SARS‑CoV‑2 is a virus of the speciesBetacoronavirus pandemicum (SARSr-CoV), as isSARS-CoV-1, the virus that caused the2002–2004 SARS outbreak.[2][17] Some animal-borne coronaviruses are more closely related to SARS-CoV-2 than SARS-CoV-1 is. The closest known relative is the BANAL-52 bat coronavirus. SARS-CoV-2 is ofzoonotic origin; its closegenetic similarity to bat coronaviruses suggests it emerged from such abat-borne virus.[18]Research is ongoing as to whether SARS‑CoV‑2 came directly from bats or indirectly through any intermediate hosts.[19] The virus shows littlegenetic diversity, indicating that thespillover event introducing SARS‑CoV‑2 to humans is likely to have occurred in late 2019.[20]
Epidemiological studies estimate that in the period between December 2019 and September 2020 each infection resulted in an average of 2.4–3.4 new infections when no members of the community wereimmune and nopreventive measures were taken.[21] Some later variants were more infectious.[22] The virus is airborne and primarily spreads between people through close contact and viaaerosols andrespiratory droplets that are exhaled when talking, breathing, or otherwise exhaling, as well as those produced from coughs and sneezes.[23][24] Itenters human cells by binding toangiotensin-converting enzyme 2 (ACE2), a membrane protein that regulates the renin–angiotensin system.[25][26]
Terminology
Sign with provisional name "2019-nCoV"
During the initial outbreak inWuhan, China, various names were used for the virus; some names used by different sources included "the coronavirus" or "Wuhan coronavirus".[27][28] In January 2020, theWorld Health Organization (WHO) recommended "2019 novel coronavirus" (2019-nCoV)[5][29] as the provisional name for the virus. This was in accordance with WHO's 2015 guidance[30] against using geographical locations, animal species, or groups of people in disease and virus names.[31][32]
On 11 February 2020, theInternational Committee on Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS‑CoV‑2).[33] To avoid confusion with the diseaseSARS, the WHO sometimes refers to SARS‑CoV‑2 as "the COVID-19 virus" in public health communications[34][35] and the name HCoV-19 was included in some research articles.[8][9][10] Referring to COVID-19 as the "Wuhan virus" has been described as dangerous by WHO officials, and asxenophobic by many journalists and academics.[36][37][38]
Human-to-humantransmission of SARS‑CoV‑2 was confirmed on 20 January 2020 during theCOVID-19 pandemic.[16][39][40][41] Transmission was initially assumed to occur primarily viarespiratory droplets from coughs and sneezes within a range of about 1.8 metres (6 ft).[42][43] Laser light scattering experiments suggest thatspeaking is an additional mode of transmission[44][45] and a far-reaching[46] one, indoors, with little air flow.[47][48] Other studies have suggested that the virus may beairborne as well, withaerosols potentially being able to transmit the virus.[49][50][51] During human-to-human transmission, between 200 and 800 infectious SARS‑CoV‑2virions are thought to initiate a new infection.[52][53][54] If confirmed, aerosol transmission has biosafety implications because a major concern associated with the risk of working with emerging viruses in the laboratory is the generation of aerosols from various laboratory activities which are not immediately recognizable and may affect other scientific personnel.[55] Indirect contact viacontaminated surfaces is another possible cause of infection.[56] Preliminary research indicates that the virus may remain viable on plastic (polypropylene) andstainless steel (AISI 304) for up to three days, but it does not survive on cardboard for more than one day or on copper for more than four hours.[10] The virus is inactivated by soap, which destabilizes itslipid bilayer.[57][58] ViralRNA has also been found instool samples and semen from infected individuals.[59][60]
The degree to which the virus is infectious during theincubation period is uncertain, but research has indicated that thepharynx reaches peakviral load approximately four days after infection[61][62] or in the first week of symptoms and declines thereafter.[63] The duration of SARS-CoV-2RNA shedding is generally between 3 and 46 days after symptom onset.[64]
A study by a team of researchers from theUniversity of North Carolina found that thenasal cavity is seemingly the dominant initial site of infection, with subsequentaspiration-mediated virus-seeding into the lungs in SARS‑CoV‑2 pathogenesis.[65] They found that there was an infection gradient from high in proximal towards low in distal pulmonary epithelial cultures, with a focal infection in ciliated cells and type 2 pneumocytes in the airway and alveolar regions respectively.[65]
Studies have identified a range of animals—such as cats, ferrets, hamsters, non-human primates, minks, tree shrews, raccoon dogs, fruit bats, and rabbits—that are susceptible and permissive to SARS-CoV-2 infection.[66][67][68] Some institutions have advised that those infected with SARS‑CoV‑2 restrict their contact with animals.[69][70]
Asymptomatic and presymptomatic transmission
On 1February 2020, theWorld Health Organization (WHO) indicated that "transmission fromasymptomatic cases is likely not a major driver of transmission".[71] One meta-analysis found that 17% of infections are asymptomatic, and asymptomatic individuals were 42% less likely to transmit the virus.[72]
However, an epidemiological model of the beginning of theoutbreak in China suggested that "pre-symptomaticshedding may be typical among documented infections" and thatsubclinical infections may have been the source of a majority of infections.[73] That may explain how out of 217 on board acruise liner that docked atMontevideo, only 24 of 128 who tested positive for viral RNA showed symptoms.[74] Similarly, a study of ninety-four patients hospitalized in January and February 2020 estimated patients began shedding virus two to three days before symptoms appear and that "a substantial proportion of transmission probably occurred before first symptoms in theindex case".[53] The authors later published a correction that showed that shedding began earlier than first estimated, four to five days before symptoms appear.[75]
Reinfection
This section needs to beupdated. Please help update this article to reflect recent events or newly available information.(May 2025)
There is uncertainty about reinfection and long-term immunity.[76] It is not known how common reinfection is, but reports have indicated that it is occurring with variable severity.[76]
The first reported case of reinfection was a 33-year-old man from Hong Kong who first tested positive on 26 March 2020, was discharged on 15 April 2020 after two negative tests, and tested positive again on 15 August 2020 (142 days later), which was confirmed by whole-genome sequencing showing that the viral genomes between the episodes belong to differentclades.[77] The findings had the implications thatherd immunity may not eliminate the virus if reinfection is not an uncommon occurrence and thatvaccines may not be able to provide lifelong protection against the virus.[77]
Another case study described a 25-year-old man from Nevada who tested positive for SARS‑CoV‑2 on 18 April 2020 and on 5 June 2020 (separated by two negative tests). Since genomic analyses showed significant genetic differences between the SARS‑CoV‑2 variant sampled on those two dates, the case study authors determined this was a reinfection.[78] The man's second infection was symptomatically more severe than the first infection, but the mechanisms that could account for this are not known.[78]
Transmission of SARS-CoV-1 and SARS‑CoV‑2 from mammals as biological carriers to humans
Nonatural reservoir for SARS-CoV-2 has been identified.[79] Prior to the emergence of SARS-CoV-2 as a pathogen infecting humans, there had been two previouszoonosis-based coronavirus epidemics, those caused bySARS-CoV-1 andMERS-CoV.[18]
The first known infections from SARS‑CoV‑2 were discovered in Wuhan, China.[80] The original source of viral transmission to humans remains unclear, as does whether the virus becamepathogenic before or after thespillover event.[9][20][81] Because many of the early infectees were workers at theHuanan Seafood Market,[82][83] it has been suggested that the virus might have originated from the market.[9][84] However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid expansion of the infections.[20][85] A March 2021 WHO-convened report stated that human spillover via an intermediate animal host was the most likely explanation, with direct spillover from bats next most likely. Introduction through the food supply chain and the Huanan Seafood Market was considered another possible, but less likely, explanation.[86] An analysis in November 2021, however, said that the earliest-known case had been misidentified and that the preponderance of early cases linked to the Huanan Market argued for it being the source.[87]
For a virus recently acquired through a cross-species transmission, rapid evolution is expected.[88] The mutation rate estimated from early cases of SARS-CoV-2 was of6.54×10−4 per site per year.[86] Coronaviruses in general have high geneticplasticity,[89] but SARS-CoV-2's viral evolution is slowed by theRNA proofreading capability of its replication machinery.[90] For comparison, the viral mutation rate in vivo of SARS-CoV-2 has been found to be lower than that of influenza.[91]
Research into the natural reservoir of the virus that caused the2002–2004 SARS outbreak has resulted in the discovery of manySARS-like bat coronaviruses, most originating inhorseshoe bats. The closest match by far, published inNature (journal) in February 2022, were virusesBANAL-52 (96.8% resemblance to SARS‑CoV‑2), BANAL-103 and BANAL-236, collected in three different species of bats inFeuang, Laos.[92][93][94] An earlier source published in February 2020 identified the virusRaTG13, collected in bats inMojiang, Yunnan, China to be the closest to SARS‑CoV‑2, with 96.1% resemblance.[80][95] None of the above are its direct ancestor.[96]
Samples taken fromRhinolophus sinicus, a species ofhorseshoe bats, show an 80% resemblance to SARS‑CoV‑2.
Bats are considered the most likely natural reservoir of SARS‑CoV‑2.[86][97] Differences between the bat coronavirus and SARS‑CoV‑2 suggest that humans may have been infected via an intermediate host;[84] although the source of introduction into humans remains unknown.[98][79]
Although the role ofpangolins as an intermediate host was initially posited (a study published in July 2020 suggested that pangolins are an intermediate host of SARS‑CoV‑2-like coronaviruses[99][100]), subsequent studies have not substantiated their contribution to the spillover.[86] Evidence against this hypothesis includes the fact that pangolin virus samples are too distant to SARS-CoV-2: isolates obtained from pangolins seized inGuangdong were only 92% identical in sequence to the SARS‑CoV‑2 genome (matches above 90 percent may sound high, but in genomic terms it is a wide evolutionary gap[101]). In addition, despite similarities in a few critical amino acids,[102] pangolin virus samples exhibit poor binding to the human ACE2 receptor.[103]
Phylogenetics and taxonomy
Genomic information
Genomic organisation of isolate Wuhan-Hu-1, the earliest sequenced sample of SARS-CoV-2
SARS‑CoV‑2 belongs to the broad family of viruses known ascoronaviruses.[28] It is apositive-sense single-stranded RNA (+ssRNA) virus, with a single linear RNA segment. Coronaviruses infect humans, other mammals, including livestock and companion animals, and avian species.[104] Human coronaviruses can cause illnesses ranging from thecommon cold to more severe diseases such asMiddle East respiratory syndrome (MERS, fatality rate ~34%). SARS-CoV-2 is the seventh known coronavirus to infect people, after229E,NL63,OC43,HKU1,MERS-CoV, and the originalSARS-CoV.[105]
Like the SARS-related coronavirus implicated in the 2003 SARS outbreak, SARS‑CoV‑2 is a member of the subgenusSarbecovirus (beta-CoV lineage B).[106][107] Coronaviruses undergo frequent recombination.[108] The mechanism of recombination in unsegmented RNA viruses such as SARS-CoV-2 is generally by copy-choice replication, in which gene material switches from one RNA template molecule to another during replication.[109] The SARS-CoV-2 RNA sequence is approximately 30,000bases in length,[110] relatively long for a coronavirus—which in turn carry the largest genomes among all RNA families.[111] Its genome consists nearly entirely of protein-coding sequences, a trait shared with other coronaviruses.[108]
A distinguishing feature of SARS‑CoV‑2 is its incorporation of apolybasic site cleaved byfurin,[102][112] which appears to be an important element enhancing its virulence.[113] It was suggested that the acquisition of the furin-cleavage site in the SARS-CoV-2 S protein was essential for zoonotic transfer to humans.[114] The furinprotease recognizes the canonicalpeptide sequenceRX[R/K]R↓X where the cleavage site is indicated by a down arrow and X is anyamino acid.[115][116] In SARS-CoV-2 the recognition site is formed by the incorporated 12codon nucleotide sequence CCT CGG CGG GCA which corresponds to the amino acid sequencePRRA.[117] This sequence is upstream of an arginine and serine which forms the S1/S2 cleavage site (PRRAR↓S) of the spike protein.[118] Although such sites are a common naturally-occurring feature of other viruses within the Subfamily Orthocoronavirinae,[117] it appears in few other viruses from theBeta-CoV genus,[119] and it is unique among members of its subgenus for such a site.[102] The closest relatives to SARS-CoV2, including BANAL-20-52, RaTG13, Pangolin P4L, and SARS-CoV-1, lack the RRAR insertion.[120] The furin cleavage site PRRAR↓ is highly similar to that of thefeline coronavirus, analphacoronavirus 1 virus.[121]
Viral genetic sequence data can provide critical information about whether viruses separated by time and space are likely to be epidemiologically linked.[122] With a sufficient number of sequencedgenomes, it is possible to reconstruct aphylogenetic tree of the mutation history of a family of viruses. By 12 January 2020, five genomes of SARS‑CoV‑2 had been isolated from Wuhan and reported by theChinese Center for Disease Control and Prevention (CCDC) and other institutions;[110][123] the number of genomes increased to 42 by 30 January 2020.[124] A phylogenetic analysis of those samples showed they were "highly related with at most seven mutations relative to acommon ancestor", implying that the first human infection occurred in November or December 2019.[124] Examination of the topology of the phylogenetic tree at the start of the pandemic also found high similarities between human isolates.[125] As of 21 August 2021,[update] 3,422 SARS‑CoV‑2 genomes, belonging to 19 strains, sampled on all continents except Antarctica were publicly available.[126]
In July 2020, scientists reported that a more infectious SARS‑CoV‑2 variant withspike protein variant G614 has replaced D614 as the dominant form in the pandemic.[128][129]
Coronavirus genomes and subgenomes encode sixopen reading frames (ORFs).[130] In October 2020, researchers discovered a possibleoverlapping gene namedORF3d, in the SARS‑CoV‑2genome. It is unknown if the protein produced byORF3d has any function, but it provokes a strong immune response.ORF3d has been identified before, in a variant of coronavirus that infectspangolins.[131][132]
Phylogenetic tree
A phylogenetic tree based on whole-genome sequences of SARS-CoV-2 and related coronaviruses is:[133][134]
This section needs to beupdated. Please help update this article to reflect recent events or newly available information.(April 2023)
False-colourtransmission electron micrograph of a B.1.1.7 variant coronavirus. The variant's increased transmissibility is believed to be due to changes in the structure of the spike proteins, shown here in green.
There are many thousands of variants of SARS-CoV-2, which can be grouped into the much largerclades.[143] Several differentclade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), whileGISAID divides them into seven (L, O, V, S, G, GH, and GR).[144]
Alpha: Lineage B.1.1.7 emerged in theUnited Kingdom in September 2020, with evidence of increased transmissibility and virulence. Notable mutations includeN501Y andP681H.
AnE484K mutation in some lineage B.1.1.7 virions has been noted and is also tracked by variouspublic health agencies.
Beta: Lineage B.1.351 emerged inSouth Africa in May 2020, with evidence of increased transmissibility and changes to antigenicity, with some public health officials raising alarms about its impact on the efficacy of some vaccines. Notable mutations includeK417N, E484K and N501Y.
Gamma: Lineage P.1 emerged inBrazil in November 2020, also with evidence of increased transmissibility and virulence, alongside changes to antigenicity. Similar concerns about vaccine efficacy have been raised. Notable mutations also include K417N, E484K and N501Y.
Delta: Lineage B.1.617.2 emerged inIndia in October 2020. There is also evidence of increased transmissibility and changes to antigenicity.
Omicron: Lineage B.1.1.529 emerged inBotswana in November 2021.
Other notable variants include 6 other WHO-designatedvariants under investigation andCluster 5, which emerged amongmink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct.[146]
Each SARS-CoV-2virion is 60–140nanometres (2.4×10−6–5.5×10−6 in) in diameter;[105][83] its mass within the global human populace has been estimated as being between 0.1 and 10 kilograms.[147] Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S (spike), E (envelope), M (membrane), and N (nucleocapsid) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create theviral envelope.[148] Coronavirus S proteins areglycoproteins and also type Imembrane proteins (membranes containing a singletransmembrane domain oriented on the extracellular side).[114] They are divided into two functional parts (S1 and S2).[104] In SARS-CoV-2, the spike protein, which has been imaged at the atomic level usingcryogenic electron microscopy,[149][150] is the protein responsible for allowing the virus to attach to and fuse with themembrane of a host cell;[148] specifically, its S1subunit catalyzes attachment, the S2 subunit fusion.[151]
As of early 2022, about 7 million SARS-CoV-2 genomes had been sequenced and deposited into public databases and another 800,000 or so were added each month.[152] By September 2023, theGISAID EpiCoV database contained more than 16 million genome sequences.[153]
SARS-CoV-2 has a linear,positive-sense, single-stranded RNA genome about 30,000 bases long.[104] Its genome has a bias againstcytosine (C) and guanine (G) nucleotides, like other coronaviruses.[154] The genome has the highest composition of U (uracil) (32.2%), followed by A (adenine) (29.9%), and a similar composition ofG (19.6%) andC (18.3%).[155] Thenucleotide bias arises from the mutation of guanines and cytosines to adenines and uracils, respectively.[156] The mutation ofCG dinucleotides is thought to arise to avoid thezinc finger antiviral protein related defense mechanism of cells,[157] and to lower the energy to unbind the genome duringreplication andtranslation (adenine and uracilbase pair via twohydrogen bonds, cytosine and guanine via three).[156] The depletion of CG dinucleotides in its genome has led the virus to have a noticeablecodon usage bias. For instance, arginine's six different codons have arelative synonymous codon usage of AGA (2.67), CGU (1.46), AGG (.81), CGC (.58), CGA (.29), and CGG (.19).[155] A similar codon usage bias trend is seen in other SARS–related coronaviruses.[158]
Replication cycle
Virus infections start when viral particles bind to host surface cellular receptors.[159]Protein modeling experiments on the spike protein of the virus soon suggested that SARS‑CoV‑2 has sufficient affinity to the receptorangiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism ofcell entry.[160] By 22 January 2020, a group in China working with the full virus genome and a group in the United States usingreverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS‑CoV‑2.[80][161][162][163] Studies have shown that SARS‑CoV‑2 has a higher affinity to human ACE2 than the original SARS virus.[149][164] SARS‑CoV‑2 may also usebasigin to assist in cell entry.[165]
Initial spike protein priming bytransmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS‑CoV‑2.[25] The host proteinneuropilin 1 (NRP1) may aid the virus in host cell entry using ACE2.[166] After a SARS‑CoV‑2 virion attaches to a target cell, the cell's TMPRSS2 cuts open the spike protein of the virus, exposing afusion peptide in the S2 subunit, and the host receptor ACE2.[151] After fusion, anendosome forms around the virion, separating it from the rest of the host cell. The virion escapes when thepH of the endosome drops or whencathepsin, a hostcysteine protease, cleaves it.[151] The virion then releases RNA into the cell and forces the cell to produce and disseminatecopies of the virus, which infect more cells.[167]
SARS‑CoV‑2 produces at least threevirulence factors that promote shedding of new virions from host cells and inhibitimmune response.[148] Whether they includedownregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).[168]
Retrospective tests collected within the Chinese surveillance system revealed no clear indication of substantial unrecognized circulation of SARS‑CoV‑2 in Wuhan during the latter part of 2019.[86]
A meta-analysis from November 2020 estimated thebasic reproduction number () of the virus to be between 2.39 and 3.44.[21] This means each infection from the virus is expected to result in 2.39 to 3.44 new infections when no members of the community areimmune and nopreventive measures are taken. The reproduction number may be higher in densely populated conditions such as those found oncruise ships.[176] Human behavior affects the R0 value and hence estimates of R0 differ between different countries, cultures, and social norms. For instance, one study found relatively low R0 (~3.5) in Sweden, Belgium and the Netherlands, while Spain and the US had significantly higher R0 values (5.9 to 6.4, respectively).[177]
There have been about 96,000 confirmed cases of infection in mainland China.[181] While the proportion of infections that result inconfirmed cases or progress to diagnosable disease remains unclear,[182] one mathematical model estimated that 75,815 people were infected on 25 January 2020 in Wuhan alone, at a time when the number of confirmed cases worldwide was only 2,015.[183] Before 24 February 2020, over 95% of all deaths fromCOVID-19 worldwide had occurred inHubei province, where Wuhan is located.[184][185] As of 10 March 2023, the percentage had decreased to0.047%.[181]
As of 10 March 2023, there were 676,609,955 total confirmed cases of SARS‑CoV‑2 infection.[181] The total number of deaths attributed to the virus was 6,881,955.[181]
^Organization WH (January 2020). Surveillance case definitions for human infection with novel coronavirus (nCoV): interim guidance v1, January 2020 (Report). World Health Organization.hdl:10665/330376. WHO/2019-nCoV/Surveillance/v2020.1.
^"Naming the coronavirus disease (COVID-2019) and the virus that causes it". World Health Organization.Archived from the original on 28 February 2020. Retrieved14 December 2020.ICTV announced "severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)" as the name of the new virus on 11 February 2020. This name was chosen because the virus is genetically related to the coronavirus responsible for the SARS outbreak of 2003. While related, the two viruses are different.
^"Naming the coronavirus disease (COVID-2019) and the virus that causes it". World Health Organization.Archived from the original on 28 February 2020. Retrieved14 December 2020.From a risk communications perspective, using the name SARS can have unintended consequences in terms of creating unnecessary fear for some populations.... For that reason and others, WHO has begun referring to the virus as "the virus responsible for COVID-19" or "the COVID-19 virus" when communicating with the public. Neither of these designations is [sic] intended as replacements for the official name of the virus as agreed by the ICTV.
^"Standing Up to Hate and Bias Related to COVID-19". National Education Association. 5 June 2020.It's racist and it creates xenophobia," University of California at Berkeley Asian American studies lecturer Harvey Dong toldThe Washington Post. "It's a very dangerous situation."
^Gstalter M (19 March 2020)."WHO official warns against calling it 'Chinese virus,' says 'there is no blame in this'".The Hill. Retrieved15 September 2022.Ryan is not the first WHO official to push back against the phrase. Director-General Tedros Adhanom Ghebreyesus said earlier this month that the term is "painful to see" and "more dangerous than the virus itself."
^Klompas M, Baker MA, Rhee C (August 2020)."Airborne Transmission of SARS-CoV-2: Theoretical Considerations and Available Evidence".JAMA.324 (5):441–442.doi:10.1001/jama.2020.12458.PMID32749495.S2CID220500293.Investigators have demonstrated that speaking and coughing produce a mixture of both droplets and aerosols in a range of sizes, that these secretions can travel together for up to 27 feet, that it is feasible for SARS-CoV-2 to remain suspended in the air and viable for hours, that SARS-CoV-2 RNA can be recovered from air samples in hospitals, and that poor ventilation prolongs the amount of time that aerosols remain airborne.
^Rettner R (21 January 2021)."Talking is worse than coughing for spreading COVID-19 indoors".Live Science. Retrieved10 October 2022.In one modeled scenario, the researchers found that after a short cough, the number of infectious particles in the air would quickly fall after 1 to 7 minutes; in contrast, after speaking for 30 seconds, only after 30 minutes would the number of infectious particles fall to similar levels; and a high number of particles were still suspended after one hour. In other words, a dose of virus particles capable of causing an infection would linger in the air much longer after speech than a cough. (In this modeled scenario, the same number of droplets were admitted during a 0.5-second cough as during the course of 30 seconds of speech.)
^Hossain MG, Tang Yd, Akter S, Zheng C (May 2022). "Roles of the polybasic furin cleavage site of spike protein in SARS-CoV-2 replication, pathogenesis, and host immune responses and vaccination".Journal of Medical Virology.94 (5):1815–1820.doi:10.1002/jmv.27539.PMID34936124.S2CID245430230.
^Temmam S, Vongphayloth K, Salazar EB, Munier S, Bonomi M, Régnault B, Douangboubpha B, Karami Y, Chretien D, Sanamxay D, Xayaphet V, Paphaphanh P, Lacoste V, Somlor S, Lakeomany K, Phommavanh N, Pérot P, Donati F, Bigot T, Nilges M, Rey F, van der Werf S, Brey P, Eloit M (February 2022). "Bat coronaviruses related to SARS-CoV-2 and infectious for human cells".Nature (604):330–336.doi:10.1038/s41586-022-04532-4.
^abcAronson JK (25 March 2020)."Coronaviruses – a general introduction".Centre for Evidence-Based Medicine, Nuffield Department of Primary Care Health Sciences, University of Oxford. Archived fromthe original on 22 May 2020. Retrieved24 May 2020.
^"Paxlovid EPAR".European Medicines Agency (EMA). 24 January 2022. Retrieved3 February 2022. Text was copied from this source which is copyright European Medicines Agency. Reproduction is authorized provided the source is acknowledged.
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