 ha Lesdi America matinay tawon.
As of March 28, 2020, U.S. states and territories have reported 122,653 U.S. COVID-19 cases to CDC, including 7,162 (5.8%) for whom data on underlying health conditions and other known risk factors for severe outcomes from respiratory infections were reported.
Ha 28 Maars 2020, lesɗe be lamordeji Lesdi America matini nyauɓe COVID-19 122 653 ha CDC, be 7 162 (5.8%) je nyau maɓɓe ɗon nyaɗi ɓe feere'en aandin ɗon no mari nyau pofɗe.
Among these 7,162 cases, 2,692 (37.6%) patients had one or more underlying health condition or risk factor, and 4,470 (62.4%) had none of these conditions reported.
Ha cakka maɓɓe nyauɓe 7 162, 2 692 (37.6%) ɗon mari no tawon nyau mala nyauji feere mala ko footi nyaɗinatta, be 4 470 (62.4%) maray ko gootel ha cakka nyauji ndu.
The percentage of COVID-19 patients with at least one underlying health condition or risk factor was higher among those requiring intensive care unit (ICU) admission (358 of 457, 78%) and those requiring hospitalization without ICU admission (732 of 1,037, 71%) than that among those who were not hospitalized (1,388 of 5,143, 27%).
Limtol nyauɓe COVID-19 be pettum man nyau feere gootel mala ko footi nyaɓinatta woni ɗuɗɗum ha cakka ɓe'en je mari no haaje suklare feerejo (ICU) (358 do 457, 78%) e ɓe'en je ɓon mari haaje wondugo ha suudu lekkibila ICU (732 do 1 037, 71%) do ɓe'en je wonday ha suudu lekki (1 388 do 5 143, 27%).
The most commonly reported conditions were diabetes mellitus, chronic lung disease, and cardiovascular disease.
Nyauji je ɓurna fu je matinama lati nyau sukar mellitus, nyau fuffu je ɗon tokkita, nyau ɓernde.
These preliminary findings suggest that in the United States, persons with underlying health conditions or other recognized risk factors for severe outcomes from respiratory infections appear to be at a higher risk for severe disease from COVID-19 than are persons without these conditions.
Arandere sappinolji ndu ɗon holla yo'o, ha Lesdi America, yimɓe je ɗon mari nyau feere mala ko footi nyaɗinatta larulaji nder pofɗe lati bana nyau COVID-19 ɓuri nyaɗugo do yimɓe je maray irin nyauji ndu.
Data from laboratory-confirmed COVID-19 cases reported to CDC from 50 states, four U.S. territories and affiliated islands, the District of Columbia, and New York City with February 12–March 28, 2020 onset dates were analyzed.
Matinolji je wurti ha suudu lartol aandini nyauɓe COVID-19 je lesɗe 50 ha CDC, lamordeji Lesdi America nay be lesɗe nder nyiyam je ɗon tardi, Distrik je Columbia, be New York City be fuɗɗorde ha 12 Feviriye–28 Maars 2020.
Cases among persons repatriated to the United States from Wuhan, China, and the Diamond Princess cruise ship were excluded.
Nyauɓe ha cakka yimɓe je warti diga Wuhan, Cayna, be je wondi no ha nder kombeewool mbiyotto Diamond Princess ha Lesdi America limay ha cakka man.
For cases with missing onset dates, date of onset was estimated by subtracting 4 days (median interval from symptom onset to specimen collection date among cases with known dates in these data) from the earliest specimen collection.
Ko larni nyauɓe je aanda wakati fuɗɗorde nde, wakati fuɗɗorde tammotto gal ustugo balɗe 4 (wakati je cakkare diga fuɗɗam mandol ha wakati hoccol leeku lartol ha cakka nyauɓe je wakati fuɗɗorde maɓɓe ɗon aandin) diga hoccol aranol leeku lartol.