atepeq/tico19 huggingface dataset:
In contrast, highly pathogenic SARS-CoV and MERS-CoV have not adapted to humans well and their transmission within humans cannot be sustained.
Na bokeseni, SARS-CoV na MERS-CoV oyo ebelisaka mingi emesana te na nzoto ya bato mpe ndenge moko te ezali mpona kokanga kopanzana na yango na kati ya bato.
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.
Ekosenga etikala mpe epanzana kaka na kati ya banyama mpe koluka libaku ya kokota na bato, mingimingi na nzela ya eloko moko to biloko mingi mpe ya malamu oyo ekoki komema yango.
SARS-CoV-2 has features that are similar to both SARS-CoV/MERS-CoV and the four community-acquired HCoVs.
SARS-CoV-2 eza na bilembo oyo ekokani na oyo ya SARS-CoV/MERS-CoV mpe HCoVs minei mosusu oyo bato bazwaka.
It is highly transmissible like community-acquired HCoVs, at least for the time being.
Epanzanaka makasi lokola ba HCoVs oyo bato bazwaka, ata kaka mpo na sikoyo.
However, it is more pathogenic than community-acquired HCoVs and less pathogenic than SARS-CoV or MERS-CoV.
Kasi, ebelisaka makasi koleka HCoVs oyo bato bazwaka kasi ebelisaka makasi te lokola SARS-CoV to 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.
Tokozela na koyeba soki ekomesana mpenza na bato mpe ekotambola na kati ya bato kozanga biloko oyo ememaka yango to banyama oyo ememaka yango.
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.
Liboso ya kolobela esika HCoVs eutaka, ekozala malamu tolobela bandimbola na yango mpe ndenge ekolaka, bozalisi, esika efandaka, bisika elekaka mpe biloko oyo ekomisaka yango HCoVs makasi.
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.
Nyama nde eza esika HCoV ekolaka soki efandi nkoko moko oyo eza na boyakani makasi na kokola ya nucleotide.
The ancestral virus is usually well adapted and non-pathogenic in this host.
Nkoko ya virisi emesana makasi mpe epesaka maladi te na eloko oyo, oyo ebombaka bango.
Likewise, a reservoir host harbours HCoV continuously and for long term.
Ndenge moko, eloko moko oyo ememaka HCoV ekomaka kobomba yango na eleko ya molai.
In both cases, the hosts are naturally infected and are the natural hosts of HCoV or its parental virus.
Na bandakisa nyonso mibale, biloko oyo ebombaka yango ezwaka maladi mpe esika ebongi mpo na kobomba HCoV to na virisi oyo ebota yango.
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.
Kasi, soki HCoV ekoti sika na esika ya malamu oyo ebombaka yango liboso to pene ya kokota na nzoto ya bato, emesanaka malamu te na esika ya sika mpe mbala mingi epesaka maladi.
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.
Esika oyo ya mibale oyo efandaka ekoki kozala banyama oyo epesaka maladi na bato mpe esalisaka mingi na kokomisa yango makasi ndenge epesaka virisi nzela ya kobota mpe na nsima kokota na nzoto ya bato mpe kopusa likolo ndenge ezali kobelisa bato mingi.
An HCoV can undergo a dead-end infection if it cannot sustain its transmission within the intermediate host.
HCoV ekoki kopesa maladi oyo ebomaka soki bakoki kokanga yango te nzela ya kopanzana kati ya eloko ya mibale oyo ebombaka yango.
On the contrary, HCoVs can also adapt to the intermediate host and even establish long-term endemicity.
Kasi, HCoVs ekoki mpe komesana na esika ya mibale oyo efandi mpe nkutu eumela na bisika efandaka.
In this case, the intermediate host becomes a natural reservoir host.
Na ndakisa oyo, esika ya mibale oyo efandaka ekomaka esika na yango ya malamu ya kofanda.
Epidemiological data revealed retrospectively that the index case of SARS had a contact history with game animals.
Bansango ya maladi mabe emonisaki ete bato oyo babelaki SARS bazalaka na lisolo ya boyokani banda kala na banyama ya kosakana.
Subsequent seroprevalence investigations indicated that animal traders had a higher prevalence of anti-SARS-CoV IgG compared with that of the general population.
Bolukiluki basalaki na maladi oyo yango epesaka emonisi ete bato batekaka banyama baza na likoki makasi ya kobundisa SARS-CoV IgG soki tokokanisi yango na bato nyonso.
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.
Banyama ebengami civette palmée masquée (Paguma larvata) mpe mbwa moko ya vivverin na bazando ya banyama ya bomoi, bamonaki na mbala ya liboso ete ezalaka na bavirisi oyo ekokani na SARS-CoV oyo eza mpenza ndenge moko na SARS-CoV.
This was indirectly supported by the fact that no further SARS was reported after killing all civets in the markets.
Basungaki yango mpo bamonaki ete ba SARS misusu emonanaki nsima ya koboma ba civette nyonso na bazando.
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.
Kasi, balobi ete ba civette palmée masquée oyo euti na zamba to na bilanga kozanga ete batya yango na bazando ya banyama ya bomoi ata mokok te ezalaki SARS-CoV, yango emonisi ete mbala mosusu ba civette wana ezalaka kaka esika ya mibale virisi SARS-CoV efandaka kasi ezali esika na yango ya libosoliboso te.
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.
Likambo ezali kobenda likebi, mpo 80% banyama oyo bazalaka na bazando ya Guangzhou bazali na ba anticorps oyo ebundisaka SARS-CoV, tokoki kokanisa mpe ete banyama mosusu ya mike bazali esika ya mibale oyo bavirisi ya SARS-CoV efandaka.
All of these appear to be dead-end hosts of SARS-CoV.
Nyonso wana ezali bisika ya suka oyo SARS-CoV efandaka.
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.
Bolukiluki mosusi na banyama oyo ebombaka SARS-CoV emonisaki boyokani makasi na ngembo ya CoV, oyo babengi SARS Rhinolophus ya ngembo CoV HKU3 (SARSr-Rh-BatCoV HKU3), oyo ezalaka na ngembo ya libende ya mpunda oyo ezalaka na Chine.
These bats are positive for anti-SARS-CoV antibodies and genome sequence of SARSr-Rh-BatCoV HKU3.
Bangembo oyo bazali na ba anti corps oyo ebundisaka SARS-CoV mpe genome ya SARSr-Rh-BatCoV HKU3.
This and other bat CoVs share 88-92% nucleotide sequence homology with SARS-CoV.
Ngembo oyo mpe ngembo ya CoVs ezali na 88-92% ya ba nucleotide ya ndenge moko na SARS-CoV.
These studies have laid the foundation for the new concept that bats host emerging human pathogens.
Balukiluki oyo esalisa mpo na kobimisa likanisi ya sika ete bangembo nde bamema maladi oyo bato bazwa.
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.
Bamona mpe ete ba CoVs (SL-CoVs) mingi oyo ezali neti SARS euta na bangembo, kasi kaka WIV1 kati na nyonso ekoki kolobama ete ezali virisi oyo ezali na bomoi.
Human angiotensin converting enzyme 2 (ACE2) is known to be the receptor of SARS-CoV.
Eyebani ete enzyme 2 (ACE2) oyo ebongolaka angiotensine ya bato nde eza ebombeli ya SARS-CoV.
WIV1 derived from fecal sample of bats was demonstrated to use bat, civet and human ACE2 as receptor for cell entry.
WIV1 oyo euti na nyei ya bangembo esalelamaki mpo na komonisa ndenge ya kosalela ngembo, civet mpe bato ACE2 neti esika ya koyamba baselile oyo ezali kokota.
Intriguingly, sera of convalescent SARS patients were capable of neutralizing WIV1.
Likambo ya ntina ezali ete, sera ya bato oyo bazalaki kobika na SARS ekokaki koboma WIV1.
Thus far, WIV1 represents the most closely related ancestor of SARS-CoV in bats, sharing 95% nucleotide sequence homology.
Kino sikoyo, WIV1 ezali nkoko ya pene ya SARS-CoV na bangembo, mpo ezali ba nucleotide 95% ya ndenge moko.
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.
Ata boyokani ezali mingi na kati ya bavirisi mibale oyo, mbala mingi bato bandimaka ete WIV1 ezali te esika ya mibale oyo virisi ya SARS-CoV efandaka mpe bangebo bazali te esika oyo SARS-CoV efandaka.
Phylogenetic analysis clusters MERS-CoV to the same group as bat CoV-HKU4 and bat CoV-HKU5.
Botaleli ya boyokani na yango ya ba MERS-CoV na etuluku moko na ngembo CoV-HKU4 mpe ngembo CoV-HKU5.
Bat CoV-HKU4 and MERS-CoV utilize the same host receptor, dipeptidyl peptidase 4 (DPP4), for virus entry.
Ngembo ya CoV-HKU4 mpe MERS-CoV esalelaka eloko moko mpo na koboya, dipeptidyl peptidase 4 (DPP4), mpo na kokotisa virisi.
RNA-dependent RNA polymerase sequences of MERS-CoV are phylogenetically closer to counterparts in bat beta-CoVs identified from Europe and Africa.
RNA-etaleli RNA polymerase oyo elandi MERS-CoV ezali maladi moke oyo ezali pene ya ngembo mosusu ya beta-CoVs oyo bamonaki na Eropa mpe na Afrika.
Up to now, no live MERS-CoV can be found in wild bats.
Kino sikoyo, tokoki komona te ata MERS-CoV moko ya bomoi na bangembo ya zamba.
MERS-CoV and its closest relative bat CoV-HKU25 share only 87% nucleotide sequence homology.
MERS-CoV mpe oyo ya libota na ye ya pene ngembo CoV-HKU25 ezali na 87% ya nucleotide ya ndenge moko.
Thus, bats might not be the immediate reservoir host of MERS-CoV.
Yango wana, bangembo bakoki te bisika ya libosoliboso oyo MERS-CoV efandaka.
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.
Kasi, bolukiluki na moyen orient emonisi ete bakamela ya dromadaire ezalaka na MERS-CoV oyo ebomaka makila oyo ebundisaka maladi, ndenge moko na bakamela euta na moyen orient oyo ezali na mikili mingi ya Afrika.
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 ya bomoi ya ndenge moko na virisi oyo bamonaka na bato, babimisaki yango na zolo ya bakamela ya dromadaire, emonisi lisisu ete bakamela ezali bisika oyo MERS-CoV efandaka.
It is also noteworthy that generally mild symptoms but massive virus shedding were observed in camels experimentally infected with MERS-CoV.
Ezali mpe ntina mpo mbala mingi bilembo ya pete kasi ya ntina mingi ya kopanzana ya virisi emonanaki na bakamela oyo batelelaki oyo ezalaka na 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.
Likambo ya ntina, bakamela oyo ezalaki na maladi epanzaki virisi kaka te na nzela ya kopema kasi mpe banda na nyei kino na monoko, yango ezali mpe nzela oyo virisi eutaka na bangembo mpe ekoteli biso.
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.
Kasi, mituna ezali kaka mpo bato mingi oyo babela MERS bakutanaki te na bakamela liboso ete maladi wana ebanda, mbala mosusu moto moko apesaki basusu to toyebi te ndenge epesamaki uta na banyama eyebani te oyo ezalaki na MERS-CoV.
SARS-CoV-2 shares 96.2% nucleotide homology with a bat CoV RaTG13 isolated from Rhinolophus affinis bats.
SARS-CoV-2 ezali na 96,2% ya ba nucleotide ya ndenge moko na ngembo CoV RaTG13 oyo bazwaki na bangembo 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.
Lokola na bandakisa ya SARS-CoV mpe MERS-CoV, bokeseni eza kati na SARS-CoV-2 mpe RaTG13 eza makasi mpenza yango wana mwaye ezali te ya koloba bauta esika moko.
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.
Elingi koloba, bangembo ekoki te esika to bisika ya mibale oyo ebombaka SARS-CoV-2 longola kaka soki tomoni oyo ezali ndenge moko na ngembo ya CoVs na mikolo ezoya.
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.
Emonani ete, nyama oyo ezali esika ya mibale ya SARS-CoV-2 esengeli kozala na kati ya banyama ya zamba oyo batekaka mpe babomaka biloko ya mbu na Huanan, esika oyo bato bakanisaka ete bavirisi mingi ya COVID-19 eutaki, emonisi ete mbala mosusu bato bazwaki yango na banyama.
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.
Bolukiluki mingi na oyo etali metagenome emonisi ete etuluku moko ya banyama oyo ezali na likama oyo babengaka bapangolin (Manis javanica) ekoki kozala bankoko ya beta-CoVs oyo ezali na boyokani na SARS-CoV-2.
These novel pangolin CoV genomes share 85-92% nucleotide sequence homology with SARS-CoV-2.
Bagenome ya pangolin ya sika ya CoV ekaboli 85-92% ya ba nucleotide ya ndenge moko na SARS-CoV-2.
However, they are equally closely related to RaTG13 with about 90% identity at the level of nucleotide sequence.
Kasi, bakokani mpenza na RaTG13 mpo ezali ndenge moko na 90% na nivo ya ba 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.
Liboke na yango na milongo mibale ya mike ya bavirisi ya SARS-CoV-2 oyo euti na nzete, oyo eza ndenge moko na esika ya kouta ndenge moko (RBD) na SARS-CoV-2, 97,4% ya amino aside na yango.
In stark contrast, the RBDs of SARS-CoV-2 and RaTG13 are more divergent, albeit a higher degree of sequence homology genome-wide.
Na kokesene makasi, RBDs ya SARS-CoV-2 mpe ya RaTG13 ekeseni mingi, ata ezali na bokokani makasi na nivo ya ba genome.
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.
Bolukiluki moko ya kala na ba pangolin oyo bakufa emonisi ete ezalaki na bavirisi na bapoumon, mpe ezalaki ndenge moko na 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.
Bolukiluki oyo esalelaka mayele mosusu mpo na kosangisa na kobikisa mpo babimisa genome oyo ezali kati ya 86,3% ya molai mobimba ya virisi ya genome.
We cannot exclude the possibility that pangolin is one of the intermediate animal hosts of SARS-CoV-2.
Tokoki koboya te ete pangolin akoki kozala moko ya bisika ya mibale oyo ebombaka 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.
Kasi, kala mingi ezali na bilembeli oyo endimisi ete SARS-CoV-2 eutaka mpenza na pangolin mpo na bokeseni oyo ezali kati ya SARS-CoV-2 mpe pangolin SARS-CoV-2 oyo ekokani na 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.
Lisusu, mosika na kati ya SARS-CoV-2 mpe RaTG13 ezali moke mpenza koleka na kati ya SARS-CoV-2 mpe SARS-CoV-2 euti na bangolin beta-CoVs.
The evolutionary pathway of SARS-CoV-2 in bats, pangolins and other mammals remains to be established.
Bokoli ya nzela ya SARS-CoV-2 na bangembo, ba pangolin mpe banyama moko eyebani naino te.
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.
Ata boyokani ya makasi ezali na kati ya RBDs na SARS-CoV-2 mpe pangolin, SARS-CoV-2- ya beta-CoVs, SARS-CoV-2 mpe RaTG13 ezali na bagenome mingi mpenza ya ndenge moko.
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.
Bato bazoloba mingi ete bokokani ya mingi makasi na kati ya RBDs ya pangolin SARS-CoV-2 ya beta-CoVs mpe SARS-CoV-2 euti na ndenge ekolaka na ndenge ya kokabwana mingi.
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.
Likanisi ekeseni mpo na bosangani na kati ya pangolin moko ya SARS-CoV-2- mpe beta-CoV na RaTG13 na molongo ya minei ya banyama ya zamba.
As a driving force in evolution, recombination is widespread among beta-CoVs.
Mayele oyo esalemaka mingi na evolution, kosangana lisusu esalemaka mingi na kati ya beta-CoVs.
The jury is still out on the immediate zoonotic origin of SARS-CoV-2.
Jury eyebi kaka te nyama nini ezali esika oyo SARS-CoV-2 eutaka.
Besides the highly pathogenic HCoVs, the zoonotic origin of HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1 have also been studied.
Longola maladi moyo HCoVs epesaka, basi bayekoli mpe soki HCoV-229E, HCoV-OC43, HCoV-NL63 mpe HCoV-HKU1 euta na banyama.
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.
Bilembeteli ya phylogenetique emonisi ete mbala mosusu HCoV-NL63 mpe HCoV-229E eutaki na ngembo CoVs, kasi bavirisi ya HCoV-OC43 mpe HCoV-HKU1 euta na ba rongeur.
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.
Barapore emonisi ete ngembo ya CoV oyo babengi ARCoV.2 (Appalachian Ridge CoV) bamonaki yango na Amerika ya norde, mpe ngembo ya langi misato ezalaki na boyokani makasi na 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.
Na ngambo mosusu, HCoV-229E ezalaka ndenge moko na CoV mosusu ya ngembo, oyo babengaki Hipposideros/GhanaKwam/19/2008, oyo bamonaki na Ghana, kasi balobaki ete esika na yango ya mibale ya kofanda ezalaki camelidés.
For clarity, the current knowledge on animal origins of known HCoVs is summarized in Figure ​1 and Table 2.
Mpo na koyeba malamu, boyebi ya sika ete HCoVs euta na banyama, bamonisi yango na mokuse na Motango​1 mpe Tablo 2.
Phylogenetic analysis has provided evidence for interspecies transmission events of HCoVs in the history.
Botaleli ya phylogenetique emonisi bilembeteli ete na lisolo na yango HCoVs euta na ekelamu moko mpe eleki na basusu.
When HCoV-OC43 crossed species to infect humans from domestic livestock around 1890, a pandemic of respiratory infection was recorded.
Ntango HCoV-OC43 eutaka na ekelamu moko mpe eleki na mosusu mpo ekota na bato longwa na bibwele pene ya 1890, balobaki ebimisaki maladi moko ya mpema.
The interspecies transmission history of HCoV-229E is less clear.
Lisolo oyo emonisi ndenge HCoV-229E eutaki na ekelamu moko mpe eleki na mosusu ezali polele te.
Bat alpha-CoVs closely related to HCoV-229E have been found.
Basi bamona ete alpha-CoVs ya ngembo ezali na boyokani makasi na HCoV-229E.
Between them there is an alpaca alpha-CoV.
Na kati na yango ezali na alpaca alpha-CoV moko.
Several lines of evidence support the transmission of virus from bats to humans directly.
Bilembetli mingi endimisi ete virisi wana eutaki na bangembo ebongo bapesaki yango mbala moko na bato.
First, humans but not alpacas might have contact with bats in a shared ecological niche.
Ya liboso, bato kasi ba alpaca te nde ekutanaki na bangembo na esika oyo bafandaka.
Instead, humans have close contact with alpacas.
Atako bongo, bato bazali na boyokani ya pembeni mpenza na ba alpaca.
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.
Ya mibale, HCoV-229E- euta na ngembo, alpha-CoVs ekeseni mpe epesaka maladi te na bangembo, kasi alpha-CoV alpaca ebimisaki maladi ya mpema na banyama oyo bazalaki na yango.
Finally, alpaca alpha-CoV has not been found in feral animals.
Na nsuka, alpha-CoV alpaca emonana te na nyei ya banyama.
Thus, the possibility cannot be excluded that alpacas obtain the HCoV-229E-related alpha-CoV from humans.
Yango wana, tokoki koboya te mbala moko ete ba alpaca bazwaki HCoV-229E ya alpha-CoV na bato.
In fact, bats are the direct source of human pathogenic viruses including rabies virus, Ebola virus, Nipah virus and Hendra virus.
Ya solo, bangembo bazali na ebandeli ya bavirisi mingi oyo ememela bato maladi, na ndakisa virisi ya bampuku, virisi ya Ebola, virisi Nipah mpe virisi Hendra.
It is therefore not too surprising that bats might transmit HCoV-229E to humans directly.
Yango wana ezali kokamwisa te soki mbala mosusu bangembo nde bato bapesaki bato mbala moko virisi HCoV-229E.
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.
To, ata alpha-CoVs ngembo yango nde epesa makila na yango na CoV-229E, ba alpaca mpe bakamela dromadaire ekoki kozala esika ya mibale oyo efandaka oyo ememelaka bato bavirisi, kaka ndenge esalemaki mpo na 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 ezali ndakisa ya malamu emonisa ndenge virisi eutaki na bangembo mpe ekomaka na bakamela dromadaire mpe longwa na bakamela dromadaire mpe ekotela bato.
The evolutionary origin of MERS-CoV from bats is known at its initial identification and has also been strengthened by subsequent findings.
Bokoli ya esika MERS-CoV euta banda na bangembo eyebani ndenge bamonaki yango na ebandeli mpe makambo bamona nsima epusaka na kondima bango.
It is obvious that bats provide a rich pool of virus species for interspecies exchange of genetic fragments and interspecies transmission.
Eyebani ete bangembo bazali na bavirisi mingi oyo ekabolamaka na kati ya bikelamu mingi mpe ndenge eutaka na ekelamu moko mpe ekotaka na ekelamu mosusu.
Longevity, densely packed colonies, close social interaction and strong ability to fly are all favourable conditions for bats to be an ideal 'virus spreader'.
Kuwemela, kofanda bituluku moko, kozala na boyokani ya pene mpenza mpe makoki makasi ya kopumbwa ezali malamu mpenza mpo bangembo bazala ekelamu ya ‘kopanza virisi’.
On the other hand, MERS-CoV has been introduced to dromedary camels for decades.
Na ngambo mosusu, MERS-CoV ekotela bakamela dromadaire banda kala.
It is well adapted to these camels that have turned from an intermediate host to a stable and natural reservoir host.
Emesana mingi na bakamela wana yango wana ezalaka lisusu te esika na yango ya mibale ya kofanda kasi esika ebonga mpe ya malamu mpo na yango.
MERS-CoV causes very mild disease and maintains a relatively low mutation rate in these animals.
MERS-CoV ebimisaka maladi ya makasi te mpe epanzanaka mingi mpenza na kati ya banyama wana.
Its sporadic transmission to humans is an accident and humans remain a dead-end host of MERS-CoV as its transmission cannot be sustained.
Ndenge ekota na bato ezali libaku mpe bato bakotikala kolata yango suka mpo kopanzana ya MERS-CoV ekoki kolanda te.
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 kokesena na mokumba ya bakamela na kopanzana ya MERS-CoV, mokumba ya bapangolin, soki ekoki kozala, na kopanzana ya SARS-CoV-2 eza ya kokesena.
Particularly, pangolin beta-CoVs are highly pathogenic in pangolins.
Mingimingi, beta-CoVs pangolin epesaka maladi mingi na bapangolin.
They might be a dead-end host for SARS-CoV-2-related beta-CoVs, similar to civets in the case of SARS-CoV.
Bakozala esika ya liwa mpona SARS-CoV-2 mpe beta-CoVs, ndenge moko na ba civette mpo na 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.
Ezali na makoki mingi mpo SARS-CoV-2 euta na ekelamu moko mpe ekota na mosusu, uta na banyama mpe ekotela bato, kasi ekosenga nde bolukiluki ya mikolo ezali koyaka nde endimisa yango.
First, bats could be the reservoir host of a SARS-CoV-2-related virus almost identical to SARS-CoV-2.
Ya liboso, bangembo ekoki kozala esika bavirisi SARS-CoV-2 efandaka oyo ekokani mpenza na SARS-CoV-2.
Humans might share the ecological niche with bats through butchering or coal mining.
Bato bakoki kokabola esika moko elongo na bangembo na nzela ya koboma bango to na mine ya makala.
Second, pangolins could be one of intermediate amplifying host to which a SARS-CoV-2-related virus had been newly introduced.
Liboso, ba pangolin bakoki kozala moko ya bisika ya mibale ya malamu oyo virisi SARS-CoV-2 ekota kala te.
Humans contract the virus through butchering and consumption of game meat.
Bato bazwaka virisi na nzela ya koboma banyama mpe kolya mosuni ya banyama.
It is possible that many mammals including domestic animals are susceptible to SARS-CoV-2.
Ekoki kozala ete banyama babengami bamamifere ata banyama efandaka na ndako ekoki kozwa SARS-CoV-2.
A survey of domestic and wild animals for antibodies is warranted.
Bolukiluki na banyama ya ndako mpe ya zamba mpo na kosala ba anticorps ebongi mpenza.
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.
Ya misato, ndenge tolobeli likolo, kosangisa lisusu mpe komesana ya SARS-CoV-2 mbala mosusu esalemaki na ekelamu ya misato oyo ekutanaki na bangembo mpe bapangolin.
The search for the animal origins of SARS-CoV-2 is still on.
Bazali kosala bolukiluki mpo na koyeba esika SARS-CoV-2 euta.
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.
Longola balolenge wana ya banyama oyo ekoki kozala na yango, makambo misato ya minene etali virisi oyo eza mpe ntina mingi mpo na kosalisa CoVs ezali kokota na bikelamu mosusu.
First of all, their relatively high mutation rates in RNA replication.
Ya liboso, ndenge etambolaka mingi na RNA mpe ebotaka.
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.
Na bokeseni na bavirisi mosusu ya RNA, ndenge CoVs etambolaka ekoki kotalelama neti “ya malamu” mpe “ya makasi” mpe echangaka na ~10-4 na mbula moko na bisika 2, na kotalela lolenge ya CoV ndenge ezali komesana na bisika na yango ya sika.
CoVs have a proof-reading exoribonuclease, deletion of which results in exceedingly high mutability and attenuation or even inviability.
CoVs ezali na botangi moko ya exoribonuclease, koboma yango ekoki kosala ete ebotama lisusu mingi mpenza mpe kokitisa bokasi na yango to nkutu ekoka kokola te.
Interestingly, the nucleotide analogue Remdesivir is known to suppress CoV replication through inhibition of this exoribonuclease and the RNA-dependent RNA polymerase.
Likambo ezali kobenda likebi ezali ete eyebani ete nucleotide ya ntina ya Remdesivir ebomaka kobotama ya CoV ndenge ekangaka exoribonuclease oyo mpe RNA oyo eutaka na polymerase RNA.
Remdesivir is one of most promising anti-SARS-CoV-2 agents to be tested in clinical trials.
Remdesivir eza moko ya bankisi ya malamu mingi ya SARS-CoV-2 oyo esengeli bameka yango na bato.
Nevertheless, mutation rates of CoVs are about a million times higher than those of their hosts.
Atako bongo, motango ya mutation ya CoVs ezali likolo pene ya milio moko koleka ya bisika oyo efandaka.
In addition, mutation rate is often high when CoVs are not well adapted to the host.
Lisusu, mbala mingi motango ya mutation ezalaki mingi soki CoVs emesani te na esika na yango ya sika.
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.
Soki tokokanisi yango na SARS-CoV oyo ezali na motango ya mutation ya likolo, emonani ete motango ya mutation ya SARS-CoV-2 ezali na nse, oyo ezali komonisa ete emesanaka mingi mpenza na bato.
Presumably, it has already been adapted to another host close to humans.
Tokoki koloba ete, esi emesana na esika mosusu ya kofanda oyo ezli pene na bato.
In addition to SARS-CoV-2, this also applies to MERS-CoV, which is well adapted to dromedary camels.
Longola SARS-CoV-2, etali mpe MERS-CoV, oyo emesana malamu na bakamela dromadaire.
Theoretically, it is unlikely that genetic drift would render vaccines and antivirals against SARS-CoV-2 ineffective quickly.
Na maloba, ezali mpo mbongwana ya genotype ekobimisa mangwele mpe bankisi ya kobundisa virisi SARS-CoV-2 mpo noki ezala makasi te.
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.
Ya mibale, genome RNA ya monene oyo ezali na CoVs ezala na mwa bopusi na mbongwana oyo esalemaka mpe na bozongi na yango, yango wana ematisaka makoki na yango ya kokola, mpe ezali malamu mpo na kobima ya CoVs ya sika ntango makambo ekobonga.
This is supported by the copious unique open reading frames and protein functions encoded towards the 3′ end of the genome.
Likambo oyo esimbami na ndenge bakadre na yango efungwamaka mpe mosala ya proteine ebimisaka 3’ nsuka ya genome.
Third, CoVs randomly and frequently switch templates during RNA replication through a unique “copy-choice” mechanism.
Ya misato, CoVs ebongolaka ndenge na yango kaka boye mpe mbala mingi ntango ebongolaka RNA na nzela ya mayele ya kokamwa ya “kopona-kopi”.
In a host that serves as the mixing vessel, strand switching occurs frequently during CoV RNA transcription.
Na esika oyo efandaka mpe oyo esalaka na kosangisa yango, ebongwanaka mbala mingi na ntango ya kokoma CoV RNA.
Highly homologous full-length and subgenomic RNAs could recombine to generate new CoVs.
Ba RNAs ya milai mingi ya ndenge moko mpe ba genome ya mike ekoki kosangana mpo na kobimisa CoVs ya sika.
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.
Bilembeteli ya phylogenetique ya kosangana ya normal emonanaki na HCoV-HKU1 mpe HCoV-OC43, mpe na CoVs nyama na ndakisa SL-CoV ngembo mpe batCoV-HKU9.
Virus-host interaction in relation to transmission
Boyakani ya virisi na esika virisi efandaka na oyo etali ndenge epanzanaka
Besides three viral factors stated above, viral interaction with host receptor is another key factor influential on interspecies transmission.
Longola makambo misato ya virisi oyo tolobeli na likolo, boyokani ya virisi na esika efandaka ezali eloko mosusu ya ntina na oyo etali ndenge eutaka na bikelamu moko mpe ekota na ekelamu mosusu.
Herein, recombination of SARS-CoV is taken as a typical example, which also showed evidence of positive selection during interspecies transmission events.
Na kati, kosangana ya SARS-CoV elobelami neti ndakisa, mpe emonisi ete epanzaka maladi ntangu ekutaka na ekelamu moko mpe ekotaka na ekelamu mosusu.
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.
Na kolanda botaleli ya kokesenisa na kati ya bato mpe nyama civet SARS-CoVs, emonani ete SARS-CoV ekokoba kobongwana noki na bisika oyo efandaka, mingimingi ndenge etambolaka na RBD ya proteine 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.
Mbala mingi, RBD ya proteine S ya CoV ezalaka na boyokani na baselile oyo ezwaka yango mpe eponamaka mingi na anticorp ya esika ekei kofanda.
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.
Na SARS-CoV, RBD ezali na aside amino ya 318 kino ya 510 na eteni ya S1 , oyo esanganaka na ACE2 ya bato mpe bisika mosusu oyo virisi ekotaka.
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 ya SARS-CoV ekoki koyeba bikoko ezwaka ACE2 ya banyama mingi, na ndakisa ngembo, civet, mpuku mpe mbwa ya zamba, yango esalisaka virisi euta na ekelamu moko mpe ekota na ekelamu mosusu.
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.
Ya solo, batika ya ba-amino aside 6 mpamba emonanaki ete ekeseni na bato mpe virisi ya civet oyo babimisaki na RBD mpe 4 kati na yango oyo ezali na eloko ezwaka yango ezalaka na boyokani na eloko ezwaka 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 civet ezali na mbongwana ya K479N mpe ya S487T na RBD na yango, mpe yango ematisaka boyakani kati ya proteine ya nsonge na ACE2 ya bato oyo ezwaka yango.
In other words, these two amino acid substitutions might be critical to viral adaption to humans.
Na maloba mosusu, biloko mibale oyo ezwaka esika ya aside amino ekoki kozala ntina mingi mpo virisi emesana na nzoto ya bato.
It is noteworthy that SARS-CoV-2 shares the same cellular receptor with SARS-CoV.
Eza ntina koyeba ete SARS-CoV-2 eza ya ndenge moko oyo ebombaka yango neti 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.
Bokeseni ya 30% na kati ya SARS-CoV-2 mpe SARS-CoV na eteni S1 ya proteine S emonisi ete boyokani ya proteine S na yango na ACE2 ya bato ekoki kobongwana.
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.
Ya solo, bolukiluki moko ya cryo-EM emonisi ete boyokani ya 10- kino 20- ya bosangani oyo koleka oyo eza kati ya ACE2 ya bato mpe SARS-CoV ya proteine S.
It will also be of interest to determine whether any other coreceptor might be required for SARS-CoV-2 transmission.
Ekozala mpe ntina na koyeba soki ekosenga eloko mosusu mpo na kopanza SARS-CoV-2.
Intriguingly, HCoV-NL63 also binds to ACE2 but with a different part of S.
Likambo ezokamwisa, HCoV-NL63 esanganaka mpe na ACE2 kasi na eteni mosusu ya S.
There exist many other HCoV receptors, such as aminopeptidase N for HCoV-229E, and 9-O-acetylated sialic acid for HCoV-OC43.
Ezali na biloko mingi mosusu oyo eyambaka HCoV, na ndakisa aminopeptidase N mpo na HCoV-229E, mpe 9-O-aside sialique acetylé mpo na HCoV-OC43.
They might also account for successful adaptation of these CoVs in humans after interspecies transmission from their animal hosts.
Ekoki mpe kosalisa na ndenge ba CoVs oyo ekokaka komesana na nzoto ya bato nsima ya kouta na banyama esika ezalaka.
In addition to cellular receptors, the outcome of interspecies transmission of HCoVs is also governed by other host dependency and restriction factors.
Longola baselila oyo eyambaka yango, matomba ya ndenge HCoVs eutaka ekelamu moko mpe ekotaka na ekelamu mosusu etambwisami na boyokani na yango na bisika mosusu oyo efandaka mpe makambo oyo ekangaka yango nzela.
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.
Bokeseni ya baproteine ya bisika oyo efandaka na kati ya bato mpe esika oyo biloko oyo ebombaka HCoVs ezalaka na ndakisa bangembo, bakamela dromadaire mpe ba rongeur ekoki kozala eloko oyo ekopekisa yango euta ne ekelamu moko mpe ekota na mosusu.
HCoVs have to usurp host dependency factors and subvert host restriction factors for a successful interspecies transmission.
HCoVs esengeli kozwa ya esika ya eloko ebomaka yango mpe kobongola makambo oyo ekangaka yango nzela mpo ezwa likoki ya kouta na ekelamu moko mpe kokota na ekelamu mosusu.
In this regard, molecular determinants in this important area of virus-host interaction remain to be identified and characterized.
Na likambo oyo, eloko esalisaka na koyeba molekile na likambo ya ntina oyo etali boyokani na kati ya virisi mpe esika efandaka eyebani kaka te mpe ekosenga kolukaluka.
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.
Depistage ya malamu ya dependance ya genome mpe makambo oyo ekangaka yango nzela mpo na SARS-CoV-2 oyo esalelaka mayele makasi ya CRISPR ekoki kosalisa.
Emergence of novel HCoVs: back to ground zero
Kobima ya HCoVs ya sika: kozonga na ebandeli
The diversity of bat CoVs provides ample opportunities for the emergence of novel HCoVs.
Bokeseni ya CoVs ngembo ezali kopesa makambo mingi mpo na kobima ya HCoVs ya sika.
In this sense, bat CoVs serve as the gene pool of HCoVs.
Na ndimbola, CoVs ngembo ezali esika oyo HCoVs eutaka.
In addition, rapid mutation and genetic recombination also drive HCoV evolution and serve as two important steps in this process.
Lisusu, mutation ya noki mpe kosangana ya ba gene esalisaka mpe na bokoli ya HCoV mpe ezalaka bitambe mibale ya ntina na likambo oyo.
For example, the acquisition or loss of novel protein-coding genes has the potential to drastically modify viral phenotypes.
Na ndakisa, kozwa to kobungisa codage ya ba gene ya proteine ezali na likoki ya kobongola mingi mpenza boyokani na kati ya bavirisi.
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.
Na kati ya biloko ya baproteine SARS-CoV, emonani ete ORF8 eza ntina mingi mpo emesana na nzoto ya bato, mpo bavirisi ya ngembo ya SARS-CoV, batyaki yango mopanzi kasi emonanaki ezalaka lolenge mosusu ya kobombana ya baproteine ORF8.
A 29-nucleotide deletion characteristic of SARS-CoVs has been found in strains isolated at the beginning of the human epidemic.
Bamonaki ete babomaki 29-nucleotide ya SARS-CoVs oyo batyaka na mopanzi na ebandeli ya maladi mabe epai ya bato.
This deletion splits ORF8 into ORF8a and ORF8b and is thought to be an adaptive mutation that promotes the switch of hosts.
Koboma oyo ekabola ORF8 na ORF8a mpe ORF8b mpe bakanisi eza eloko oyo esalisaka yango elongwa na esika mpe ekota na bisika mosusu.
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.
Lisusu, SARS-CoV ekoki kosangana lisusu na molongo ya alpha- mpe gamma-CoVs, esika bosangani mingi ya mikemike emonanaki na RNA oyo euta na RNA ya polymerase.
Recombination locations were also identified in the nsp9, most of nsp10, and parts of nsp14.
Bisika ya kosangisa yango emonanaki mpe na nsp9, mingi ya nsp10, mpe biteni ya 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.
Ndenge moko, emonani ete maladi mabe ya MERS-CoV esanganaki na kati ya milongo mingi, oyo esalemaki na bakamela dromadaire ya Arabie Saudite.
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.
Longola SARS-CoV mpe MERS-CoV, makambo ya kosangana emonanaki mpe na ba HCoVs mosusu, na kati na yango HCoVs esanganaki na CoVs ya nyama mosusu na ba gene na yango.
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.
Esengeli mpe kokeba mpo kopona oyo ya lokuta ekoki komema na mbongwana tokanaki te ya ba genome oyo ememaka bavirisi, mpe ekoki ete elembisa bavirisi na bopusi oyo ezali kokutana na yango, na ndakisa mikrobe oyo ebundisaka maladi na nzoto ya bato oyo bazalo na yango.
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.
Na ndakisa moko ya makambo wana ezali kobungisa mobimba ya ORF4 na HCoV-229E prototype, oyo esalemaki mpo babomaki ba nucleotide mibale.
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.
Ata ORF4 oyo ebebi te ekoki komonana na ngembo mpe na bavirisi ya bakamela oyo ezali na boyokani na HCoV-229E, alpha-CoV alpaca emonisaki kobakisama ya nucleotide moko, esalaki ete kadre ebongwana.
Last but not least, the evolution of novel HCoVs is also driven by the selection pressure in their reservoir hosts.
Ya nsuka kasi ya ntina, kokola ya HCoVs ya sika euti na bopusi ezali na bisika efandaka.
Asymptomatic or only mild symptoms were detected when bats were infected with CoVs, indicating the mutual adaptation between CoVs and bats.
Kozanga bilembo to kozala na bilembo kaka moke emonanaki ntango bangembo bazwaki CoVs, yango emonisi komesana na kati ya CoVs mpe bangembo.
It appeared that bats are well adapted to CoVs anatomically and physiologically.
Emonani ete bangembo emeseni mpenza na CoVs na makambo ya anatomie mpe ya physiologie.
For example, defects in the activation of pro-inflammatory response in bats efficiently reduce the pathology triggered by CoVs.
Na ndakisa, bambeba na kobimisa mukusa malamumalamu na bangembo ekitisaki maladi oyo CoVs ekoki kobimisa.
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.
Lisusu, selile oyo ebomaka bangembo ekufaki mpo bamatisaki selile oyo ebomaka yango mpenza NKG2/CD94 mpe emonisaki nivo ya nse ya histocompatibilié ya makasi ya mindondomindondo ya bamolecule ya kelasi I.
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.
Lisusu, nivo ya makasi ya bandakisa ya oxygene (ROS) oyo eutaka na metabolisme makasi ya bangembo ekoki koboma CoV to ebotama mpe kozala na bopusi na botangi na yango na nzela ya exoribonuclease, yango wana esalisaka na kopona bopusi ya bavirisi oyo epesaka mpenza maladi soki ekoki na esika ya sika.
More pathogenic CoV strains might also evolve by recombination, leading to the acquisition of novel proteins or protein features for host adaptation.
Maladi mingi ya CoV ekoki mpe kokola na nzela ya kosangana, ekomema na kozwa baproteine ya sika to baproteine mpo na komesana na esika ya efandi.
Thus, it is not by chance that three novel HCoVs have emerged in the past two decades.
Yango wana, eza te kaka chance ndenge ba HCoVs misato ya sika ebimaki na bambula ntuku mibale oyo eleki.
CoVs are non-pathogenic or cause mild symptoms in their reservoir hosts such as bats and camels.
CoVs epeska te maladi to ebimisaka te bilembo ya mike na bisika efandaka na ndakisa na bangembo mpe na bakamela.
They replicate robustly without eliciting a strong host immune response.
Ebotamaka mingi kozanga kosalela mikrobe ebundisaka maladi ya moto oyo aza na yango.
Herein lie the secrets of why asymptomatic carriers are seen and what causes the severe cases in human infection.
Awa nde esika baseleke ya koyeba soki bato oyo bazali na bilembo te bamonana mpe oyo esalaka ete ebelisa bato makasi mpenza.
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.
Bilembo ya makasi euti mingimingi na hyperactivation ya mikrobe oyo ebundisaka maladi mpe ba cytokine mingi na esika mikrobe oyo ebundisaka maladi ezalaka makasi, mpe yango ebebisaka poumon mingi.
In contrast, in asymptomatic carriers, the immune response has been de-coupled from CoV replication.
Na kokesena, na bato ya maladi oyo bazali na bilembo te, mikrobe oyo ebundisaka maladi oyo euti na kobotama ya CoV esalaka mbala mibale.
The same strategy of delinking the immune response might have beneficial effects in anti-SARS-CoV-2 therapy.
Mayele ya lolenge moko kolongola mikrobe oyo ebundisaka maladi ekoki kozala na bopusi malamu na nkisi ya SARS-CoV-2.
The interferon response is particularly strong in bats.
Interferon esalaka makasi mpenza mingimingi na bangembo.
Thus, administration of type I interferon at least in the early phase of SARS-CoV-2 infection in humans should be beneficial.
Yango wana, kopesa interferon ya lolenge I ata kaka na ebandeli ya maladi ya SARS-CoV-2 na nzoto ya bato esengeli esalisa mingi.
In addition, NLRP3 inflammasome activation in bats is defective.
Lisusu, koningisa NLRP3 na inflammasome na bangembo esimbaka te.
By this reasoning, inhibition of NLRP3 inflammasome with MCC950 might be useful in the treatment of COVID-19.
Na kotalela makanisi oyo, koningisa NLRP3 na inflammasome elongo na MCC950 ekoki kosalisa na kozwa nkisi ya COVID-19.
The emergence of SARS-CoV-2 follows the general theme by which SARS-CoV and MERS-CoV arose.
Kobima ya SARS-CoV-2 ezali kolanda moto ya likambo moko oyo esalaka ete SARS-CoV mpe MERS-CoV ebima.
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.
Ata emonana ete beta-CoV ya ngembo ezali na 95% ya nucleotide ya ndenge moko na SARS-CoV, bat-CoV ezali na 96% ya ba nucleotide ya ndenge moko na 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.
Ata emonanaki ete ba civet mpe banyama mosusu na bazando ezali na bavirisi ya lolenge moko na SARS-CoV, bisika ya sika oyo SARS-CoV-2 ekendaka kofanda ezali ndenge moko.
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.
Emonani ete beta-CoVs ya pangolin ekokani mingi mpenza na SARS-CoV-2, emonisi ete bapangolin bakoki kozala esika moko oyo bavirisi wana efandaka to beta-CoVs ya bapangolin esalisaka na kokabola ba gene ya nsuka ya SARS-CoV-2.
Although questions remain, there is no evidence that SARS-CoV-2 is man-made either deliberately or accidentally.
Ata mituna ezali kaka, ezali te na bilembeteli emonisi ete SARS-CoV-2 esalemi na bato ezali na nko to na kidiba.
CoVs have returned to the limelight due to the recent outbreak of SARS-CoV-2.
Bato bazongeli kolobela mingi CoVs mpo na epalangana ya sika ya SARS-CoV-2.