atepeq/tico19 huggingface dataset:
Bat alpha-CoVs closely related to HCoV-229E have been found.
Alpha-CoV alïïk thääny thok kek HCoV-229E aacï yɔ̈k.
Between them there is an alpaca alpha-CoV.
Kam ken ala alpaka alpha-CoV.
Several lines of evidence support the transmission of virus from bats to humans directly.
Käjuëc aa të ye köm tɛk piny bï jäl aliɛ̈k gup ku kɔc gup nyinic.
First, humans but not alpacas might have contact with bats in a shared ecological niche.
Tueŋ, aa kɔc aa kek cï dhiɛl yɔ̈k kek aliɛ̈k ku aace lääi cɔl alpaka.
Instead, humans have close contact with alpacas.
Ku na ye keya, kɔc aa thiääk ke alpaka.
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.
Rɔu, HCoV-229E thiääk thok kek alpha-CoV alïïk aa kiith iic ku aacïn thuou dït aliɛk iic, ku alpha-CoV alpaka e yen cï tuany riɛl ic wɛ̈i jɔk lääi cï luaŋ iic.
Finally, alpaca alpha-CoV has not been found in feral animals.
Thökde, alpha-CoV alpaka akïc yɔ̈k lääi rɔɔr gup.
Thus, the possibility cannot be excluded that alpacas obtain the HCoV-229E-related alpha-CoV from humans.
Acïn të lɛ̈u bï yen guɔ thiöök cɔ̈k lɔn ade ka alpaka ala guop HCoV-229E ke thiääk thok kek alpha-CoV alɔŋ kɔc.
In fact, bats are the direct source of human pathogenic viruses including rabies virus, Ebola virus, Nipah virus and Hendra virus.
Ku yic adhïl, aliɛ̈k aa kek la gup käm kɔc luaŋ ku aala iic alïïŋ pan Autharalia, köm Ebola, köm Nipah ku köm Hendra.
It is therefore not too surprising that bats might transmit HCoV-229E to humans directly.
Acï lɛ̈u bï kɔc gɔ̈i lɔn ade ka aliɛ̈k aa HCoV-229E tɛk kɔc gup nyinic.
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.
Ku këdɛ̈t aya, alpha-CoV alïïk e yen të ye HCoV-229E yɔ̈k thïn, alpaka ku thɔ̈rɔ̈ɔ̈l baai aalɛ̈u bïk ya të ye käm tɛk kɔc gup thïn, cïmen tuɛny 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 e yen ke pɛɛth yen nyuɔth lɔn ye tuany jäl tën aliɛ̈k le tën thɔ̈rɔ̈ɔ̈l ku tën thɔ̈rɔ̈ɔ̈r le tën kɔc.
The evolutionary origin of MERS-CoV from bats is known at its initial identification and has also been strengthened by subsequent findings.
Të a jɔ̈k MERS-CoV alɔŋ aliɛ̈k mɛ̈nɛ̈ wär cï yen ŋic ku acï käk cï ke yɔ̈k akuën ic cɔl aril.
It is obvious that bats provide a rich pool of virus species for interspecies exchange of genetic fragments and interspecies transmission.
Aŋic lɔn ye aliɛ̈k käk la gup käm la lääi kök gup ku bïk käk guop waar ku tek rɔt lääi kök gup.
Longevity, densely packed colonies, close social interaction and strong ability to fly are all favourable conditions for bats to be an ideal 'virus spreader'.
Kam bäric, akuöt nhom den, rɛ̈ɛ̈r ye kek rɛ̈ɛ̈r akut ku riɛl ye kek pär aliɛ̈k cɔl aye kek köm tɛk piny.
On the other hand, MERS-CoV has been introduced to dromedary camels for decades.
Ku tëdɛ̈t, MERS-CoV acï rɔt yɔ̈k thɔ̈rɔ̈ɔ̈l gup run juëc.
It is well adapted to these camels that have turned from an intermediate host to a stable and natural reservoir host.
E ŋiɛc dom thɔ̈rɔ̈ɔ̈l gup cï ya të ye köm yɔ̈k ku bï ya keek tuany dhiɛ̈th.
MERS-CoV causes very mild disease and maintains a relatively low mutation rate in these animals.
MERS-CoV e tuany thiin kor jɔk ku e dhiɛ̈th amäth lääi kä gup.
Its sporadic transmission to humans is an accident and humans remain a dead-end host of MERS-CoV as its transmission cannot be sustained.
La de kɔc gup ece kën acï guir ic ku kɔc aa kek ye MERS-CoV rɛ̈ɛ̈r thïn rin cï tekde piny rɔt lɛ̈u bï rot duut.
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.
Ku kë wääc kë ye thɔ̈rɔ̈ɔ̈l loi ic tek piny MERS-CoV, luɔi pangolin, te le yen ke ye kä looi, tek piny SARS-CoV-2 a loi thok
Particularly, pangolin beta-CoVs are highly pathogenic in pangolins.
Kën rot, thuou a dït tën beta-CoV pangolin ic.
They might be a dead-end host for SARS-CoV-2-related beta-CoVs, similar to civets in the case of SARS-CoV.
Abï dhiɛl ya të ye SARS-CoV-2 thääny thok kek beta-CoV thou thïn, ku a thööŋ kek aŋääth alɔŋ 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.
Tek pinyy SARS-CoV-2 jäl lääi gup le kɔc gup a dhil kuum alöŋ thïn wula kuum aɣer.
First, bats could be the reservoir host of a SARS-CoV-2-related virus almost identical to SARS-CoV-2.
Tueŋ, aliɛ̈k aabï dhiɛl ya kek ye SARS-CoV-2 thääny thok kek köm aa thööŋ kek SARS-CoV-2.
Humans might share the ecological niche with bats through butchering or coal mining.
Kɔc aa rɔm tok kek aliɛ̈k alɔŋ nääkde ku wɛ̈cwɛ̈cde atiɔp mac ic.
Second, pangolins could be one of intermediate amplifying host to which a SARS-CoV-2-related virus had been newly introduced.
Rɔu, pangolin aa dhil a kek cï yɔ̈k keye të ye SARS-CoV-2 rɛ̈ɛ̈r ke gup.
Humans contract the virus through butchering and consumption of game meat.
Kɔc aacï köm yɔ̈k nääk ku ciɛ̈mciɛ̈m rïŋ lääi rɔɔr.
It is possible that many mammals including domestic animals are susceptible to SARS-CoV-2.
Abï dhiɛl ya yic lɔn lääi juëc dhiɛ̈th aala gup SARS-CoV-2.
A survey of domestic and wild animals for antibodies is warranted.
Cɛɛth cï looi lääi baai ku lääi rɔɔr la gup tuany acï gam.
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.
Diäk, cïmen cï yen luel nhial të tui, nuɛ̈tnuɛ̈t ku döm SARS-CoV-2 e ciɛ̈t kë cï la tueŋ län ye kek diäk guop cï römm kek aliɛ̈k ku pangolin.
The search for the animal origins of SARS-CoV-2 is still on.
Të ye tuany SARS-CoV-2 yɔ̈k thïn lääi gup aŋuɔt yɔ̈p.
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.
Tën kuat lääi ye tuany rɛ̈ɛ̈r ke gup, käŋ kä diäk köm kuɔny aa muɣɛm ku bï të ye CoV la lääi kök gup thïn kuɔny.
First of all, their relatively high mutation rates in RNA replication.
Tueŋ, juɛ̈ŋ rot dhiɛnhden RNA ic.
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.
Të thɔ̈ɔ̈ŋ kek käm kök tɔ̈u RNA ic, dhiënh ye CoV atɔ̈u "ciɛl" le "nhial" kek awɛ̈rde ye tëcït tën 10-4 ruon ic arak 2, ku e lui tëcït të ye CoV lui thïn.
CoVs have a proof-reading exoribonuclease, deletion of which results in exceedingly high mutability and attenuation or even inviability.
Kuat CoV aala të ye ke kuen thïn exoribonuclease, cothden wei ku e yen të ye yen rot juak thïn nyuɔth ku tɛ̈ŋde ic wula piɛ̈rde.
Interestingly, the nucleotide analogue Remdesivir is known to suppress CoV replication through inhibition of this exoribonuclease and the RNA-dependent RNA polymerase.
Ke path, nucleotide Remdesivir aŋic te yen CoV thany piny tëcït ye yen rot juak thïn exoribonuclease ku RNA ku käk RNA bɛ̈i.
Remdesivir is one of most promising anti-SARS-CoV-2 agents to be tested in clinical trials.
Remdesivir e yen wäl tööŋ SARS-CoV-2 diɛ̈t dem ke lɛ̈u bï them panakim.
Nevertheless, mutation rates of CoVs are about a million times higher than those of their hosts.
CoV e dhiɛ̈th arak juëc malion ka wäär län ye kek rɛ̈ɛ̈r ye guop.
In addition, mutation rate is often high when CoVs are not well adapted to the host.
Ku bï mat thïn, dhiɛ̈ɛ̈th köm e tɔ̈u nhial apɛi të kilc CoV dom kën ye kek rɛ̈ɛ̈r ke gup.
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.
Kë cï thɔ̈ɔ̈ŋ kek të ye SARS-CoV dhiɛ̈th thïn, dhiɛ̈nh SARS-CoV-2 atɔ̈u piiny, ku e yen ye nyuɔth lɔn lëu bï yen dom kɔc gup.
Presumably, it has already been adapted to another host close to humans.
Thɔ̈ɔ̈ŋ ic de, yenn acï dom apath tën kë dɛ̈t thɔ̈ɔ̈ŋ kek kɔc.
In addition to SARS-CoV-2, this also applies to MERS-CoV, which is well adapted to dromedary camels.
Të met SARS-CoV-2, kën alɛ̈u bï luɔ̈i alɔŋ MERS-CoV, këye kë cï dom apath tën thɔ̈rɔ̈ɔ̈l.
Theoretically, it is unlikely that genetic drift would render vaccines and antivirals against SARS-CoV-2 ineffective quickly.
Të ŋïc yen, të ye köm cɛɛth thïn abï wäl ku käk guop tiit ice tuany SARS-CoV-2 cɔl acï lɔc yɔ̈k.
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.
Rɔu, abaŋ dït RNA CoV ic e lui ke cïn ke rɛc guop ic të ye guop rot waar thïn e dhiëëth ku nuɛ̈tnuɛt, ku e yen tuany cɔl ajuak rot alɔŋ lääi cï thɔ̈ɔ̈ŋ ku e yen kë path tën kuat CoV të cï aliir ic piath.
This is supported by the copious unique open reading frames and protein functions encoded towards the 3′ end of the genome.
Kën aye akuën cï looi ke ŋaany kuɔny cɔ̈k kä tɔ̈u ye kɛ̈c ku të ye protin lui thïn cï kek waar iic alɔŋ 3' të ye guop lui thïn
Third, CoVs randomly and frequently switch templates during RNA replication through a unique “copy-choice” mechanism.
Diäk, kuat CoV aa rɔ̈t waar ku aa rɔ̈t wäc kamken dhaman RNA të ye kek yen "kuany-thïn" bïk lui.
In a host that serves as the mixing vessel, strand switching occurs frequently during CoV RNA transcription.
Tën të ye käm rɛ̈ɛ̈r thïn ke ye kën käŋ liääp, wɛ̈c rot e rot looi dhaman thok ebën të tek CoV RNA rot.
Highly homologous full-length and subgenomic RNAs could recombine to generate new CoVs.
Të thɔ̈ɔ̈ŋ RNA ku luɔi den alɛ̈u bï rɔ̈t mat ku bïk kuat CoV yam bɛ̈i.
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.
Acï kë cï kuen nyuɔth lɔn nuɛ̈tnuɛ̈t HCoV-HKU1 ku HCoV-OC43, acï yɔ̈k, agut CoV lääi cïmen SL-CoV ku batCoV-HKU9.
Virus-host interaction in relation to transmission
Të ye köm rɛ̈ɛ̈r thïn ku tekde rot piny
Besides three viral factors stated above, viral interaction with host receptor is another key factor influential on interspecies transmission.
Tën dhɔ̈ɔ̈l kä diäk ye köm yɔ̈k cï ke luel nhial të tui, të ye köm rɛ̈ɛ̈r thïn kek ye yen rɛ̈ɛ̈r ye guop e kë pɛth dɛ̈t lɛ̈u bï kɔc kony të ye köm rot tɛk piny thïn lääi loi thook gup.
Herein, recombination of SARS-CoV is taken as a typical example, which also showed evidence of positive selection during interspecies transmission events.
E tën, mɛ̈n ic SARS-CoV acï nyai ke ye kït, ku acï yic nyuɔth ke alɔŋ kuɛ̈nykuɛ̈ny path dhaman loi të ye köm rot tɛk lääi loi thook gup.
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.
Tëcït tën thɔ̈ɔ̈ŋ kɔ̈u cï looi kam kɔc cï kek tek thook ku SARS-CoV aŋɔu, acï tak ka SARS-CoV e lac dom käjuëc gup, ku e dhiɛ̈th alɔŋ RBD protin 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.
RBD tɔ̈u S protin CoV e liääp kek riɛm ku acï guop ye köm rɛ̈ɛ̈r kuany.
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.
SARS-CoV ic, RBD atɔ̈u nimra 318 le 510 amino acid abaŋ S1, ku e rɔt nuɛt ACE2 raan ic ku e yen tëde tën dhɔ̈ɔ̈l ye köm tɛ̈k.
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 SARS-CoV alɛ̈u bï ACE2 tɔ̈u lääi gup ŋic, ku aala iic alïïk, aŋau, lɔk ku jɔ̈ŋ rakuun, ku tek piny tuany kam lääi cï liääp puöl.
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.
Ku yic, amino acid kä 6 aa kek cï ke tïŋ ke looi thöök tën ran ku köm aŋau cï tek thok RBD ic ku käŋ kä 4 aa tɔ̈u të ye kek rɛ̈ɛ̈r thïn ku bï ACE2 lui.
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 aŋau ala K479N ku S487T dhiɛ̈th RBD, ku e mäth den juakic spike protin kek ACE2 tɔ̈u raan guop.
In other words, these two amino acid substitutions might be critical to viral adaption to humans.
Të luel yen wɛ̈l kök, awɛ̈r ic amino acid kärɔu abï ic dhiɛl riɛl to köm ku bï dom raan guop.
It is noteworthy that SARS-CoV-2 shares the same cellular receptor with SARS-CoV.
Eke path ku bï ŋic lɔn rɔm SARS-CoV-2 ɣɔ̈ɔ̈n ye riɛm ke cath thïn kek 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.
Abaŋ 30% SARS-CoV-2 tek ic kek SARS-CoV alɔŋ S1 abaŋ protin S aye nyuɔth ka mäth protin S kek ACE2 raan acï rɔt war.
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.
Ku adhïl, kë cï cryo-EM kuen aye nyuɔth ka 10 le 20 abaŋ mäth ce ic dol kën nuɛ̈tnuɛ̈t kën tën kën kam ACE2 raan ku protin S SARS-CoV.
It will also be of interest to determine whether any other coreceptor might be required for SARS-CoV-2 transmission.
Abï piath ku bï ŋic lɔn le yen kë bï wïc ku bï SARS-CoV-2 rɔt tɛk piny.
Intriguingly, HCoV-NL63 also binds to ACE2 but with a different part of S.
Kë kɔc tut emɛ̈nɛ̈, HCoV-NL63 e rot mat kek ACE2 ku kek abaŋ S loi thok.
There exist many other HCoV receptors, such as aminopeptidase N for HCoV-229E, and 9-O-acetylated sialic acid for HCoV-OC43.
Anaŋ käjuëc kök ye HCoV rɛ̈ɛ̈r ke gup, cïmen aminopeptidase N ke ye ke;n HCoV-229E, ku 9-O akut acid lui guop ic ke ye kën HCoV-OC43
They might also account for successful adaptation of these CoVs in humans after interspecies transmission from their animal hosts.
Kek aalɛ̈u bï ke kuën rin kuat CoV dom kɔc gup apath wën cï kek tɛk piny e lääi rɛ̈ɛ̈r kek ke gup.
In addition to cellular receptors, the outcome of interspecies transmission of HCoVs is also governed by other host dependency and restriction factors.
Ku kë mɛt thïn alɔŋ käk dom guop ic, kën bɛ̈n bei tek rot piny lääi loi thok gup alɔŋ kuat HCoV aye mac kë dɛ̈t ɣäc ku käk cï pɛ̈n.
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.
Kë wääc protin kam kɔc ku ɣɔ̈ɔ̈n ye kuat HCoV yɔ̈k thïn cïmen aliɛ̈k, thɔ̈rɔ̈ɔ̈l baai ku luɔk aalɛ̈u bïk tuany tɛk piny.
HCoVs have to usurp host dependency factors and subvert host restriction factors for a successful interspecies transmission.
Kuat HCoV aalɛ̈u bïk käk ye kek rɛ̈ɛ̈r thïn dom ku rɛc kä kek ku naŋ të tek käm rɔ̈t piny lääi loi thook gup.
In this regard, molecular determinants in this important area of virus-host interaction remain to be identified and characterized.
Ku rin kën, kën käk guop cɔl a lui alɔŋ muɣɛm te ye köm rɛ̈ɛ̈r thïn aŋuɔt ŋot kïc tïŋ ku tɛ̈u akutde ic.
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.
Lui CRISPR bï ke SARS-CoV-2 tïŋ të ye yen lui thïn guop ic ku käk cï kek pɛ̈n aa lɛ̈i bï naŋ kë bï kä.
Emergence of novel HCoVs: back to ground zero
Ke wïc bï rot lac looi alɔŋ kuat HCoV: bi kɔc dhuk piny ic.
The diversity of bat CoVs provides ample opportunities for the emergence of novel HCoVs.
Juɛëc ye bat CoVs juëc e kuat HCoVs cɔl ajuak rɔ̈t aya.
In this sense, bat CoVs serve as the gene pool of HCoVs.
Ku rin kën, kuat bat CoVs e yen të ye kuat HCoVs yɔ̈k thïn.
In addition, rapid mutation and genetic recombination also drive HCoV evolution and serve as two important steps in this process.
Ku kë mɛt thïn, dhiɛ̈th ye köm dhiɛ̈th ku nuɛ̈tnuɛ̈tde aa ke HCoV cɔl a jɔk rot ku aa kek lui keye dhɔ̈ɔ̈l kärɔu e dhël kën ic.
For example, the acquisition or loss of novel protein-coding genes has the potential to drastically modify viral phenotypes.
Cïmen, yɔ̈kyɔ̈k wula mär protin e naŋ kë ye looi ku bï të ye köm lui thïn kek aliir cɔ̈k piny.
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.
Kam SARS-CoV protin, ORF8 acï tak lɔn ye yen muɣɛm dömde kɔc gup, ke SARS-CoV thääny thok ke käm aliik cï tek thok ku aacï yɔ̈k ke cï rɔ̈t mat ORF8 protin ic.
A 29-nucleotide deletion characteristic of SARS-CoVs has been found in strains isolated at the beginning of the human epidemic.
Coth wei 29-nucleotide të ye kuat SARS-CoV acï yɔ̈k rïŋ cï lel thok mɛ̈nɛ̈ jɔk tuany rot tën kɔc.
This deletion splits ORF8 into ORF8a and ORF8b and is thought to be an adaptive mutation that promotes the switch of hosts.
Coth wei acï ORF8 ku bi ya ORF8a ku ORF8b ku acï tak bï të köm rɔt jak thïn ku e yen lääi wääc.
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.
Ku e tën, kuat SARS-CoV ala anyïköl nuɛ̈tnuɛ̈t rɔt ke kuat dhiɛ̈ɛ̈th alpa - ku kuat gamma-CoV, ku e yen tën acï abaŋ thiin kor cï rɔ̈t nuet tïŋ thïn RNA polymerase ic.
Recombination locations were also identified in the nsp9, most of nsp10, and parts of nsp14.
Të ye kek rɔ̈t nuet thïn acï yɔ̈k nsp9 ic, ku abaŋ dït nsp10, ku abaŋ 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.
Cïmen deaya, acï nyuɔth ka tuɛny MERS-CoV acï dhɔ̈ɔ̈l ye kek rɔ̈t nuet yɔ̈k kam kuat dhiɛ̈th loi thook, ku e rɛ̈ɛ̈r thɔ̈rɔ̈ɔ̈l baai pan Saudi Arabia.
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.
Tën SARS-CoV ku MERS-CoV, të ye kuat HCoVs rɔ̈t nuɛt thïn acï tïŋ , ku e yen të ye kuat HCoVs rɔ̈t nuɛt thïn kek kuat CoV lääi kök alɔŋ të ke cak thïn gup ken iic.
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.
Awïc bï ŋiɛc looi apath rin kuɛ̈nykuɛ̈ny alɛ̈u bï awɛ̈r rot cï wïc looi käm guop ic, ku e lac bɛ̈n bei të pɛ̈l käm alɔŋ kuɛ̈nykuɛny cï looi riɛl, cïmen të ye të ye kek rɛ̈ɛ̈r thïn lui thïn.
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.
Ku kën yen nyuɔth yen kë cï rot looi e määr ORF4 HCoV-229E iic ebën, ku aŋuɔt awïc coth wei nucleotide kärɔu.
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.
Ku ke ORF4 kïc riäk lɛ̈u bï tïŋ alïïk ku käm thɔ̈rɔ̈l gup thääny thook kek HCoV-229E, alpha-CoV alpaka e nucleotide tök yen aye nyuɔth tɛ̈ɛ̈u thïn, ku e yen käk coth wei ku mɛt thïn nyuɔth.
Last but not least, the evolution of novel HCoVs is also driven by the selection pressure in their reservoir hosts.
Thökde ku ace yen kor, jɔ̈k cɔ̈k kuat HCoV aye kuɛnynuɛny thɔɔc cɔ̈k të ye kek rɛ̈ɛ̈r thïn.
Asymptomatic or only mild symptoms were detected when bats were infected with CoVs, indicating the mutual adaptation between CoVs and bats.
Ke yï cïn guop kïït tuany wula kïït thii tuany aa ke cï ke tïŋ wën cï aliɛ̈k luaŋ kuat CoV, ku e të ye kek rɔ̈t dam thïn kam kuat CoV ku aliɛ̈k.
It appeared that bats are well adapted to CoVs anatomically and physiologically.
Acï tuöl lɔn ka aliɛk aa ŋiɛc dom kuat CoV raan guop alɔ̈ŋ thïn ku të yë guop lui.
For example, defects in the activation of pro-inflammatory response in bats efficiently reduce the pathology triggered by CoVs.
Cïmen, të le yen kë jɔ̈ɔ̈r alɔŋ käk guop cɔl atuc aliɛ̈k ic ku e thuou cï kuat CoV dhuök piny.
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.
Tëdɛ̈t, kën nɛ̈k aliɛ̈k iic aye thany piny rin cɔl kën yen ɣääc käk NKG2/CD94 ku abaŋ kor anyïköl kek cɔl acï thɔ̈ɔ̈ŋ käk guop tueŋ ic.
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.
Ku keya, abaŋ të dït alɔŋ aliir wɛ̈i (ROS) ye yɔ̈k käk ye cam alɔŋ aliɛ̈k aalɛ̈u bï CoV thany piny ku alɛ̈u bï kuɛ̈n ben ke kuen jɔ̈ɔ̈r exoribonuclease, ku keya e akuɛ̈ny gam të ye köm lui la ic thuou të cï yen ɣäth län dɛ̈t guop.
More pathogenic CoV strains might also evolve by recombination, leading to the acquisition of novel proteins or protein features for host adaptation.
CoV dït thuou thïn aalɛ̈u bïk jɔk ke ye nuɛ̈t yen cï kek rɔ̈t nuet, ku e yen protin kuöt ic wula protin e lui bï dom.
Thus, it is not by chance that three novel HCoVs have emerged in the past two decades.
Tuɛnytuɛny kuat HCoV kä diäk kä aa ke cï bɔ̈ path ruon thiärɔu cï jäl.
CoVs are non-pathogenic or cause mild symptoms in their reservoir hosts such as bats and camels.
Kuat CoV aace näk wula kïït tuany aa lïk lääi ɣɛ̈ɛ̈c ke gup cïmen aliɛ̈k ku thɔ̈rɔ̈ɔ̈l.
They replicate robustly without eliciting a strong host immune response.
Aa rɔ̈t juak ke ril ke cïn ke ril kek cɔl a lui kë rɛ̈ɛ̈r kek ye guop.
Herein lie the secrets of why asymptomatic carriers are seen and what causes the severe cases in human infection.
Kën ala ic kë cï thiän yeŋɔ̈ kë ye län ɣɛ̈ɛ̈c tuany ye ke tïŋ ku yeŋɔ̈ kën tuany cɔl a dït kɔc iic.
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.
Kïït kä e rin ye kek lui guop ic apɛi ku luɔi cytokine ku të ye guop ye dhuök nhom thïn, e yen të ye cuɛ̈ny riɛ̈k thïn.
In contrast, in asymptomatic carriers, the immune response has been de-coupled from CoV replication.
Ku kë wääc, tën lääi cï kïït tuany ŋic thïn, të ye guop ye dhuök nhom thïn acï dhuk piny arak rɔu juɛ̈ŋ ic CoV.
The same strategy of delinking the immune response might have beneficial effects in anti-SARS-CoV-2 therapy.
Dhel lɛ̈u bï të ye guop lui thïn tek thok alɛ̈u bï naŋ kuɔny e yäp wäl SARS-CoV-2.
The interferon response is particularly strong in bats.
Të ye interferon këdäŋ dhuök thïn a ril apɛi aliɛ̈k iic.
Thus, administration of type I interferon at least in the early phase of SARS-CoV-2 infection in humans should be beneficial.
Ku këya, të ye abaŋ I interferon gam thïn të puɔc SARS-CoV-2 jɔk kɔc iic alɛ̈u bï naŋ këpath.
In addition, NLRP3 inflammasome activation in bats is defective.
Ku kë mɛt thïn, luɔi ye kuat NLRP3 protin lui aliɛ̈k iic ace lui apath.
By this reasoning, inhibition of NLRP3 inflammasome with MCC950 might be useful in the treatment of COVID-19.
Ku rin wɛ̈tkën, juɛ̈ŋ rot NLRP3 inflammasome kek MCC950 aalɛ̈u bï piath elace COVID-19 ic.
The emergence of SARS-CoV-2 follows the general theme by which SARS-CoV and MERS-CoV arose.
Kë wïc alɔŋ SARS-CoV-2 abuɔth tën a jɔk SARS-CoV ku MERS-CoV thïn.
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.
Beta-CoV alïïk a rɔm 95% nucleotide kek SARS-CoV acï yɔ̈k, ku ala CoV-alïïk rɔm 96% nucleotide kek 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.
Aŋääth ku lääi tɔ̈u thuök aacï kek yɔ̈k ke ɣɛ̈ɛ̈c käm thɔ̈ɔ̈ŋ kek SARS-CoV, ku kën ɣɛ̈ɛ̈c ke ye kë rɛ̈ɛ̈r SARS-CoV-2 ye guop akïc tïŋ.
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.
Kuat Beta-CoV pangolin ret ke lui SARS-CoV-2 acï yɔk, ku aye nyuɔth lɔn lɛ̈u pangolin köm ɣääc wula kuat beta-CoV pangolin ale kë lëu bï juak te ye guop lui thïn ku bï SARS-CoV-2 jäl bɛ̈n bei.
Although questions remain, there is no evidence that SARS-CoV-2 is man-made either deliberately or accidentally.
Cɔk alɔn le yen kïït thiëc ŋuɔt ke ŋoot, acïn kën yen nyuɔth lɔn adë ka SARS-CoV-2 e raan yen aloi ye ke ŋic wula loi ke kuc.
CoVs have returned to the limelight due to the recent outbreak of SARS-CoV-2.
Kuat CoV aacï dhuk nhial rin tuany SARS-CoV-2 cï jɔk kën.
The study of CoVs in bats and other animals has drastically changed our perception of the importance of zoonotic origins and animal reservoirs of HCoVs in human transmission.
Kuën kuen kuat CoVs aliɛ̈k iic ku lääi kök dhiɛ̈ɛ̈th acï të ye ok muɣɛma lääi tïŋ war ku lääi ye ke kuat HCoVs yɔ̈k thïn tekde piny ran guop.
Pervasive evidence has shown that SARS-CoV, MERS-CoV and SARS-CoV-2 have a bat origin and are transmitted to humans via intermediate hosts.
Wɛ̈t yic kɔc dɔk nhïïm acï nyuɔth lɔn ka SARS-CoV, MERS-CoV ku SARS-CoV-2 ala te ye yɔ̈k alïïk guop ku aala kɔc gup dhɔ̈ɔ̈l kɔc rom ke kek.
Given that SARS-CoV infection originates from the contact between humans and civets in the markets, closing wet markets and killing civets therein could have effectively ended the SARS epidemic.
Rin cï yen yɔ̈k lɔn ka SARS-CoV a jɔ̈k rɔ̈m kam kɔc ku aŋääth thuök iic, thiök thok thuök tiɔp ku nääk aŋääth alɛ̈u bï tuɛny SARS cɔl ajäl.
By the same reasoning, pangolins should be removed from wet markets to prevent zoonotic transmission, in view of the discovery of multiple lineages of pangolin beta-CoVs closely related to SARS-CoV-2.
Ku rin wɛ̈t tööŋ, pangolin aa wïc bï kek nyai thuök tiɔp iic ku bï tek piny tuɛnytuɛny lääi gɛ̈l, ku rin kë cï yɔ̈k kuat dhiɛ̈nh kuat beta-CoV pangolin thääny thok ke SARS-CoV-2.
However, whether and how SARS-CoV-2 is transmitted to humans through pangolins and other mammals remain to be clarified in future investigations.
Ku këya, cɔk alɔn wula të ye SARS-CoV-2 tɛk piny thïn tën kɔc ke jäl tën pangolin ku kuat lääi kök dhiɛ̈th aŋuɔt aŋot ke bï jam ic aköl ciɛ̈n.
On the other hand, MERS-CoV has existed in dromedary camels for a long time.
Ku tëdɛ̈t, MERS-CoV acï rɛ̈ɛ̈r thɔ̈rɔ̈ɔ̈l baai gup kam bär kɔ̈u.
These camels serve as an important tool for transportation as well as a main source of meat, milk, leather and wool products for the local people.
Thɔ̈rɔ̈ɔ̈l aa kek ye luɔ̈i ke ye käŋ ɣääc ku aaye cuet aya, aala caŋ, biok ku nhiɛ̈mden aye kɔc lui.
They are widely distributed across the Middle East and Africa.
Kek aacï rɔ̈t tɛk piny apɛi Middle East ku Afrika.
It is therefore impossible to sacrifice all camels for the control of MERS, as what was done in wild animal markets in China to prevent the spreading of SARS-CoV and SARS-CoV-2.
Ku yen a ril ic bï thɔ̈rɔ̈ɔ̈l juar rin bï ke MERS-CoV gɛ̈l, cïmen ke cï looi tën lääi rɔɔr thuök China in ku bï SARS-CoV ku SARS-CoV-2 gɛ̈l.
To stop the recurrent outbreaks of MERS, a comprehensive approach should be taken to develop effective vaccines against MERS-CoV for camels, in combination with other infection control measures.
Ku bï MERS gɛ̈l bï cï la tueŋ, anɔŋ dhɔ̈ɔ̈l puɔth wïc bï kek nyai ku bï wäl MERS-CoV thɔ̈rɔ̈ɔ̈l cak, ku mat ke iic kek dhɔ̈ɔ̈l bï tuɛnytuɛny kök gɛ̈l.
As we are not able to eliminate these viruses, new genotypes might emerge to cause outbreaks.
Rin cïn të lɛ̈u bï ok käm kä cɔl a jäl ebën, kën yam alɛ̈u bï tuɛnytuɛny cɔl a ben jɔ̈.
A variety of zoonotic CoVs are circulating in the wild.
Kuat CoV lääi juëc aa rɔ̈t göt lääi rɔɔr ic.
Particularly, bat CoVs with zoonotic potential are so diverse.
Ku kë loi thok, kuat bat CoV kek kuat tuɛnytuɛny lääi aa kiith iic.
There are plenty of opportunities that these zoonotic CoVs evolve and recombine, resulting in the emergence of new CoVs that are more transmissible and/or deadly in humans in future.
Anɔŋ dhɔ̈ɔ̈l juëc lɛ̈u bï kuat CoV lääi rɔ̈t cak ku nuɛ̈t kä rɔ̈t, ku e yen të cï kuat CoV yam bɛ̈n nhial thïn rɔ̈t guɔ tek piny ku/wula thuou kɔc ic aköl tueŋ.
The culture of eating wild animals in some places of China should be abandoned to reduce unnecessary contact between humans and animals.
Cääm ye kɔc cam lääi rɔɔr gɛth kök pan China awïc bï puöl ku bï tuɛnytuɛny lääi kɔc dom dhuök piny.
With the ordeals of SARS, MERS and COVID-19, a better preparedness and response plan should be in place.
Ku kek athɛ̈m SARS, MERS ku COVID-19, aguiɛr path ku t-dhɔ̈ɔ̈l bï ke gɛ̈l aa dhil täu nyiɛnden.
In fact, many viruses have existed in the planet for a very long time.
Ku yic adïl, käm juëc aacï rɛ̈ɛ̈r piny kam bär kɔ̈u.
They stay in their own natural reservoirs until there is a chance for spillover.
Aa rɛ̈ɛ̈r ɣɔ̈ɔ̈n ken ye kek yɔ̈ thïn ɣet dhaman bï kek rɔ̈t tɛk piny.
Although bats have many features that favours the spreading of viruses, the chance for humans to be in contact with bats and other wildlife species can be minimized if people are educated to stay away from them.
Cɔk alɔn le aliɛ̈k käk tuany cɔl aweer rot piny, dhɔ̈ɔ̈l lɛ̈u bï kɔc rɔ̈m kek aliɛ̈k ku lääi rɔɔr kök alɛ̈u bï kuɔr nyin të cï kɔc piɔɔc ku bïk rɔ̈t aa mɛc wëi ke lɔm.
Continuous surveillance in mammals is necessary for better understanding of the ecology of CoVs and their natural hosts, which will prove useful in preventing animal-to-human transmission and future outbreaks.
La tueŋ cɛɛth ye lääi dhiɛ̈th caath gup apath ku bï të ye kuat CoV ku të ye kek rɛ̈ɛ̈r thïn tiɛt thïn, ka bï kuɔny cɔk ke path ku bï tek piny tuany jäl lɔŋ lääi le raan guop ku kë bï rot looi aköl ciɛ̈n.
To conclude, the most effective way to prevent viral zoonosis is for humans to stay away from the ecological niches of the natural reservoirs of the zoonotic viruses.
Ku bï thiök cɔ̈k, dhel lɛ̈u bï tuɛnytuɛny lääi tiɛt wei e ku bï kɔc rɔ̈t ya mɛc wei të den ye kek rɛ̈ɛ̈r thïn kek käm lääi.
Several pieces in the puzzle of the zoonotic origin of SARS-CoV-2 are still missing.
Käk juëc alɔŋ käk ye nyuɔth lɔn ye SARS-CoV-2 tuɛny lääi aa ŋuɔt ke liu.
First, if bats transmit an ancestral virus of SARS-CoV-2 to pangolins, it will be of interest to see under what circumstances bats and pangolins could share the same ecological niche.
Tök, na lɛ̈u aliɛ̈k bïk köm SARS-CoV-2 ɣäth pangolin gup, ka path bï tïŋ ye dhaman yïndë ye aliɛ̈k ku pangolin tö rɔm.
Second, if bats play a more direct role in human transmission, how humans get into contact with bats should be determined.
Rɔu, të le yen ke ye aliɛ̈k looi tek piny tuany raan guop, ka të kɔc ɔ̈m thïn kek aliɛ̈k a dhil yɔ̈p bï ŋic.
Third, if a third mammal acts as the true intermediate host, how it interacts with the different species including humans, bats and pangolins has to be clarified.
Diäk, na ye län ye kek diäk yen ye köm rɛ̈ɛ̈r ye guop, ka të ye yen rɔ̈m thïn kek lääi kök agut kɔc, aliɛ̈k ku pangolin a dhil cɔ̈k ic apath.
Finally, since many mammals including domestic animals might be susceptible to SARS-CoV-2, both surveillance and experimental infection should be conducted.
Thökde, rin cï lääi dhiɛ̈th la iic lääi ye mac bai aalɛ̈u bïk gup naŋ SARS-CoV-2, kë cï caath ku kë cï yɔ̈k të ye yen dom a dhil looi.
Should it be a bat, a pangolin or another mammal, it is expected that SARS-CoV-2 or its parental viruses that are almost identical will be identified in its natural hosts in future.
Të yɔ̈k yen ke ye alïïk, pangolin wula län dɛ̈t dhiɛ̈th, ka bï dhiɛl tiit lɔn ka SARS-CoV-2 wula käk a dhiɛ̈th köm thɔ̈ɔ̈ŋ aabï kek tïŋ ke ye kek ye käm yɔ̈k thïn aköl ciɛ̈n.
Continued investigations in this area will elucidate the evolutionary pathway of SARS-CoV-2 in animals, with important implications in the prevention and control of COVID-19 in humans.
Giɛ̈k cï looi kela tueŋ alɔŋ kën abï të ye SARS-CoV-2 jɔk thïn lääi gup tet ic apath, ku e muɣɛm të bï COVID-19 gɛ̈l thïn ku muökde kɔc gup.
Preliminary Estimates of the Prevalence of Selected Underlying Health Conditions Among Patients with Coronavirus Disease 2019 — United States, February 12–March 28, 2020
Käk cï kek thɔ̈ɔ̈ŋ ic la tueŋ käk cï ke kuany ke ye käk jɔ̈ɔ̈r pial guop kam kɔc tuany Coronavirus 2019 - United States, pɛi Rɔu aköl nïïn 12 le pɛi Diäk aköl nïïn 28, ruon 2020
On March 11, 2020, the World Health Organization declared Coronavirus Disease 2019 (COVID-19) a pandemic.
Pɛi Diäk aköl nïïn 11, ruon 2020, Manadhama lui käk pial guop pinynhom acï coronavirus 2019 (COVID-19) cal keye tuɛny pinynhom.
As of March 28, 2020, a total of 571,678 confirmed COVID-19 cases and 26,494 deaths have been reported worldwide.
Ku na ye aköl nïïn 28, pɛi Diäk ruon 2020, ka adat kɔc cï luaŋ COVID-19 e ye 571,678 ku ran 26,494 ke cï thou ecï cal pinynhom ebën.
Reports from China and Italy suggest that risk factors for severe disease include older age and the presence of at least one of several underlying health conditions.
Käk cï ke yɔ̈k pan China ku Italy aaye ke nyuöth ka käk jɔ̈ɔ̈r e tuany kën ic aala iic kɔc cï dït ku kë tööŋ alɔŋ käk kɔc jɔ̈ɔ̈r alɔŋ pial guop.
U.S. older adults, including those aged ≥65 years and particularly those aged ≥85 years, also appear to be at higher risk for severe COVID-19–associated outcomes; however, data describing underlying health conditions among U.S. COVID-19 patients have not yet been reported.
Kɔc cï dït pan U.S. agut kɔc la ruon 65 le tueŋ ku a kɔc la ruon 85, aaye ke tïŋ ke lɛ̈u bï COVID-19 kek dom, athɔ̈r käk jɔ̈ɔ̈r pial guop ic nyuɔth kam kɔc tuany COVID-19 pan U.S akïc cal.
As of March 28, 2020, U.S. states and territories have reported 122,653 U.S. COVID-19 cases to CDC, including 7,162 (5.8%) for whom data on underlying health conditions and other known risk factors for severe outcomes from respiratory infections were reported.
Pɛi Diäk aköl nïïn 28 ruon 2020, U.S ku bɛ̈ɛ̈i thiääk kek yen aacï ran 122,653 kɔc pan U.S cal kek cï luaŋ COVID-19 të ye tuɛnytuɛny gɛ̈l thïn cɔl CDC, ku ala ic ran 7,162 (5.8%) ke ye të ye kɔc pïïr thïn nyuɔth ku kä kök jɔ̈ɔ̈r bɛ̈n bei tuɛnytuɛny wɛ̈i iic.
Among these 7,162 cases, 2,692 (37.6%) patients had one or more underlying health condition or risk factor, and 4,470 (62.4%) had none of these conditions reported.
Kɔc cï luaŋ kä iic aa 7,162, 2,692 (37.6%) kɔc cï tuany aala tök wula tuɛnytuɛny juëc, ku ran 4,470 (62.4%) aacïn kë ril ic kä.
The percentage of COVID-19 patients with at least one underlying health condition or risk factor was higher among those requiring intensive care unit (ICU) admission (358 of 457, 78%) and those requiring hospitalization without ICU admission (732 of 1,037, 71%) than that among those who were not hospitalized (1,388 of 5,143, 27%).
Abaŋ të dït kam kɔc tuany COVID-19 la kë töŋ jɔ̈ɔ̈r alɔŋ pial guop wula käk ril iic pail guop ic e dït kam kɔc wïc kuɔny (ICU) alɔŋ tɛ̈ɛ̈c (358 e 457, 78%) ku kɔc wïc tɛ̈ɛ̈c ke cïn kuɔny alɔŋ ICU (732 e 1,037, 71%) tën abaŋ kɔc kïc ke tääc (1,388 e 5,143, 27%).
The most commonly reported conditions were diabetes mellitus, chronic lung disease, and cardiovascular disease.
Käk ril iic ke iic lac bɛr e thukari milletuth, tuɛny cuɛ̈ny, ku tuɛnytuɛny puou.
These preliminary findings suggest that in the United States, persons with underlying health conditions or other recognized risk factors for severe outcomes from respiratory infections appear to be at a higher risk for severe disease from COVID-19 than are persons without these conditions.
Käk cï kek yɔ̈k kä aaye kä luel ela pan United States, kɔc la kä jɔ̈ɔ̈r ke guop alɔŋ pial guop wula kä kök cï kek tïŋ ke jɔ̈ɔ̈r tuɛnytuɛny ye yɔ̈k wɛ̈i ic aaye COVID-19 taap apɛi tën kɔc cïn kä jɔ̈ɔ̈r tɔ̈u ke gup.
Data from laboratory-confirmed COVID-19 cases reported to CDC from 50 states, four U.S. territories and affiliated islands, the District of Columbia, and New York City with February 12–March 28, 2020 onset dates were analyzed.
Thɛ̈m cï yɔ̈k ɣɔ̈n ye kɔc them gup thïn acï COVID-19 luɛl tën CDC gɛth 50 ic, akɛth U.S. kä ŋuan ku Island thiääk ke kek, gen Columbia, ku gendit New York kek Pɛi Rɔu, aköl 12 le pɛi Diäk aköl nïïn 28 ruon 2020 aake cï caath.
Cases among persons repatriated to the United States from Wuhan, China, and the Diamond Princess cruise ship were excluded.
Kam kɔc tuany cï kek tuɔ̈c United State pan Wuhan, China, ku riän wïïr Diamond Princess aa kïc kek mat thïn.
For cases with missing onset dates, date of onset was estimated by subtracting 4 days (median interval from symptom onset to specimen collection date among cases with known dates in these data) from the earliest specimen collection.
Kɔc tuany kïc nïïn ken yɔ̈k, aköl a jɔk yen rɔt acï thɔ̈ɔ̈ŋ ic ke nïïn kä 4 cï nyai thïn (kam ciɛl mɛ̈nɛ̈ jɔ̈k tuany le aköl cï riim kɔc nyai bï ke them nïïn kam nïïn kɔc cï yɔ̈k ke ci luaŋ) mɛ̈nɛ̈ nyɛi riim bï ke them.
Public health departments reported cases to CDC using a standardized case report form that captures information (yes, no, or unknown) on the following conditions and potential risk factors: chronic lung disease (inclusive of asthma, chronic obstructive pulmonary disease [COPD], and emphysema); diabetes mellitus; cardiovascular disease; chronic renal disease; chronic liver disease; immunocompromised condition; neurologic disorder, neurodevelopmental, or intellectual disability; pregnancy; current smoking status; former smoking status; or other chronic disease.
Alɔŋ kɔc lɛ̈k alɔŋ pial guop acï CDC lɛ̈k acï athɔ̈r la ic wɛ̈t (e yic, lueth, wula akuc) kä ril kä iic ku käk bï kɔc jɔ̈ɔ̈r: tuɛny cuɛ̈ny (ku aala iic athama, tuany puou cuök ic [COPD], ku emphyɛema); thukari mellituth; tuany puou; tuany cuɛ̈ny cɔl acï lui apath, tuany cuɛ̈ny liɔ̈ɔ̈i guop, nhom liäp nyith, jɔ̈k tuany nhom, riɛr nhom; liɛ̈c, tëcït të ye yïn mɛth thïn, të ye yïn mɛth thïn thɛɛr, wula tuɛnytuɛny kök ril iic.
Data reported to CDC are preliminary and can be updated by health departments over time; critical data elements might be missing at the time of initial report; thus, this analysis is descriptive, and no statistical comparisons could be made.
Wɛ̈l cï kek lɛ̈k CDC a jɔ̈ɔ̈kden ku aalɛ̈u bï kek ben juak iic kɔc lui bɛ̈ɛ̈i akïïm ic kuat dhaman thok ebën, wɛ̈l cïc kek aalɛ̈u bïk liu dhaman loi lɛ̈k; ku këya cɛɛth kën ekë cï tet ic, ku acïn thɔ̈ɔ̈ŋ cï looi.
The percentages of patients of all ages with underlying health conditions who were not hospitalized, hospitalized without ICU admission, and hospitalized with ICU admission were calculated.
Adan dït kɔc tuany kuat run kela käk jɔ̈ɔ̈r pial guopden ic ke kïc tääc, kïc kek tääc ICU ic, ku kɔc cï tääc ICU ic aacï kek kuen/mat iic.
Percentages of hospitalizations with and without ICU admission were estimated for persons aged ≥19 years with and without underlying health conditions.
Adan dït kɔc cï kek tääc kela ku acïn kuony tɛ̈ɛ̈c wïc kä ICU aake cï thɔ̈ɔ̈ŋ iic tën kɔc la uon 19 le tueŋ kɔc la kä jɔ̈ɔ̈r pial guop ic ku kɔc cï kë jɔ̈ɔ̈r.
This part of the analysis was limited to persons aged ≥19 years because of the small sample size of cases in children with reported underlying health conditions (N = 32).
Abaŋ kä caath ic kën ecï looi tën akut la ruon 19 le tueŋ rin athem thïïn kor tɔ̈u mïïth iic la kä jɔ̈ɔ̈r alɔŋden pial guop (N = 32).
To account for missing data among these preliminary reports, ranges were estimated with a lower bound including cases with both known and unknown status for hospitalization with and without ICU admission as the denominator and an upper bound using only cases with known outcome status as the denominator.
Ku bï wɛ̈l liu kuen kam wɛ̈l cï kek lɛ̈k kɔc kä, të ye kek jɔk thïn acï thɔ̈ɔ̈ŋ ic kek të kor ku ala ic adat kɔc kuc ku kɔc ŋic keek ke cï tääc ICU ku kɔc kïc tääc ke ye nimra kor ku kë nhial ke adat kɔc cï tuany ŋic kë cï bɛ̈n bei keye nimra.
Because of small sample size and missing data on underlying health conditions among COVID-19 patients who died, case-fatality rates for persons with and without underlying conditions were not estimated.
Rin abaŋ thiin kor cï kuany ku wɛ̈t abaŋ liu thïn alɔŋ käk jɔ̈ɔ̈r pial guop ic kam kɔc tuany COVID-19 ci thou, abaŋ thuou tën kɔc la kä jɔ̈ɔ̈r ku kɔc cïn kë jɔ̈ɔ̈r aakïc kek thɔ̈ɔ̈ŋ iic.
As of March 28, 2020, a total of 122,653 laboratory-confirmed COVID-19 cases (Figure) and 2,112 deaths were reported to CDC.
Ku na ye pɛi Diäk aköl nïïn 28, ruon 2020, ka adat 122,653 aacï yɔ̈k ɣɔ̈n ye kɔc them gup thïn ke tuany COVID-19 (Thura) ku ran 2,112 ke cï thou aake cï lɛ̈k CDC.
Case report forms were submitted to CDC for 74,439 (60.7%) cases.
Athɔ̈ɔ̈r ye kɔc lɛ̈k aake cï gam tën CDC kën ran 74,439 (60.7%) cï luaŋ.
Data on presence or absence of underlying health conditions and other recognized risk factors for severe outcomes from respiratory infections (i.e., smoking and pregnancy) were available for 7,162 (5.8%) patients (Table 1).
Wɛ̈t tɔ̈u wula aliu alɔŋ käk jɔ̈ɔ̈r pial guop ic ku jɔ̈l aa kä kök ril iic rɔ̈t yɔ̈k tuɛnytuɛnywɛ̈i iic (cïmen mäth ku liɛ̈c) aake tɔ̈u ke ye 7,162 (5.8%) kɔc cï tuany (Agït 1).
Approximately one third of these patients (2,692, 37.6%), had at least one underlying condition or risk factor.
Ku bï thɔ̈ɔ̈ŋ ic abaŋ tök diäk (2,692. 37.6%) kɔc cï tuany, aala tök ke jɔ̈ɔ̈r wula ke ril ic alɔŋ pial guopden ic.
Diabetes mellitus (784, 10.9%), chronic lung disease (656, 9.2%), and cardiovascular disease (647, 9.0%) were the most frequently reported conditions among all cases.
Thukari mellituth (784, 10.9%), tuany cuɛ̈ny (656, 9.2%), ku tuany puou (647, 9.0%) aa kek käk cï kek lac a yɔ̈k kam kɔc cï luaŋ.
Among 457 ICU admissions and 1,037 non-ICU hospitalizations, 358 (78%) and 732 (71%), respectively occurred among persons with one or more reported underlying health condition.
Kam ran 457 cï tääc ic ku ran 1,037 kïc tääc ICU, 358 (78%) ku 732 (71%), aacï ke yɔ̈k kam kɔc la kë töŋ jɔ̈ɔ̈r wula käk cï ke yɔ̈k ke jɔ̈ɔ̈r pial guop ic.
In contrast, 1,388 of 5,143 (27%) COVID-19 patients who were not hospitalized were reported to have at least one underlying health condition.
Ku wɛ̈cden ic, 1,388 a 5,143 (27%) kɔc cï tuany COVID-19 ke kïc tääc acï luel lɔn le kek töŋ jɔ̈ɔ̈r pial guopden ic.
Among patients aged ≥19 years, the percentage of non-ICU hospitalizations was higher among those with underlying health conditions (27.3%–29.8%) than among those without underlying health conditions (7.2%–7.8%); the percentage of cases that resulted in an ICU admission was also higher for those with underlying health conditions (13.3%–14.5%) than those without these conditions (2.2%–2.4%) (Table 2).
Kam kɔc cï tuany la ruon 19 le tueŋ, adat kɔc kïc tääc ICU e dït kam kɔc la käk jɔ̈ɔ̈r pial guopden ic (27.3%-29.8%) tën kɔc cïn ke jɔ̈ɔ̈r pial guopden ic (7.2%-7.8%); adat kɔc cï kek tääc ICU e dït aya tën kɔc la kë jɔ̈ɔ̈r pial guopden ic (13.3%-14.5%) tën kɔc liu kek thïn (2.2%-2.4) (Agït 2).
Small numbers of COVID-19 patients aged &lt; 19 years were reported to be hospitalized (48) or admitted to an ICU (eight).
Adat kor kɔc la ruon 19 le tueŋ cï tuany COVID-19 aake cï cal lɔn cï kek tääc (48) wula aacï tääc ICU ic (bɛ̈t).
In contrast, 335 patients aged &lt; 19 years were not hospitalized and 1,342 had missing data on hospitalization.
Wɛ̈cden ic, ran 335 la ruon 19 le tueŋ ci tuany aake kïc tääc ku ran 1,342 acïn kë cï göt alɔŋ tɛ̈ɛ̈cden.
Among all COVID-19 patients with complete information on underlying conditions or risk factors, 184 deaths occurred (all among patients aged ≥19 years); 173 deaths (94%) were reported among patients with at least one underlying condition.
Kam kɔc cï tuany COVID-19 la wɛ̈t cï yɔ̈k alɔŋ käk jɔ̈ɔ̈r wula kä ril iic alɔŋ pial guopden ic, ran 184 acï thou (kam kɔc la ruon 19 le tueŋ tuany); ran 173 cï thou (94%) eye kam kɔc tuany la gup kë töŋ jɔ̈ɔ̈r alɔŋ pial guop.
Among 122,653 U.S. COVID-19 cases reported to CDC as of March 28, 2020, 7,162 (5.8%) patients had data available pertaining to underlying health conditions or potential risk factors; among these patients, higher percentages of patients with underlying conditions were admitted to the hospital and to an ICU than patients without reported underlying conditions.
Kam kɔc cï tuany COVID-19 pan U.S ran 122,653 ecï lɛ̈k CDC pɛi Diäk aköl nïïn 28, ruon 2020, ran 7,162 (5.8%) kɔc tuany ala kë ŋic alɔŋ käk jɔ̈ɔ̈r wula kä ril iic ye tïŋ; ku kam kɔc tuany kä, adat dït kam kɔc tuany la käk jɔ̈ɔ̈r alɔŋ pial guop aake cï kek tääc panakïm ku ICU tën kɔc tuany cï kë jɔ̈ɔ̈r tën kek.
These results are consistent with findings from China and Italy, which suggest that patients with underlying health conditions and risk factors, including, but not limited to, diabetes mellitus, hypertension, COPD, coronary artery disease, cerebrovascular disease, chronic renal disease, and smoking, might be at higher risk for severe disease or death from COVID-19.
Käk cï ke yɔ̈k aa thɔ̈ɔ̈ŋ kek käk cï kek yɔ̈k China ku Italy, ku acï luel lɔn ka kɔc la käk jɔ̈ɔ̈r alɔŋ pial guop ku kä ril ic, ku aala iic, ku ace kek ke pɛ̈c, thukari melittuth, jɔ̈n rot riɛm, COPD, tuany rääl ic, tuany kɔc thɔ̈ɔ̈ŋ, tuany ce cuɛ̈ny lui apath, mäth, aalɛ̈u bï tuany kek bau wula thuou alɔŋ COVID-19.
This analysis was limited by small numbers and missing data because of the burden placed on reporting health departments with rapidly rising case counts, and these findings might change as additional data become available.
Cɛɛth kën ecï kuɔr piny adat kor ku rin wɛ̈l liu rin luɔi ril cï täu kɔc lui panakïm ku tuany ajuak rot, ku käk cï yɔ̈k kä aalɛ̈u bïk rɔ̈t waar ke wɛ̈l juëc aŋuɔt ke bɔ̈u nhial.
It is not yet known whether the severity or level of control of underlying health conditions affects the risk for severe disease associated with COVID-19.
Aŋuɔt kuc yen rɛ̈c wula të ye käk jɔ̈ɔ̈r alɔŋ pial guop tuany thiääk thok ke COVID-19 rɛ̈c thïn.
Many of these underlying health conditions are common in the United States: based on self-reported 2018 data, the prevalence of diagnosed diabetes among U.S. adults was 10.1%, and the U.S. age-adjusted prevalence of all types of heart disease (excluding hypertension without other heart disease) was 10.6% in 2017.
Kuat käk jɔ̈ɔ̈ alɔŋ pial guop kä aa tɔ̈u U.S: tëcït të cï yen luel thïn athɔ̈r ruon 2018, rɛ̈ɛ̈r thukari kam kɔc dït U.S e 10.1%, ku run cï ke cök piny U.S kela kuat tuɛnytuɛny puou (ku däkät aliu thïn ku ke tuɛnytuɛny puou liu thïn) e ye 10.6% ruon 2017.
The age-adjusted prevalence of COPD among U.S. adults is 5.9%, and in 2018, the U.S. estimated prevalence of current asthma among persons of all ages was 7.9%.
Run cï ke cök piny täu COPD kam kɔc dït U.S e 5.9%, ku ruon 2018 ic, Adhiama pan U.S acï yɔ̈k kuat run ic ebën e 7.9%.
CDC continues to develop and update resources for persons with underlying health conditions to reduce the risk of acquiring COVID-19.
CDC aŋuɔt ye dhɔ̈l bï ke COVID-19 dhuk piny cak ku e athɔ̈r waar ic tën kɔc la gup käk jɔ̈ɔ̈r guopden ic alɔŋ pial guop.
The estimated higher prevalence of these conditions among those in this early group of U.S. COVID-19 patients and the potentially higher risk for more severe disease from COVID-19 associated with the presence of underlying conditions highlight the importance of COVID-19 prevention in persons with underlying conditions.
Rɛ̈ɛ̈r cï thɔ̈ɔ̈ŋ ic rin kä jɔ̈ɔ̈r kam akut tueŋ tuany COVID-19 pan U.S ku kä ril iic ye tïŋ alɔŋ tuany rɛc COVID-19 thääny thook ke käk jɔ̈ɔ̈r e ke nyuöth muɣema bï COVID-19 gɛ̈l kɔc la gup käk jɔ̈ɔ̈r.
The findings in this report are subject to at least six limitations.
Käk cï ke yɔ̈k athɔ̈rkën ic aacï kek kuɔr piny käŋ kädëtem iic.
First, these data are preliminary, and the analysis was limited by missing data related to the health department reporting burden associated with rapidly rising case counts and delays in completion of information requiring medical chart review; these findings might change as additional data become available.
Tueŋ, wɛ̈lkä a jɔ̈kden, ku cɛɛth eci dhuök piny rin wɛ̈l liu thääny thook kek kɔc lui panakïm luɔi dït thääny thok kek juɛ̈ŋ rot tuany ku gäu kïc wɛ̈l wïc panakïm; wɛ̈lkä aalɛ̈u bï rɔ̈t waar të le yen wɛ̈l kök tɔ̈u thïn.
Information on underlying conditions was only available for 7,162 (5.8%) of 122,653 cases reported to CDC.
Wɛ̈t rin käk jɔ̈ɔ̈r etɔ̈u tën ran 7,162 (5.8%) ran 122,653 kɔc cï tuany cï ke lɛ̈k CDC.