atepeq/tico19 huggingface dataset:
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.
Domin wannan ya faru, HCoVs na bukatar su rubanya a cikin mutane zuwa isasshen mataki don ba da damar tattaruwar maye gurbi da zai ci galabar dalilan ƙuntatawa na mafaka.
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.
Ta wannan hanyar, tsawon lokacin fashewa da SARS-CoV-2 ya ci gaba kuma mutane da yawa suna cutar dashi, mafi girma damar cewa zai cikakken daidaita da ga mutane.
If it adapts well, its transmission in humans would be difficult to stop by quarantine or other infection control measures.
Idan har ta samu gindin zama sosai, yaduwarta tsakanin mutum zuwa mutum zai zama da matukar wahala ta hanyar killacewa ko kuma sauran matakan kare bazuwar cuta.
For many years, the four community-acquired CoVs circulate in human populations, triggering common cold in immunocompetent subjects.
Shekaru da yawa, al'umma huɗu sun samo CoVs suna kewayawa cikin yawan mutane, yana haifar da sanyin mura cikin kwararun masun garkuwa.
These viruses do not need an animal reservoir.
Wadannan kwayoyin cutar basa bukatar zama a jikin mutum ko dabba.
In contrast, highly pathogenic SARS-CoV and MERS-CoV have not adapted to humans well and their transmission within humans cannot be sustained.
Sabanin haka, SARS-CoV da MERS-CoV masu sanya cuta ba su daidaita da mutane ba da kyau kuma yaduwarsu a mutane ba za a iya cigaba da shi ba.
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.
Suna da bukatar ci gaba da rayuwa a jikin dabbobin da ke dauke da su domin su sami damar shiga jikin mutane ta hanyar mutum guda ko fiye da samo ta daga dabbobin.
SARS-CoV-2 has features that are similar to both SARS-CoV/MERS-CoV and the four community-acquired HCoVs.
Cutar SARS-CoV-2 tana da kamanni irin na cutar SARS-CoV/MERS-CoV da kuma sauran masu dauke da nau’in cutar HCoVs.
It is highly transmissible like community-acquired HCoVs, at least for the time being.
Wannan abu ne da za'a iya yaduwa sosai kamar kamuwar HCOVs a cikin al'umma, aƙalla a lokacin da muke a ciki.
However, it is more pathogenic than community-acquired HCoVs and less pathogenic than SARS-CoV or MERS-CoV.
Duk da haka, ya fi zaman mai daukar kwayar cuta fiye da al’uma da aka sami HCoVs kuma ƙasa da mai daukar kwayar cutan fiye da SARS-CoV ko 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.
Ya rage a gani ko zai iya dacewa da mutane sosai kuma ya kewaya cikin mutane ba tare da wurin ajiya ba ko mafaka ta tsakiya a jikin dabbobi.
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.
Kafin tattauna asalin dabbobin dabbobi na HCoVs, zai taimaka mana sosai mu tattauna kan ma’anoni da halayen juyin halitta, na halitta, tafki, matsakaici da haɓaka mafakar HCoVs.
An animal serves as the evolutionary host of an HCoV if it harbours a closely related ancestor sharing high homology at the level of nucleotide sequence.
Dabba da ta zama wata mafaka ta juyin halitta ta HCoV idan ta tanadi asalin magabata mai kusanci wadda suke babban kama ta haɗin dangantaka a matakin jerin nucleotide.
The ancestral virus is usually well adapted and non-pathogenic in this host.
Kwayar cutar ta asali galibi ana rayuwa da ita kuma bata zama illa ga inda dama take rayuwa.
Likewise, a reservoir host harbours HCoV continuously and for long term.
Hakanan, mai yin tafki mai tashar jiragen ruwa HCoV yana ci gaba kuma tsawon lokaci.
In both cases, the hosts are naturally infected and are the natural hosts of HCoV or its parental virus.
A dukkan halayen, masu rukunin suna kamuwa da cuta ta dabi'a kuma sune ainihin rukunin HCoV ko ƙwayar mahaifa.
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.
Sabanin haka, idan sabon HCoV ya gabatar da sabon matsakaici a gabanin ko a kusa da gabatarwar sa ga mutane, ba a daidaita shi da sabon mai masaukin ba kuma yawanci shine pathogenic.
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.
Wannan da kwayar cutar ta samu gindin zama jikinsa, zai iya zama tushen da cutar da za ta shafa kuma ya taka muhimmiyar rawa wajen bai wa kwayar cutar damar ta hayayyafa inda za ta iya harbin dan adam daga nan.
An HCoV can undergo a dead-end infection if it cannot sustain its transmission within the intermediate host.
HCoV na iya yin gwajin cutar mutu-karshen idan har ba zai iya ci gaba da yada ta ba a cikin matsakaiciyar mai watsa shiri.
On the contrary, HCoVs can also adapt to the intermediate host and even establish long-term endemicity.
Sai dai wani abin da zai zama wanda ya saba da hakan, cutar HCoVs kan iya rayuwa jikin wani abu na daban kuma ya iya haifar da illar gaske da za ta dauki lokaci gabanin bayyanarta.
In this case, the intermediate host becomes a natural reservoir host.
A nan kuma, wanda cutar ta kasance a jikinsa na karshe to zai zama wanda ainihin inda cutar ta samo asali tun da farko.
Epidemiological data revealed retrospectively that the index case of SARS had a contact history with game animals.
Bayanan cututtukan dabbobi sun bayyana bita da kullun cewa yanayin binciken SARS yana da tarihin hulɗa tare da dabbobin wasa.
Subsequent seroprevalence investigations indicated that animal traders had a higher prevalence of anti-SARS-CoV IgG compared with that of the general population.
Binciken seroprevalence mai zuwa ya nuna cewa yan kasuwar dabbobi sun sami karuwar SARS-CoV IgG idan aka kwatanta da na sauran jama'a.
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.
Dabbobin civet masu rufaffen tafi (Paguma larvata) da karen racoon dake cikin kasuwancin dabbobi su ne aka fara ganowa suna ɗauke da ƙwayoyin cuta masu kama da wadanda suke kusan iri ɗaya ne ga SARS-CoV.
This was indirectly supported by the fact that no further SARS was reported after killing all civets in the markets.
Wannan ya tallafawa kai tsaye ta hanyar cewa ba a sake samun ƙarin rahoton SARS ba bayan kashe duk wasu dabbobin Sivets cikin kasuwannin.
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.
Duk da haka, an ba da rahoton cewa dabban itacen giginya wato civets daga cikin daji ko gonaki ba tare da fuskantar kasuwannin dabbobi masu rai ba sun kasance da cutar SARS-CoV ba, wadda ke nunar da cewa civets masu rufaffen tafi watakila kawai su zama mafakar tsakiya mai fadadawa ga SARS-CoV amma ba mafakan sa ba.
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.
Musamman ma, tunda kashi 80% na dabbobi daban-daban a cikin kasuwanni a Guangzhou suna da rigakafin SARS-CoV da yiwuwar cewa yawancin nau'in kananan dabbobi masu shayarwa suma zasu iya zama matsakaicin fadada rundunonin SARS-CoV ba za'a iya cire su ba.
All of these appear to be dead-end hosts of SARS-CoV.
Dukkanin wadannan sun kasance inda cutar SARS-CoV take mutuwa a jikinsu.
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.
Bincike mai zuwa don rundunar dabba ta SARS-CoV sun nuna wata jemage mai zaman kusa da CoV da ake kira SARS-Jemagen Rhinolophus CoV HKU3 (SARSr-Rh-JemageCoV HKU3), wanda yake a cikin jikunan dawakai na kasar Sin.
These bats are positive for anti-SARS-CoV antibodies and genome sequence of SARSr-Rh-BatCoV HKU3.
Wadannan jemagun suna dauke da kwayoyin halitta masu maganin SARS-CoV da kwayoyin tsuhen halitta masu ajin SARSr-Rh-BatCoV HKU3.
This and other bat CoVs share 88-92% nucleotide sequence homology with SARS-CoV.
Wannan da sauran CoVs na jemagu suna da nasaba kashi 88-92% ta jerin kwayoyin nucleotide tare da SARS-CoV.
These studies have laid the foundation for the new concept that bats host emerging human pathogens.
Wadannan karatuttukan sun aza harsasai ga sabuwar manufar da jemagu ke karbar bakuncin cututtukan dan adam.
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.
Yawancin CoVs (SL-CoVs) masu kama da SARS an kuma gano su daga jemagu, amma babu wani idan ba guda kawai da aka tsara WIV1 da za a iya warewa a zaman ƙwayar cuta mai rai.
Human angiotensin converting enzyme 2 (ACE2) is known to be the receptor of SARS-CoV.
Kayan mutum wanda yake canza enzyme 2 (ACE2) an san shi mai karɓar SARS-CoV.
WIV1 derived from fecal sample of bats was demonstrated to use bat, civet and human ACE2 as receptor for cell entry.
Kwayar WIV1 da aka samo daga kashin jemagu an yi amfani da shi ne a jemagen da kyanwa da kuma ACE2 na mutum a matsayin masu karbar kwayar halittar.
Intriguingly, sera of convalescent SARS patients were capable of neutralizing WIV1.
Abin ban sha'awa, fama da cutar SARS wanda suna samun sauki sun iya wargazawar WIV1.
Thus far, WIV1 represents the most closely related ancestor of SARS-CoV in bats, sharing 95% nucleotide sequence homology.
Har zuwa yau, WIV1 tana wakiltar asalin magabata na SARS-CoV a cikin jemage, yana kamanni mataki na 95% nucleotide jerin homology.
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.
Duk da haka, akwai babban tsarin alaƙa tsakanin waɗannan ƙwayoyin cuta guda biyu, gabaɗaya an yi imanin cewa WIV1 ba ƙwayar cuta ce ta iyaye na nan take na SARS-CoV kuma jemagu ba shine reshe na kai tsaye na SARS-CoV ba.
Phylogenetic analysis clusters MERS-CoV to the same group as bat CoV-HKU4 and bat CoV-HKU5.
Binciken ƙwayar Phylogenetic ta mahaɗar MERS-CoV zuwa rukuni guda na Jemage CoV-HKU4 da baton CoV-HKU5.
Bat CoV-HKU4 and MERS-CoV utilize the same host receptor, dipeptidyl peptidase 4 (DPP4), for virus entry.
CoV-HKU4 na jemage da MERS-CoV suna yin amfani da mai karɓa guda, da dipeptidyl peptidase 4 (DPP4), don shigowar ƙwayar cutar virus.
RNA-dependent RNA polymerase sequences of MERS-CoV are phylogenetically closer to counterparts in bat beta-CoVs identified from Europe and Africa.
Jerin kwayoyin halittar RNA-dependent da kuma na miyau RNA suna daga cutar MERS-CoV suna kama ne da jemagun da ake gani a nahiyar Turai da kuma Afirka.
Up to now, no live MERS-CoV can be found in wild bats.
Har ya zuwa maganan nan da muke yanzu, babu wata alamar kwayar cutar MERS-CoV da take rayuwa a jikin jemagun daji.
MERS-CoV and its closest relative bat CoV-HKU25 share only 87% nucleotide sequence homology.
Kwayar cutar MERS-CoV da kuma wacce tafi kama da ita ta jemage mai suna CoV-HKU25 suna da nasaba ta kashi 87% a kwayoyin halittarsu masu kamanceceniya da juna.
Thus, bats might not be the immediate reservoir host of MERS-CoV.
Don haka jemagu watakila ba sune ke dauke da kwayar cutar MERS-CoV.
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.
A gefe guda, bincike a Gabas ta Tsakiya ya nuna cewa raƙuman masu tozo guda suna da matsalar virus ga ƙwayoyin magance ƙwayoyin cuta na MERS-CoV, daidai da raƙuman masu asalin daga gabas ta Tsakiya wadanda ke cikin ƙasashen Afirka da yawa.
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 mai raye daidai ne da cutar da aka samu a cikin mutane an ware ta daga kwarfatar hanci na raƙuman maso tozo guda, wanda ke cigaba da nuna cewa rakuma suna aiki a matsayin taskar mafaka ta MERS-CoV.
It is also noteworthy that generally mild symptoms but massive virus shedding were observed in camels experimentally infected with MERS-CoV.
Hakanan abin lura ne cewa yawancin alamu masu saukin kai amma an lura da zubar da kwayar cutar a cikin raƙuma na gwaji yayin kamuwa da MERS-CoV.
Notably, infected camels shed viruses not only through respiratory route but also through fecal-oral route, which is also the main route for virus shedding from bats.
Musamman, raƙuma masu kamuwa da cuta suna zubar da ƙwayoyin cuta ba kawai ta hanyar numfashi ba amma har ma ta hanyar fecal-na baka, wanda kuma shine babban hanyar cutar zubar da kwari daga jemagu.
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.
Koyaya, tambayoyi har yanzu suna kasancewa tunda masu kamuwa da MERS su da yawa sun tabbatar da cewa ba su da tarihin hulɗa da raƙuma kafin farawa samun alamar cuta, wanda ake dangantawa watsuwa tskanin mutum-zuwa-mutum ko ta hanyoyi da ba a sani ba wadanda suka shafi nau'in dabbobi da ba a gano su ba wadanda suke dauke da MERS-CoV.
SARS-CoV-2 shares 96.2% nucleotide homology with a bat CoV RaTG13 isolated from Rhinolophus affinis bats.
SARS-CoV-2 na raba kashi 96.2% na nucleotide homology tare da wata bature CoV RaTG13 da aka ware daga jemagun affinis Rhinolophus.
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.
Kamar yadda ya faru da SARS-CoV da MERS-CoV, rarrabewa tsakanin SARS-CoV-2 da RaTG13 ya yi girma da yawa don sanya dangantakar iyaye.
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.
Abin nufi shine, jemagu bazai kasance mai masaukin na kai tsaye na SARS-CoV-2 ba sai dai idan an samo kusan kwatankwacin batutuwan CoVs masu zuwa nan gaba.
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.
Wataƙila, rundunan dabbobi masu matsakaici na SARS-CoV-2 ya kamata ya kasance cikin nau'in namun daji da aka sayar kuma an kashe shi a Kasuwar sayar da abincin teku, wanda yawancin farkon damuwar COVID-19 suke da alaƙa, alamu ne na yiwuwar watsawar cutan daga dabbobi-zuwa-mutum.
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.
Yawancin binciken da aka yi kwanan nan dangane da jerin hanyoyin metagenomic sun nunar da wasu ƙananan dabbobi masu shayarwa dake haɗarin bata, wadanda aka sani da pangolins (Manis javanica) suna iya kasancewa masu dauke da magabata beta-CoVs wanda ya dangantaka da SARS-CoV-2.
These novel pangolin CoV genomes share 85-92% nucleotide sequence homology with SARS-CoV-2.
Wadannan sabbin kwayoyin genome na pangolin CoV suna hadakar kwayoyin genomes 85-92% na tsarin kwayoyin nucleotide homology tare da SARS-CoV-2.
However, they are equally closely related to RaTG13 with about 90% identity at the level of nucleotide sequence.
Ko yaya, suna da alaƙa da RaTG13 da kusan kasha 90 bisa dari Asali a matakin nucleotide.
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.
Suna tattaruwa cikin sassan biyu na SARS-CoV-2-kamar ƙwayoyin cuta a cikin bishiyar phylogenetic, ɗayan wanda ya raba yanki mai ɗaukar nauyi mai rikodin mai karɓa (RBD) tare da SARS-CoV-2, tare da 97.4% shaidar asalin jerin amino asid.
In stark contrast, the RBDs of SARS-CoV-2 and RaTG13 are more divergent, albeit a higher degree of sequence homology genome-wide.
Ko yaya dai, yawan maye gurbi RBDs na SARS-CoVs-2 da RaTG13 su na daban-daban kusan sau miliyan ne fiye da wanda ke daukar su.
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.
Wani binciken da ya gabata a kan pangolins masu cutuka shi ma ya ba da labarin gano alamun kwayar cutar virus daga samfuran huhu, wanda ya yi kama da masu alaƙa da 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.
Wannan binciken ya karɓi hanyoyi daban-daban na haɗuwa da kundin jagora don samar da jerin abubuwan genome wanda ya ƙunshi kimanin kashi 86.3% na cikakkiyar ƙwayoyin cuta ta genome.
We cannot exclude the possibility that pangolin is one of the intermediate animal hosts of SARS-CoV-2.
Ba za mu kawar da yiwuwar cewa dabbar pangolin din tana daga cikin dabbobin da suke dauke da kwayar cutar 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.
Duk da haka, a halin yanzu babu wata shaida a cikin goyon bayan asalin pangolin kai tsaye na SARS-CoV-2 saboda rarrabewar jerin tsakanin SARS-CoV-2 da pangolin hadedeyar-SARS-CoV-2 da beta-CoVs.
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.
Kari akan haka, nisan da ke tsakanin SARS-CoV-2 da RaTG13 ya fi guntu fiye da wancan tsakanin SARS-CoV-2 da pangolin SARS-CoV-2 masu hade da beta-CoVs.
The evolutionary pathway of SARS-CoV-2 in bats, pangolins and other mammals remains to be established.
Rikidar cutar SARS-CoV-2 a jikin jemagu da kuma dabbobin pangolin da ma sauransu ya zama wani abi da za a kafa hujja kansa.
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.
Ganin cewa mafi girman jerin kwayoyin an samo cikin RBDs tsakanin SARS-CoV-2 da pangolin, SARS-CoV-2-beta-CoVs, beta-CoVs masu alaka da SARS-CoV-2 da RaTG13 suna kama mafi girma a jerin kwayoyin halittar jini.
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.
Abun hasashe ne babba cewa girman matsayin dake kamance tsakanin RBDs na pangolin SARS-CoV-2-beta-CoV-beta da SARS-CoV-2 ana haifar da shi ne ta hanyar juyin halitta wanda yake rikidewa.
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.
Neman shawara ya dace da sake hadewa tsakanin SARS-CoV-2 da aka hada da beta-CoV da RaTG13 a cikin dabbobin daji na uku.
As a driving force in evolution, recombination is widespread among beta-CoVs.
A matsayin ƙarfin tuki a cikin juyin halitta, sake haɗa abubuwa da ke yaɗuwa sosai tsakanin beta-CoVs.
The jury is still out on the immediate zoonotic origin of SARS-CoV-2.
Har yanzu masu yanke hukunci suna kan asalin SARS-CoV-2 na zoonotic.
Besides the highly pathogenic HCoVs, the zoonotic origin of HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1 have also been studied.
Idan ka cire batun rikidar kwayar cutar HcoVs data samo asali daga jikin dabbobi an kuma nazarci na’ukan HCoV-229E da HCoV-OC43 da HCoV-NL63 da HCoV-HKU1.
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.
Shaidar ilimin halittun dabbobi ya nuna cewa duka HCoV-NL63 da HCoV-229E za su iya samo asali ne daga jemage CoVs, yayin da aka sami ƙwayoyin cuta na iyaye na HCoV-OC43 da HCoV-HKU1 a cikin beraye.
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.
An ba da rahoton cewa wata CoV ta jemage da ake kira ARCoV.2 (Appalachian Ridge CoV) wacce aka gano a jemage mai kala uku a Arewacin Amurka ta sami dangantaka mai kusanci da 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.
A wata gefe guda, HCoV-229E yana da alaƙar alaƙa da wani jigon CoV, ana kiran shi Hipposideros / GhanaKwam / 19/2008, wanda aka gano a Gana, yayin da kuma ana zargin raƙumin a matsayin mai ba da taimakon sa.
For clarity, the current knowledge on animal origins of known HCoVs is summarized in Figure ​1 and Table 2.
Don ba da haske, ilimin zamani game da asalin dabbobi na sananniyar HCoVs an taƙaita su a cikin Hoto na 1 da Tebur 2.
Phylogenetic analysis has provided evidence for interspecies transmission events of HCoVs in the history.
Nazarin Phylogenetic ya ba da hujja ga abubuwan da suka faru na watsa abubuwan HCoV a cikin tarihin.
When HCoV-OC43 crossed species to infect humans from domestic livestock around 1890, a pandemic of respiratory infection was recorded.
Lokacin da HCoV-OC43 ya haɗu da jinsin don cutar da mutane daga dabbobin gida a shekarar 1890, an yi rikodin annoba ta numfashi.
The interspecies transmission history of HCoV-229E is less clear.
Tarihin yaduwar cutar HCoV-229E ba wani karin haske sosai a kansa.
Bat alpha-CoVs closely related to HCoV-229E have been found.
An gano kwayar cutar daga jemage CoVs wacce ta yi kama sosai da cutar HCoV-229E.
Between them there is an alpaca alpha-CoV.
Tsakanin su akwai alpha mai suna 'alpaca-CoV.
Several lines of evidence support the transmission of virus from bats to humans directly.
Akwai hujjoji da dama da suke nuna cewa cutar ta yadu ne daga jemagu kai tsaye zuwa jikin dan adam.
First, humans but not alpacas might have contact with bats in a shared ecological niche.
Da farko, mutane amma ba almasas ba zasu iya hulɗa da jemagu a cikin raba kimiyyar muhalli.
Instead, humans have close contact with alpacas.
Maimakon haka, mutane suna kusanci da alpacas.
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.
Na biyu, HCoV-229E mai hade da batutuwan al-CoVs suna da bambanci kuma marasa tsari a cikin jemagu, alhali kuwa Alpha-CoV ya haifar da barkewar cutar ta hanu a cikin dabbobi masu kamuwa.
Finally, alpaca alpha-CoV has not been found in feral animals.
A ƙarshe, ba a sami alpaca alpha-CoV ba a cikin dabbobin feral.
Thus, the possibility cannot be excluded that alpacas obtain the HCoV-229E-related alpha-CoV from humans.
Don haka, baza a kawar da tunanin yiyuwar cutar HCoV-229E ta samo asali ne daga kwayoyin halittar CoV daga dan jikin dan adam.
In fact, bats are the direct source of human pathogenic viruses including rabies virus, Ebola virus, Nipah virus and Hendra virus.
Hakika, jemagu sune tushen kai tsaye na ƙwayoyin cuta na mutum wanda ya haɗa da kwayar cutar rabies, ƙwayar cutar Ebola, ƙwayar cutar Nipah da ƙwayar cutar Hendra.
It is therefore not too surprising that bats might transmit HCoV-229E to humans directly.
Don haka ba abin mamaki bane cewa jemagu na iya yada HCoV-229E ga mutane kai tsaye.
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.
A wata hanya, yayin da alpha-CoVs suna aiki ne a matsayin hanyar samar da hanyar HCoV-229E, alpacas da raƙuman ruwa na iya zama matsakaiciyar runduna waɗanda ke aika ƙwayoyin cuta ga mutane, daidai kamar yadda yake a cikin yanayin 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 ya zama wani kyakkyawan misali game da watsa sadarwa daga jemage zuwa raƙuman dabbobi da kuma raƙumi zuwa ga mutane.
The evolutionary origin of MERS-CoV from bats is known at its initial identification and has also been strengthened by subsequent findings.
Asalin juyin halitta na MERS-CoV daga jemagu an san shi a farkon ganowarsa kuma ya sami ƙarfafuwa sakamakon binciken da ya biyo baya.
It is obvious that bats provide a rich pool of virus species for interspecies exchange of genetic fragments and interspecies transmission.
A fili take cewa jemagu sune matattarar da ke dauke da cututtukan da za su iya yada su daga dabbobi zuwa mutane.
Longevity, densely packed colonies, close social interaction and strong ability to fly are all favourable conditions for bats to be an ideal 'virus spreader'.
Dogon lokaci, dauloli masu cike da tarin yawa, kusanci da zamantakewa da kuma karfin ƙarfi don tashi duka yanayi ne da ya dace da jemage don zama kyakkyawan 'mai yada kwayoyin cutar.
On the other hand, MERS-CoV has been introduced to dromedary camels for decades.
A wata gefe guda, MERS-CoV an gabatar dashi ga raƙuman dromedary shekaru da yawa.
It is well adapted to these camels that have turned from an intermediate host to a stable and natural reservoir host.
Ya dace da waɗannan raƙuma waɗanda suka juya daga matsakaici mai ban sha'awa zuwa barikin mai tsaro da na ɗabi'a na dabi'a.
MERS-CoV causes very mild disease and maintains a relatively low mutation rate in these animals.
MERS-CoV yana haifar da ciwo mai laushi kuma yana riƙe da ƙarancin maye gurbi a cikin waɗannan dabbobi.
Its sporadic transmission to humans is an accident and humans remain a dead-end host of MERS-CoV as its transmission cannot be sustained.
Bazuwarta zuwa mutane ya faru haka kwatsam kmua mutane sune inda cutar MERS-CoV ba za ta iya sake fita ba sakamakon yadda bai iya fita daga nan.
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.
Ya bambanta da rawar raƙuma a cikin watsa MERS-CoV, rawar pangolins, idan akwai wani, a cikin watsawar SARS-CoV-2 ya bambanta.
Particularly, pangolin beta-CoVs are highly pathogenic in pangolins.
Musamman ma kwayoyin cutar jemagen pangolin beta-CoVs wanda sun fi rayuwa a jikin jemagun pangolins.
They might be a dead-end host for SARS-CoV-2-related beta-CoVs, similar to civets in the case of SARS-CoV.
Zasu iya zama mafakar karshe ga SARS-CoV-2-beta-CoVs masu dangantaka, da kama da dabbobin civets a yanayin 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.
Yawancin yuwuwar watsuwa tsakanin jinsuna na SARS-CoV-2 daga dabbobi zuwa mutane dole ne a yi watsi da su ko a amince da su a nazari gaba.
First, bats could be the reservoir host of a SARS-CoV-2-related virus almost identical to SARS-CoV-2.
Na farko, jemagu za su iya zama babban reshin raunin da ke da alaƙa da ƙwayar SARS-CoV-2 kusan iri ɗaya ce ga SARS-CoV-2.
Humans might share the ecological niche with bats through butchering or coal mining.
Yan-Adam na iya hadakar muhalli tare da jemagu ta hanyar yankan nama ko kuma hakar kwal.
Second, pangolins could be one of intermediate amplifying host to which a SARS-CoV-2-related virus had been newly introduced.
Na biyu, pangolins na iya zama ɗayan tsaka-tsakin fadadawa wanda aka gabatar da sabon ƙwayar cuta ta SARS-CoV-2.
Humans contract the virus through butchering and consumption of game meat.
Yan-Adam suna kamuwa da kwayar cutar ta fannin yanka da cin naman dabba.
It is possible that many mammals including domestic animals are susceptible to SARS-CoV-2.
Yana yiwuwa yawancin dabbobi masu shayarwa ciki har da dabbobin gida suna da saukin kamuwa da SARS-CoV-2.
A survey of domestic and wild animals for antibodies is warranted.
Lallai ne akwai bukatar gudanar da wani bincike kan dabbobin cikin gida da kuma na dawa/daji domin kariya ga jiki.
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.
Na uku, kamar yadda aka ambata a sama, sake sakewa da daidaitawa da SARS-CoV-2 na iya faruwa a cikin jinsin na uku wanda ke da alaƙa tare da jemage da kuma pangolins.
The search for the animal origins of SARS-CoV-2 is still on.
Binciken asalin SARS-CoV-2 daga dabba har yanzu ana kan yi.
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.
Baya ga mabanbanta dabbobin da ke daukar cutar, akwai wasu ababuwa uku muhimmai game da cutar wajen tsallakawa da halittun CoVs daga masu hana su fita.
First of all, their relatively high mutation rates in RNA replication.
Da farko dai, yawan adadin su na maye gurbi a cikin rabawar RNA.
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.
Idan aka kwatanta da sauran ƙwayoyin RNA guda ɗaya, masu ƙididdigar adadin maye gurbi na CoVs za'a iya ɗauka su azaman “Matsakaici” zuwa “babba” tare da matsakaicin sauyawa mai aiki wanda ya zama ~ 10-4 sauyawa a kowace shekara ta rukunin yanar gizon 2, gwargwadon tsarin karbuwa na CoV zuwa runduna mai labari.
CoVs have a proof-reading exoribonuclease, deletion of which results in exceedingly high mutability and attenuation or even inviability.
CoVs suna da hujjar sake-karantar exoribonuclease, sharewa wanda yake haifar da babban rikitarwa sosai da rashiwa ko mara dorewa.
Interestingly, the nucleotide analogue Remdesivir is known to suppress CoV replication through inhibition of this exoribonuclease and the RNA-dependent RNA polymerase.
Sai dai abin sha’awa a nan, asalin halittar cutar wanda galibi yake takura kwayar CoV ta hanyar haduwa da miyau ta sinadaran RNA.
Remdesivir is one of most promising anti-SARS-CoV-2 agents to be tested in clinical trials.
Remdesivir yana daya daga cikin masu ba da rigakafin maganin SARS-CoV-2 da za a gwada su a gwajin asibiti.
Nevertheless, mutation rates of CoVs are about a million times higher than those of their hosts.
Ko yaya dai, yawan maye gurbi na CoVs ya ninka sau miliyan sama da na ƙungiyar sojojinsu.
In addition, mutation rate is often high when CoVs are not well adapted to the host.
Bugu da kari, yawan maye gurbi yakan zama mafi girma yayin da CoVs ba su dace da mai zama da su ba.
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.
Idan aka kwatanta da SARS-CoV da babban maye gurbi, adadin maye gurbi na SARS-CoV-2 na kasa sosai, bayar da shawarar mafi girman matakin karbuwa ga mutane.
Presumably, it has already been adapted to another host close to humans.
Wataƙila, an riga an saba da shi ga wata mai zama da cutar da ke kusa da mutane.
In addition to SARS-CoV-2, this also applies to MERS-CoV, which is well adapted to dromedary camels.
Baya ga SARS-CoV-2, wannan kuma ya shafi MERS-CoV, wanda ya dace da raƙuma masu tozo guda.
Theoretically, it is unlikely that genetic drift would render vaccines and antivirals against SARS-CoV-2 ineffective quickly.
A ka’idodi, ba lallai bane cewa tsaran kwayoyin halitta zai iya samar da alluran rigakafi da rigakafi akan SARS-CoV-2 marasa tasiri da sauri.
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.
Na biyu kuma, babbar kwayar halittar RNA a jikin cutar CoVs ya nuna asalin sauyawa da rikida da tushen kwayoyin halitta suke yi, wanda hakan ke kara haifar da bazuwarsu tsakanin halittu wanda ya taimaka wajen bullar cututtukan CoVs masu shuhura a lokacin da suka samu dacewar yanayin da suke so.
This is supported by the copious unique open reading frames and protein functions encoded towards the 3′ end of the genome.
Wannan yana da goyan bayan yalwar budaddun faifan karatu na musamman da amfanin furotin mai lamba ta wurin ƙarshen 3′ na genome.
Third, CoVs randomly and frequently switch templates during RNA replication through a unique “copy-choice” mechanism.
Na uku, Covs na iya canza jiki barkatai da akai-akai lokacin rabuwar RNA ta hanyar “kwafin-zabi” na musamman.
In a host that serves as the mixing vessel, strand switching occurs frequently during CoV RNA transcription.
A cikin mafakar da take zama wurin gaurayuwa, canzawar sassa yana faruwa akai-akai a lokacin kwafar CoV RNA.
Highly homologous full-length and subgenomic RNAs could recombine to generate new CoVs.
Cigaba da cikakken-tsawon da bangarn genomic na RNAs mai sake haduwa don samar da sabbin abubuwan CoV.
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.
An samu shaidar asalin halitta daga yadda aka halicce take a jikin duka HCoV-HKU1 da kuma HCoV-OC43, har ma da jikin dabbobi CoVs kamar su jemagu SL-CoV da batCoV-HKU9.
Virus-host interaction in relation to transmission
Mu’amalar kwayar cuta daga inda take zama da kuma na yadda take bazuwa.
Besides three viral factors stated above, viral interaction with host receptor is another key factor influential on interspecies transmission.
Baya ga abubuwa guda uku da aka ambata a sama game da kwayar cutar, hulɗar kwayar cuta tare da mafaka mai karba wani abu ne dake tasiri akan watsuwa tsakanin jinsunar kwayar halittar.
Herein, recombination of SARS-CoV is taken as a typical example, which also showed evidence of positive selection during interspecies transmission events.
Anan, an sake haɗawa da SARS-CoV a zaman misali na yau da kullum, wanda kuma ya nuna tabbataccen zaɓi na ɗabi'a yayin watsuwa tsakanin jinsuna.
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.
Ta la'akari da gwajin kwatanci tsakanin keɓaɓɓun abu na SARS-CoVs din ɗan-adam da civet, Ana tunanin SARS-CoV zai iya yin saurin daidaituwa cikin mafaka daban-daban, musamman tare da maye gurbi a cikin furotin RBD na 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.
Gabaɗaya, RBD a cikin furotin na S na CoV yana hulɗa tare da tantanin halita mai karban sako da mai martini abin kare jiki.
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.
A cikin SARS-CoV, RBD yana cikin 318th zuwa 510 na amino acid din akan gungun S1, wanda ya daure wa dan Adam ACE2 kazalika hade da mai karban don shigar kwayar cuta.
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 na SARS-CoV yana da ikon sanin masu karɓar ACE2 na dabbobi daban-daban, gami da jemage, civet, bera da karen raccoon, wadda ke ba da izinin watsuwa tsakanin jinsuna kwayar cutar.
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.
A zahiri, amino acid guda 6 ne kawai da aka lura ya bambanta da na mutum kuma ƙwayar civet viral ta ware a cikin RBD kuma 4 daga cikinsu suna cikin motsi mai ɗaukar abubuwa don hulɗa da mai karɓar 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.
SARS-CoV na dabba Sivet yana da rikice-rikicen K479N da S487T a cikin RBD, wanda zai iya ƙara kusancin hulɗa da ma'adinin furotin tare da mai karɓar ACE2 na mutum.
In other words, these two amino acid substitutions might be critical to viral adaption to humans.
A takaice dai, wadannan maye gurbi na amino acid na iya zama mai matukar mahimmanci ga karbar kwayar cuta a jikin mutum.
It is noteworthy that SARS-CoV-2 shares the same cellular receptor with SARS-CoV.
Abin lura ne cewa SARS-CoV-2 yana raba tantanin halita mai karban sako (cellular receptor) iri daya da 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.
Bambanci kashi 30% tsakanin SARS-CoV-2 da SARS-CoV a cikin sashin S1 na furotin S yana nuna cewa ƙarshen dangantakar S furotin da dan adam ACE2 zai iya canzawa.
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.
Tabbas, binciken cryo-EM yana nuna dangantakar mafi girma ta 10 zuwa 20 daga wannan abin da aka ɗauka sama da wanda ke tsakanin ɗan adam na ACE2 da furotin na SARS-CoV S.
It will also be of interest to determine whether any other coreceptor might be required for SARS-CoV-2 transmission.
Hakanan zai kasance mai ban sha'awa don sanin ko za a buƙaci kowane sauran abokin karba don watsuwar SARS-CoV-2.
Intriguingly, HCoV-NL63 also binds to ACE2 but with a different part of S.
Mai ban sha'awa, HCoV-NL63 kuma yana ɗaure wa ACE2 amma tare da wani sashi na S.
There exist many other HCoV receptors, such as aminopeptidase N for HCoV-229E, and 9-O-acetylated sialic acid for HCoV-OC43.
Akwai sauran masu karɓar HCoV, kamar aminopeptidase N don HCoV-229E, da acid 9-O-acetylated sialic acid don HCoV-OC43.
They might also account for successful adaptation of these CoVs in humans after interspecies transmission from their animal hosts.
Zasu iya dauka nauyin samun nasarar daidaita wadatar waɗannan CoVs a cikin mutane bayan watsa nau'in halittu daga wurin dakaru dabbobin su.
In addition to cellular receptors, the outcome of interspecies transmission of HCoVs is also governed by other host dependency and restriction factors.
Baya ga tantanin halita mai karban sako, sakamakon watsuwar HCoVs ta tsakanin jinsuna shi ma ana sarrafa shi ta hanyar sauran abubuwan dogaro na mafaka da abubuwan ƙuntatawa.
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.
Rarraba waɗannan sunadaran masu kariya tsakanin ɗan adam da rarar halitta na rukunin HCoVs kamar jemagu, raƙumi da bera na iya zama cikas ga watsawar ma'amala.
HCoVs have to usurp host dependency factors and subvert host restriction factors for a successful interspecies transmission.
HCoVs dole su rinjayi dogaro kan mafaka sannan su fi karfin ƙuntatawar mafakarsu don nasarar watsuwa tsakanin jinsina daban-daban.
In this regard, molecular determinants in this important area of virus-host interaction remain to be identified and characterized.
Dangane da wannan, masu fayyace kwayoyin halitta a wannan muhimmin fannin na hulɗar kwayar cuta da mafakarta sun kasance har yanzu ana gano su kuma za a iya sanin su.
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.
Binciken yanayin rashin daidaituwa game da dogaro na mafaka da abubuwan ƙuntatawa don SARS-CoV-2 ta amfani da fasahar zamani ta CRISPR na iya zama mai amfani.
Emergence of novel HCoVs: back to ground zero
Fitowar HCoVs: Koma baya ga sifili
The diversity of bat CoVs provides ample opportunities for the emergence of novel HCoVs.
Bambancin CoVs na jemage yana bayar da isasshe dama ga fitowar sabon HCoVs da ke daban.
In this sense, bat CoVs serve as the gene pool of HCoVs.
Bisa wannan hujjar, cututtukan jemage na CoVs sune tushen cututtukan HCoVs.
In addition, rapid mutation and genetic recombination also drive HCoV evolution and serve as two important steps in this process.
Bugu da kari, saurin maye gurbi da sake halittar gado shima yana fitar da cigaban HCoV kuma yana zama matakai biyu masu mahimmanci a wannan aikin.
For example, the acquisition or loss of novel protein-coding genes has the potential to drastically modify viral phenotypes.
Alal misali, siyarwa ko asarar kwayoyin halittar furotin dana duniya suna da damar canza kwayar cutar kwayar halitta ta wata hanya.
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.
Daga cikin furotin na kariya na SARS-CoV, ORF8 ana tsammanin yana da mahimmanci a cikin dacewa da mutane, kamar yadda SARS-CoV masu hade da ƙwayoyin cuta jemage wanda aka keɓancewa amma an sami sinadarai masu bambam da furotin na ORF8.
A 29-nucleotide deletion characteristic of SARS-CoVs has been found in strains isolated at the beginning of the human epidemic.
An gano rugujewar kwayar halittar 29 daga yanayin SARS-CoVs a jini a farkon lokacin da aka fara gano annobar a jikin dan adam.
This deletion splits ORF8 into ORF8a and ORF8b and is thought to be an adaptive mutation that promotes the switch of hosts.
Wannan sharewa ta shiga ORF8 zuwa ORF8a da ORF8b kuma ana zaton shine maye gurbi wanda yake inganta canjin mafaka.
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.
Bayan haka, SARS-CoV yana da yiwuwar sake duba tarihin tare da layin alpha- da gamma-CoVs, inda aka gano yawancin adadin yankuna masu rarrafe a cikin polymrase ɗin RNA da suke dogara da RNA.
Recombination locations were also identified in the nsp9, most of nsp10, and parts of nsp14.
An kuma gano wuraren sake canzawa a cikin nsp9, mafi yawan nsp10, da kuma sassan 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.
Hakanan, an nuna cewa annobar MERS-CoV ta sami abubuwan sake haduwa tsakanin layuka daban-daban, wanda ya faru a cikin raƙuman masu tozo guda a Saudiya.
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.
Gefen wannan SARS-CoV da MERS-CoV, an kuma lura da abubuwan sake maye a cikin wasu HCoVs, wanda HCoVs suka sake haɗuwa da wasu CoVs na dabba a cikin abubuwan halittar da basu da tsari.
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.
Hakanan ya kamata a yi gargaɗin cewa zaɓin ɗan adam zai iya ba da gudummawa ga canje-canjen da ba a yi tsammani ba a kwayoyin halittar, wataƙila ana haifar da sauƙaƙe ƙwayoyin cuta daga matsanancin zaɓi, kamar su tsarin garkuwar jiki.
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.
Misalin waɗannan tasirin shine asarar cikakken tsawon ORF4 a cikin ƙwayar samfurin HCoV-229E, sakamakon shafewar nucleotide guda biyu.
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.
Duk da yake ana iya lura da ingantaccen ORF4 a cikin ƙwayoyin cutar jemage da raƙumi waɗanda ke da alaƙa da HCoV-229E, alpha-CoV ta rakumin alpaca yana nuna guda ɗaya na nucleotide, wanda ya haifar da sauyin frameshift.
Last but not least, the evolution of novel HCoVs is also driven by the selection pressure in their reservoir hosts.
Daga ƙarshe amma ba ƙarami ba, juyin halittar sabbin HCoVs yana kuma faruwa ne ta hanyar matsi na zabin a cikin mafakar taskokinsu.
Asymptomatic or only mild symptoms were detected when bats were infected with CoVs, indicating the mutual adaptation between CoVs and bats.
Mai nuna ya kamu da cuta ko kawai bayyanar cututtuka ne aka gano yayin da Jemagu sun kamu da cuta na CoVs, yana nuna daidaitawar juna tsakanin CoVs da jemagu.
It appeared that bats are well adapted to CoVs anatomically and physiologically.
Ta bayyana cewa jemagu sune matattarar kwayoyin halittar CoVs lura da yanayin jikinsu da kuma yadda gabobin jikin nasu ke aiki.
For example, defects in the activation of pro-inflammatory response in bats efficiently reduce the pathology triggered by CoVs.
Alal misali, lahani a cikin faifan martani na maganin kumburi-kumburi a cikin jemagu yadda yakamata ya rage cutarwar da CoVs tayi.
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.
Bayan haka, ayyukan kwayar halittar kisa a cikin jemagu tana lalacewa sakamakon hauhawar mai hana karbar kwayar halittar kisa NKG2/CD94 da ƙarancin matakin bayyana manyan kwayoyin halittun aji I hadaddu masu dacen jini.
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.
Haka kuma, babban nau'in nau'in oxygen mai aiki (ROS) wanda aka samo asali daga ayyukan kwayoyi na jemagu na iya murkushe kwafin kwayar CoV kuma yana shafar karantawa ta hanyar karba-karba, ta haka ne samar da matsin zabi na tsararrakin kwayar cuta mai matukar birgeshi yayin gabatar da shi cikin sabon mai watsa shiri.
More pathogenic CoV strains might also evolve by recombination, leading to the acquisition of novel proteins or protein features for host adaptation.
Haka kuma cututtukan CoV na pathogenic CoV na iya canzawa ta hanyar sake halittar, wanda ke haifar da sifofin furotin ko littafin fasalin furotin don karbuwa.
Thus, it is not by chance that three novel HCoVs have emerged in the past two decades.
Don haka, babu wat hanya ba ne cewa uku na HCoVs sun fito a cikin shekaru ashirin da suka gabata.
CoVs are non-pathogenic or cause mild symptoms in their reservoir hosts such as bats and camels.
CoVs ba cuta ba ne ko haifar karamin alamu cuta a cikin ɗakunan masu kamu da su kamar gemage da raƙuma.
They replicate robustly without eliciting a strong host immune response.
Suna iya rarrabawa sosai ba tare nuna garkuwar jiki daga mai zama da ciwon ba.
Herein lie the secrets of why asymptomatic carriers are seen and what causes the severe cases in human infection.
Anan ne aka samu sirrin me ya sa marasa nuna alamar kamuwa ake ganinsu da kuma abun da yake haifar da mummunan lamura a kamuwa da cutar a mutum.
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.
Radadin alamun cutar suna faruwa ne sakamakon yadda kwayoyin halittar jikin mutum masu yaki da cuta suke kokarin yakar cutar wanda idan aka samu karfin nasu sosai hakan zai kuma yi illar gaske ga huhun mutum.
In contrast, in asymptomatic carriers, the immune response has been de-coupled from CoV replication.
Sabanin haka, a cikin marasa nuna alamar kamuwa da cutar, amsa rigakafi ya kasance kasa ga yaduwar Cov.
The same strategy of delinking the immune response might have beneficial effects in anti-SARS-CoV-2 therapy.
Dabarun iri daya ta raba cudanya da amsawar rigakafin iya samun sakamako masu amfani a cikin maganin anti-SARS-CoV-2.
The interferon response is particularly strong in bats.
Amsar interferon tana da ƙarfi musamman a cikin jemagu.