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SARS-CoV-2

December 01, 2023

This article is about the virus that causes COVID-19. For the virus that causes SARS, see SARS-CoV-1.

Severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2)[2] is a strain of coronavirus that causes COVID-19, the respiratory illness responsible for the COVID-19 pandemic.[3] The virus previously had the provisional name 2019 novel coronavirus (2019-nCoV),[4][5][6][7] and has also been called human coronavirus 2019 (HCoV-19 or hCoV-19).[8][9][10][11] First identified in the city of Wuhan, Hubei, China, the World Health Organization designated the outbreak a public health emergency of international concern from January 30, 2020, to May 5, 2023.[12][13][14] SARS‑CoV‑2 is a positive-sense single-stranded RNA virus[15] that is contagious in humans.[16]

Severe acute respiratory syndrome coronavirus 2
Colourised transmission electron micrograph of SARS-CoV-2 virions with visible coronae
Model of the external structure of the SARS-CoV-2 virion[1]
● Blue:envelope
● Turquoise:spike glycoprotein (S)
● Pink:envelope proteins (E)
● Green:membrane proteins (M)
● Orange:glycan
Virus classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Pisuviricota
Class: Pisoniviricetes
Order: Nidovirales
Family: Coronaviridae
Genus: Betacoronavirus
Subgenus: Sarbecovirus
Species:
Severe acute respiratory syndrome–related coronavirus
Virus:
Severe acute respiratory syndrome coronavirus 2
Notable variants
Synonyms
  • 2019-nCoV

SARS‑CoV‑2 is a virus of the species severe acute respiratory syndrome–related coronavirus (SARSr-CoV), related to the SARS-CoV-1 virus that caused the 2002–2004 SARS outbreak.[2][17] Despite its close relation to SARS-CoV-1, its closest known relatives, with which it forms a sister group, are the derived SARS viruses BANAL-52 and RaTG13.[18] The virus is of zoonotic origin and has close genetic similarity to bat coronaviruses, suggesting it emerged from a bat-borne virus.[19] Research is ongoing as to whether SARS‑CoV‑2 came directly from bats or indirectly through any intermediate hosts.[20] The virus shows little genetic diversity, indicating that the spillover event introducing SARS‑CoV‑2 to humans is likely to have occurred in late 2019.[21]

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 were immune and no preventive measures were taken.[22] However, some subsequent variants have become more infectious.[23] The virus is airborne and primarily spreads between people through close contact and via aerosols and respiratory droplets that are exhaled when talking, breathing, or otherwise exhaling, as well as those produced from coughs and sneezes.[24][25] It enters human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane protein that regulates the renin–angiotensin system.[26][27]

Terminology

 
Sign with provisional name "2019-nCoV"

During the initial outbreak in Wuhan, China, various names were used for the virus; some names used by different sources included "the coronavirus" or "Wuhan coronavirus".[28][29] In January 2020, the World Health Organization (WHO) recommended "2019 novel coronavirus" (2019-nCoV)[5][30] as the provisional name for the virus. This was in accordance with WHO's 2015 guidance[31] against using geographical locations, animal species, or groups of people in disease and virus names.[32][33]

On 11 February 2020, the International Committee on Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS‑CoV‑2).[34] To avoid confusion with the disease SARS, the WHO sometimes refers to SARS‑CoV‑2 as "the COVID-19 virus" in public health communications[35][36] 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 as xenophobic by many journalists and academics.[37][38][39]

Infection and transmission

Main article: Transmission of COVID-19

Human-to-human transmission of SARS‑CoV‑2 was confirmed on 20 January 2020 during the COVID-19 pandemic.[16][40][41][42] Transmission was initially assumed to occur primarily via respiratory droplets from coughs and sneezes within a range of about 1.8 metres (6 ft).[43][44] Laser light scattering experiments suggest that speaking is an additional mode of transmission[45][46] and a far-reaching[47] one, indoors, with little air flow.[48][49] Other studies have suggested that the virus may be airborne as well, with aerosols potentially being able to transmit the virus.[50][51][52] During human-to-human transmission, between 200 and 800 infectious SARS‑CoV‑2 virions are thought to initiate a new infection.[53][54][55] 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.[56] Indirect contact via contaminated surfaces is another possible cause of infection.[57] Preliminary research indicates that the virus may remain viable on plastic (polypropylene) and stainless 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 its lipid bilayer.[58][59] Viral RNA has also been found in stool samples and semen from infected individuals.[60][61]

The degree to which the virus is infectious during the incubation period is uncertain, but research has indicated that the pharynx reaches peak viral load approximately four days after infection[62][63] or in the first week of symptoms and declines thereafter.[64] The duration of SARS-CoV-2 RNA shedding is generally between 3 and 46 days after symptom onset.[65]

A study by a team of researchers from the University of North Carolina found that the nasal cavity is seemingly the dominant initial site of infection, with subsequent aspiration-mediated virus-seeding into the lungs in SARS‑CoV‑2 pathogenesis.[66] 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.[66]

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.[67][68][69] Some institutions have advised that those infected with SARS‑CoV‑2 restrict their contact with animals.[70][71]

Asymptomatic and presymptomatic transmission

On 1 February 2020, the World Health Organization (WHO) indicated that "transmission from asymptomatic cases is likely not a major driver of transmission".[72] One meta-analysis found that 17% of infections are asymptomatic, and asymptomatic individuals were 42% less likely to transmit the virus.[73]

However, an epidemiological model of the beginning of the outbreak in China suggested that "pre-symptomatic shedding may be typical among documented infections" and that subclinical infections may have been the source of a majority of infections.[74] That may explain how out of 217 on board a cruise liner that docked at Montevideo, only 24 of 128 who tested positive for viral RNA showed symptoms.[75] 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 the index case".[54] The authors later published a correction that showed that shedding began earlier than first estimated, four to five days before symptoms appear.[76]

Reinfection

There is uncertainty about reinfection and long-term immunity.[77] It is not known how common reinfection is, but reports have indicated that it is occurring with variable severity.[77]

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 different clades.[78] The findings had the implications that herd immunity may not eliminate the virus if reinfection is not an uncommon occurrence and that vaccines may not be able to provide lifelong protection against the virus.[78]

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.[79] The man's second infection was symptomatically more severe than the first infection, but the mechanisms that could account for this are not known.[79]

Reservoir and origin

Further information: Investigations into the origin of COVID-19
 
Transmission of SARS-CoV-1 and SARS‑CoV‑2 from mammals as biological carriers to humans

No natural reservoir for SARS-CoV-2 has been identified.[80] Prior to the emergence of SARS-CoV-2 as a pathogen infecting humans, there had been two previous zoonosis-based coronavirus epidemics, those caused by SARS-CoV-1 and MERS-CoV.[19]

The first known infections from SARS‑CoV‑2 were discovered in Wuhan, China.[81] The original source of viral transmission to humans remains unclear, as does whether the virus became pathogenic before or after the spillover event.[9][21][82] Because many of the early infectees were workers at the Huanan Seafood Market,[83][84] it has been suggested that the virus might have originated from the market.[9][85] However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid expansion of the infections.[21][86] 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.[87] 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.[88]

For a virus recently acquired through a cross-species transmission, rapid evolution is expected.[89] The mutation rate estimated from early cases of SARS-CoV-2 was of 6.54×10−4 per site per year.[87] Coronaviruses in general have high genetic plasticity,[90] but SARS-CoV-2's viral evolution is slowed by the RNA proofreading capability of its replication machinery.[91] For comparison, the viral mutation rate in vivo of SARS-CoV-2 has been found to be lower than that of influenza.[92]

Research into the natural reservoir of the virus that caused the 2002–2004 SARS outbreak has resulted in the discovery of many SARS-like bat coronaviruses, most originating in horseshoe bats. The closest match by far, published in Nature (journal) in February 2022, were viruses BANAL-52 (96.8% resemblance to SARS‑CoV‑2), BANAL-103 and BANAL-236, collected in three different species of bats in Feuang, Laos.[93][94][95] An earlier source published in February 2020 identified the virus RaTG13, collected in bats in Mojiang, Yunnan, China to be the closest to SARS‑CoV‑2, with 96.1% resemblance.[81][96] None of the above are its direct ancestor.[97]

 
Samples taken from Rhinolophus sinicus, a species of horseshoe bats, show an 80% resemblance to SARS‑CoV‑2.

Bats are considered the most likely natural reservoir of SARS‑CoV‑2.[87][98] Differences between the bat coronavirus and SARS‑CoV‑2 suggest that humans may have been infected via an intermediate host;[85] although the source of introduction into humans remains unknown.[99][80]

Although the role of pangolins 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[100][101]), subsequent studies have not substantiated their contribution to the spillover.[87] Evidence against this hypothesis includes the fact that pangolin virus samples are too distant to SARS-CoV-2: isolates obtained from pangolins seized in Guangdong 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[102]). In addition, despite similarities in a few critical amino acids,[103] pangolin virus samples exhibit poor binding to the human ACE2 receptor.[104]

Phylogenetics and taxonomy

Genomic information
 
Genomic organisation of isolate Wuhan-Hu-1, the earliest sequenced sample of SARS-CoV-2
NCBI genome ID86693
Genome size29,903 bases
Year of completion2020
Genome browser (UCSC)

SARS‑CoV‑2 belongs to the broad family of viruses known as coronaviruses.[29] It is a positive-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.[105] Human coronaviruses are capable of causing illnesses ranging from the common cold to more severe diseases such as Middle East respiratory syndrome (MERS, fatality rate ~34%). SARS-CoV-2 is the seventh known coronavirus to infect people, after 229E, NL63, OC43, HKU1, MERS-CoV, and the original SARS-CoV.[106]

Like the SARS-related coronavirus implicated in the 2003 SARS outbreak, SARS‑CoV‑2 is a member of the subgenus Sarbecovirus (beta-CoV lineage B).[107][108] Coronaviruses undergo frequent recombination.[109] 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.[110] The SARS-CoV-2 RNA sequence is approximately 30,000 bases in length,[111] relatively long for a coronavirus—which in turn carry the largest genomes among all RNA families.[112] Its genome consists nearly entirely of protein-coding sequences, a trait shared with other coronaviruses.[109]

 
Transmission electron micrograph of SARS‑CoV‑2 virions (red) isolated from a patient during the COVID-19 pandemic

A distinguishing feature of SARS‑CoV‑2 is its incorporation of a polybasic site cleaved by furin,[103][113] which appears to be an important element enhancing its virulence.[114] 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.[115] The furin protease recognizes the canonical peptide sequence RX[R/K] R↓X where the cleavage site is indicated by a down arrow and X is any amino acid.[116][117] In SARS-CoV-2 the recognition site is formed by the incorporated 12 codon nucleotide sequence CCT CGG CGG GCA which corresponds to the amino acid sequence P RR A.[118] This sequence is upstream of an arginine and serine which forms the S1/S2 cleavage site (P RR A R↓S) of the spike protein.[119] Although such sites are a common naturally-occurring feature of other viruses within the Subfamily Orthocoronavirinae,[118] it appears in few other viruses from the Beta-CoV genus,[120] and it is unique among members of its subgenus for such a site.[103] The furin cleavage site PRRAR↓ is highly similar to that of the feline coronavirus, an alphacoronavirus 1 strain.[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 sequenced genomes, it is possible to reconstruct a phylogenetic 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 the Chinese Center for Disease Control and Prevention (CCDC) and other institutions;[111][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 a common 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, 3,422 SARS‑CoV‑2 genomes, belonging to 19 strains, sampled on all continents except Antarctica were publicly available.[126]

On 11 February 2020, the International Committee on Taxonomy of Viruses announced that according to existing rules that compute hierarchical relationships among coronaviruses based on five conserved sequences of nucleic acids, the differences between what was then called 2019-nCoV and the virus from the 2003 SARS outbreak were insufficient to make them separate viral species. Therefore, they identified 2019-nCoV as a virus of Severe acute respiratory syndrome–related coronavirus.[127]

In July 2020, scientists reported that a more infectious SARS‑CoV‑2 variant with spike protein variant G614 has replaced D614 as the dominant form in the pandemic.[128][129]

Coronavirus genomes and subgenomes encode six open reading frames (ORFs).[130] In October 2020, researchers discovered a possible overlapping gene named ORF3d, in the SARS‑CoV‑2 genome. It is unknown if the protein produced by ORF3d has any function, but it provokes a strong immune response. ORF3d has been identified before, in a variant of coronavirus that infects pangolins.[131][132]

Phylogenetic tree

A phylogenetic tree based on whole-genome sequences of SARS-CoV-2 and related coronaviruses is:[133][134]

SARS‑CoV‑2 related coronavirus

(Bat) Rc-o319, 81% to SARS-CoV-2, Rhinolophus cornutus, Iwate, Japan[135]

Bat SL-ZXC21, 88% to SARS-CoV-2, Rhinolophus pusillus, Zhoushan, Zhejiang[136]

Bat SL-ZC45, 88% to SARS-CoV-2, Rhinolophus pusillus, Zhoushan, Zhejiang[136]

Pangolin SARSr-CoV-GX, 85.3% to SARS-CoV-2, Manis javanica, smuggled from Southeast Asia[137]

Pangolin SARSr-CoV-GD, 90.1% to SARS-CoV-2, Manis javanica, smuggled from Southeast Asia[138]

Bat RshSTT182, 92.6% to SARS-CoV-2, Rhinolophus shameli, Steung Treng, Cambodia[139]

Bat RshSTT200, 92.6% to SARS-CoV-2, Rhinolophus shameli, Steung Treng, Cambodia[139]

(Bat) RacCS203, 91.5% to SARS-CoV-2, Rhinolophus acuminatus, Chachoengsao, Thailand[134]

(Bat) RmYN02, 93.3% to SARS-CoV-2, Rhinolophus malayanus, Mengla, Yunnan[140]

(Bat) RpYN06, 94.4% to SARS-CoV-2, Rhinolophus pusillus, Xishuangbanna, Yunnan[133]

(Bat) RaTG13, 96.1% to SARS-CoV-2, Rhinolophus affinis, Mojiang, Yunnan[141]

(Bat) BANAL-52, 96.8% to SARS-CoV-2, Rhinolophus malayanus, Vientiane, Laos[142]

SARS-CoV-2

SARS-CoV-1, 79% to SARS-CoV-2


Variants

Main article: Variants of SARS-CoV-2
 
False-colour transmission 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 larger clades.[143] Several different clade nomenclatures have been proposed. Nextstrain divides the variants into five clades (19A, 19B, 20A, 20B, and 20C), while GISAID divides them into seven (L, O, V, S, G, GH, and GR).[144]

Several notable variants of SARS-CoV-2 emerged in late 2020. The World Health Organization has currently declared five variants of concern, which are as follows:[145]

  • Alpha: Lineage B.1.1.7 emerged in the United Kingdom in September 2020, with evidence of increased transmissibility and virulence. Notable mutations include N501Y and P681H.
  • Beta: Lineage B.1.351 emerged in South 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 include K417N, E484K and N501Y.
  • Gamma: Lineage P.1 emerged in Brazil 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 in India in October 2020. There is also evidence of increased transmissibility and changes to antigenicity.
  • Omicron: Lineage B.1.1.529 emerged in Botswana in November 2021.

Other notable variants include 6 other WHO-designated variants under investigation and Cluster 5, which emerged among mink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct.[146]

Virology

Virus structure

 
Structure of a SARSr-CoV virion

Each SARS-CoV-2 virion is 60–140 nanometres (2.4×10−6–5.5×10−6 in) in diameter;[106][84] 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 the viral envelope.[148] Coronavirus S proteins are glycoproteins and also type I membrane proteins (membranes containing a single transmembrane domain oriented on the extracellular side).[115] They are divided into two functional parts (S1 and S2).[105] In SARS-CoV-2, the spike protein, which has been imaged at the atomic level using cryogenic electron microscopy,[149][150] is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell;[148] specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion.[151]

 
SARS‑CoV‑2 spike homotrimer with one protein subunit highlighted. The ACE2 binding domain is magenta.

Genome

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, the GISAID 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.[105] Its genome has a bias against cytosine (C) and guanine (G) nucleotides, like other coronaviruses.[154] The genome has the highest composition of U (32.2%), followed by A (29.9%), and a similar composition of G (19.6%) and C (18.3%).[155] The nucleotide bias arises from the mutation of guanines and cytosines to adenosines and uracils, respectively.[156] The mutation of CG dinucleotides is thought to arise to avoid the zinc finger antiviral protein related defense mechanism of cells,[157] and to lower the energy to unbind the genome during replication and translation (adenosine and uracil base pair via two hydrogen bonds, cytosine and guanine via three).[156] The depletion of CG dinucleotides in its genome has led the virus to have a noticeable codon usage bias. For instance, arginine's six different codons have a relative 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 receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism of cell entry.[160] By 22 January 2020, a group in China working with the full virus genome and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS‑CoV‑2.[81][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 use basigin to assist in cell entry.[165]

Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS‑CoV‑2.[26] The host protein neuropilin 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 a fusion peptide in the S2 subunit, and the host receptor ACE2.[151] After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it.[151] The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells.[167]

SARS‑CoV‑2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response.[148] Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).[168]

 
 
Digitally colourised scanning electron micrographs of SARS-CoV-2 virions (yellow) emerging from human cells cultured in a laboratory

Treatment and drug development

Very few drugs are known to effectively inhibit SARS‑CoV‑2. Masitinib is a clinically safe drug and was recently found to inhibit its main protease, 3CLpro and showed >200-fold reduction in viral titers in the lungs and nose in mice. However, it is not approved for the treatment of COVID-19 in humans as of August 2021.[169][needs update] In December 2021, the United States granted emergency use authorization to Nirmatrelvir/ritonavir for the treatment of the virus;[170] the European Union, United Kingdom, and Canada followed suit with full authorization soon after.[171][172][173] One study found that Nirmatrelvir/ritonavir reduced the risk of hospitalization and death by 88%.[174]

COVID Moonshot is an international collaborative open-science project started in March 2020 with the goal of developing an un-patented oral antiviral drug for treatment of SARS-CoV-2.[175]

Epidemiology

Main article: COVID-19 pandemic

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.[87]

A meta-analysis from November 2020 estimated the basic reproduction number ( ) of the virus to be between 2.39 and 3.44.[22] 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 are immune and no preventive measures are taken. The reproduction number may be higher in densely populated conditions such as those found on cruise 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]

Reproductive value R0 of SARS-CoV-2 variants
Variant R0 Source
Reference/ancestral strain ~2.8 [178]
Alpha (B.1.1.7) (40-90% higher than previous variants) [179]
Delta (B.1.617.2) ~5 (3-8) [180]

There have been about 96,000 confirmed cases of infection in mainland China.[181] While the proportion of infections that result in confirmed 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 from COVID-19 worldwide had occurred in Hubei province, where Wuhan is located.[184][185] As of 10 March 2023, the percentage had decreased to 0.047%.[181]

As of 10 March 2023, there have been 676,609,955 total confirmed cases of SARS‑CoV‑2 infection in the ongoing pandemic.[181] The total number of deaths attributed to the virus is 6,881,955.[181]

See also

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Further reading

  • Bar-On YM, Flamholz A, Phillips R, Milo R (April 2020). "SARS-CoV-2 (COVID-19) by the numbers". eLife. 9. arXiv:2003.12886. Bibcode:2020arXiv200312886B. doi:10.7554/eLife.57309. PMC 7224694. PMID 32228860.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  • Brüssow H (May 2020). "The Novel Coronavirus - A Snapshot of Current Knowledge". Microbial Biotechnology. 13 (3): 607–612. doi:10.1111/1751-7915.13557. PMC 7111068. PMID 32144890.
  • Cascella M, Rajnik M, Aleem A, Dulebohn S, Di Napoli R (January 2020). "Features, Evaluation and Treatment Coronavirus (COVID-19)". StatPearls. PMID 32150360. from the original on 6 April 2020. Retrieved 4 April 2020.
  • Laboratory testing for coronavirus disease 2019 (COVID-19) in suspected human cases (Report). World Health Organization. 2 March 2020. hdl:10665/331329.
  • Zoumpourlis V, Goulielmaki M, Rizos E, Baliou S, Spandidos DA (October 2020). "[Comment] The COVID‑19 pandemic as a scientific and social challenge in the 21st century". Molecular Medicine Reports (Review). 22 (4): 3035–3048. doi:10.3892/mmr.2020.11393. PMC 7453598. PMID 32945405.

External links

 
Scholia has a profile for SARS-CoV-2 (Q82069695).

December 01, 2023
sars, this, article, about, virus, that, causes, covid, virus, that, causes, sars, sars, severe, acute, respiratory, syndrome, coronavirus, sars, strain, coronavirus, that, causes, covid, respiratory, illness, responsible, covid, pandemic, virus, previously, p. This article is about the virus that causes COVID 19 For the virus that causes SARS see SARS CoV 1 Severe acute respiratory syndrome coronavirus 2 SARS CoV 2 2 is a strain of coronavirus that causes COVID 19 the respiratory illness responsible for the COVID 19 pandemic 3 The virus previously had the provisional name 2019 novel coronavirus 2019 nCoV 4 5 6 7 and has also been called human coronavirus 2019 HCoV 19 or hCoV 19 8 9 10 11 First identified in the city of Wuhan Hubei China the World Health Organization designated the outbreak a public health emergency of international concern from January 30 2020 to May 5 2023 12 13 14 SARS CoV 2 is a positive sense single stranded RNA virus 15 that is contagious in humans 16 Severe acute respiratory syndrome coronavirus 2Colourised transmission electron micrograph of SARS CoV 2 virions with visible coronaeModel of the external structure of the SARS CoV 2 virion 1 Blue envelope Turquoise spike glycoprotein S Pink envelope proteins E Green membrane proteins M Orange glycanVirus classification unranked VirusRealm RiboviriaKingdom OrthornaviraePhylum PisuviricotaClass PisoniviricetesOrder NidoviralesFamily CoronaviridaeGenus BetacoronavirusSubgenus SarbecovirusSpecies Severe acute respiratory syndrome related coronavirusVirus Severe acute respiratory syndrome coronavirus 2Notable variantsAlpha B 1 1 7 Beta B 1 351 Gamma P 1 Delta B 1 617 2 Omicron B 1 1 529 Full listSynonyms2019 nCoVSARS CoV 2 is a virus of the species severe acute respiratory syndrome related coronavirus SARSr CoV related to the SARS CoV 1 virus that caused the 2002 2004 SARS outbreak 2 17 Despite its close relation to SARS CoV 1 its closest known relatives with which it forms a sister group are the derived SARS viruses BANAL 52 and RaTG13 18 The virus is of zoonotic origin and has close genetic similarity to bat coronaviruses suggesting it emerged from a bat borne virus 19 Research is ongoing as to whether SARS CoV 2 came directly from bats or indirectly through any intermediate hosts 20 The virus shows little genetic diversity indicating that the spillover event introducing SARS CoV 2 to humans is likely to have occurred in late 2019 21 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 were immune and no preventive measures were taken 22 However some subsequent variants have become more infectious 23 The virus is airborne and primarily spreads between people through close contact and via aerosols and respiratory droplets that are exhaled when talking breathing or otherwise exhaling as well as those produced from coughs and sneezes 24 25 It enters human cells by binding to angiotensin converting enzyme 2 ACE2 a membrane protein that regulates the renin angiotensin system 26 27 Contents 1 Terminology 2 Infection and transmission 2 1 Asymptomatic and presymptomatic transmission 2 2 Reinfection 3 Reservoir and origin 4 Phylogenetics and taxonomy 4 1 Phylogenetic tree 4 1 1 Variants 5 Virology 5 1 Virus structure 5 2 Genome 5 3 Replication cycle 6 Treatment and drug development 7 Epidemiology 8 See also 9 References 10 Further reading 11 External linksTerminology nbsp Sign with provisional name 2019 nCoV During the initial outbreak in Wuhan China various names were used for the virus some names used by different sources included the coronavirus or Wuhan coronavirus 28 29 In January 2020 the World Health Organization WHO recommended 2019 novel coronavirus 2019 nCoV 5 30 as the provisional name for the virus This was in accordance with WHO s 2015 guidance 31 against using geographical locations animal species or groups of people in disease and virus names 32 33 On 11 February 2020 the International Committee on Taxonomy of Viruses adopted the official name severe acute respiratory syndrome coronavirus 2 SARS CoV 2 34 To avoid confusion with the disease SARS the WHO sometimes refers to SARS CoV 2 as the COVID 19 virus in public health communications 35 36 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 as xenophobic by many journalists and academics 37 38 39 Infection and transmissionMain article Transmission of COVID 19 This section has multiple issues Please help improve it or discuss these issues on the talk page Learn how and when to remove these template messages This section needs to be updated Please help update this article to reflect recent events or newly available information August 2021 This section needs additional medical references for verification Please help improve this article by adding appropriate references Unsourced or poorly sourced material may be challenged and removed Find sources SARS CoV 2 news newspapers books scholar JSTOR August 2021 Learn how and when to remove this template message Human to human transmission of SARS CoV 2 was confirmed on 20 January 2020 during the COVID 19 pandemic 16 40 41 42 Transmission was initially assumed to occur primarily via respiratory droplets from coughs and sneezes within a range of about 1 8 metres 6 ft 43 44 Laser light scattering experiments suggest that speaking is an additional mode of transmission 45 46 and a far reaching 47 one indoors with little air flow 48 49 Other studies have suggested that the virus may be airborne as well with aerosols potentially being able to transmit the virus 50 51 52 During human to human transmission between 200 and 800 infectious SARS CoV 2 virions are thought to initiate a new infection 53 54 55 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 56 Indirect contact via contaminated surfaces is another possible cause of infection 57 Preliminary research indicates that the virus may remain viable on plastic polypropylene and stainless 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 its lipid bilayer 58 59 Viral RNA has also been found in stool samples and semen from infected individuals 60 61 The degree to which the virus is infectious during the incubation period is uncertain but research has indicated that the pharynx reaches peak viral load approximately four days after infection 62 63 or in the first week of symptoms and declines thereafter 64 The duration of SARS CoV 2 RNA shedding is generally between 3 and 46 days after symptom onset 65 A study by a team of researchers from the University of North Carolina found that the nasal cavity is seemingly the dominant initial site of infection with subsequent aspiration mediated virus seeding into the lungs in SARS CoV 2 pathogenesis 66 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 66 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 67 68 69 Some institutions have advised that those infected with SARS CoV 2 restrict their contact with animals 70 71 Asymptomatic and presymptomatic transmission On 1 February 2020 the World Health Organization WHO indicated that transmission from asymptomatic cases is likely not a major driver of transmission 72 One meta analysis found that 17 of infections are asymptomatic and asymptomatic individuals were 42 less likely to transmit the virus 73 However an epidemiological model of the beginning of the outbreak in China suggested that pre symptomatic shedding may be typical among documented infections and that subclinical infections may have been the source of a majority of infections 74 That may explain how out of 217 on board a cruise liner that docked at Montevideo only 24 of 128 who tested positive for viral RNA showed symptoms 75 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 the index case 54 The authors later published a correction that showed that shedding began earlier than first estimated four to five days before symptoms appear 76 Reinfection There is uncertainty about reinfection and long term immunity 77 It is not known how common reinfection is but reports have indicated that it is occurring with variable severity 77 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 different clades 78 The findings had the implications that herd immunity may not eliminate the virus if reinfection is not an uncommon occurrence and that vaccines may not be able to provide lifelong protection against the virus 78 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 79 The man s second infection was symptomatically more severe than the first infection but the mechanisms that could account for this are not known 79 Reservoir and originFurther information Investigations into the origin of COVID 19 nbsp Transmission of SARS CoV 1 and SARS CoV 2 from mammals as biological carriers to humansNo natural reservoir for SARS CoV 2 has been identified 80 Prior to the emergence of SARS CoV 2 as a pathogen infecting humans there had been two previous zoonosis based coronavirus epidemics those caused by SARS CoV 1 and MERS CoV 19 The first known infections from SARS CoV 2 were discovered in Wuhan China 81 The original source of viral transmission to humans remains unclear as does whether the virus became pathogenic before or after the spillover event 9 21 82 Because many of the early infectees were workers at the Huanan Seafood Market 83 84 it has been suggested that the virus might have originated from the market 9 85 However other research indicates that visitors may have introduced the virus to the market which then facilitated rapid expansion of the infections 21 86 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 87 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 88 For a virus recently acquired through a cross species transmission rapid evolution is expected 89 The mutation rate estimated from early cases of SARS CoV 2 was of 6 54 10 4 per site per year 87 Coronaviruses in general have high genetic plasticity 90 but SARS CoV 2 s viral evolution is slowed by the RNA proofreading capability of its replication machinery 91 For comparison the viral mutation rate in vivo of SARS CoV 2 has been found to be lower than that of influenza 92 Research into the natural reservoir of the virus that caused the 2002 2004 SARS outbreak has resulted in the discovery of many SARS like bat coronaviruses most originating in horseshoe bats The closest match by far published in Nature journal in February 2022 were viruses BANAL 52 96 8 resemblance to SARS CoV 2 BANAL 103 and BANAL 236 collected in three different species of bats in Feuang Laos 93 94 95 An earlier source published in February 2020 identified the virus RaTG13 collected in bats in Mojiang Yunnan China to be the closest to SARS CoV 2 with 96 1 resemblance 81 96 None of the above are its direct ancestor 97 nbsp Samples taken from Rhinolophus sinicus a species of horseshoe bats show an 80 resemblance to SARS CoV 2 Bats are considered the most likely natural reservoir of SARS CoV 2 87 98 Differences between the bat coronavirus and SARS CoV 2 suggest that humans may have been infected via an intermediate host 85 although the source of introduction into humans remains unknown 99 80 Although the role of pangolins 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 100 101 subsequent studies have not substantiated their contribution to the spillover 87 Evidence against this hypothesis includes the fact that pangolin virus samples are too distant to SARS CoV 2 isolates obtained from pangolins seized in Guangdong 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 102 In addition despite similarities in a few critical amino acids 103 pangolin virus samples exhibit poor binding to the human ACE2 receptor 104 Phylogenetics and taxonomyGenomic information nbsp Genomic organisation of isolate Wuhan Hu 1 the earliest sequenced sample of SARS CoV 2NCBI genome ID86693Genome size29 903 basesYear of completion2020Genome browser UCSC SARS CoV 2 belongs to the broad family of viruses known as coronaviruses 29 It is a positive 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 105 Human coronaviruses are capable of causing illnesses ranging from the common cold to more severe diseases such as Middle East respiratory syndrome MERS fatality rate 34 SARS CoV 2 is the seventh known coronavirus to infect people after 229E NL63 OC43 HKU1 MERS CoV and the original SARS CoV 106 Like the SARS related coronavirus implicated in the 2003 SARS outbreak SARS CoV 2 is a member of the subgenus Sarbecovirus beta CoV lineage B 107 108 Coronaviruses undergo frequent recombination 109 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 110 The SARS CoV 2 RNA sequence is approximately 30 000 bases in length 111 relatively long for a coronavirus which in turn carry the largest genomes among all RNA families 112 Its genome consists nearly entirely of protein coding sequences a trait shared with other coronaviruses 109 nbsp Transmission electron micrograph of SARS CoV 2 virions red isolated from a patient during the COVID 19 pandemicA distinguishing feature of SARS CoV 2 is its incorporation of a polybasic site cleaved by furin 103 113 which appears to be an important element enhancing its virulence 114 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 115 The furin protease recognizes the canonical peptide sequence RX R K R X where the cleavage site is indicated by a down arrow and X is any amino acid 116 117 In SARS CoV 2 the recognition site is formed by the incorporated 12 codon nucleotide sequence CCT CGG CGG GCA which corresponds to the amino acid sequence P RR A 118 This sequence is upstream of an arginine and serine which forms the S1 S2 cleavage site P RR A R S of the spike protein 119 Although such sites are a common naturally occurring feature of other viruses within the Subfamily Orthocoronavirinae 118 it appears in few other viruses from the Beta CoV genus 120 and it is unique among members of its subgenus for such a site 103 The furin cleavage site PRRAR is highly similar to that of the feline coronavirus an alphacoronavirus 1 strain 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 sequenced genomes it is possible to reconstruct a phylogenetic 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 the Chinese Center for Disease Control and Prevention CCDC and other institutions 111 123 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 a common 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 On 11 February 2020 the International Committee on Taxonomy of Viruses announced that according to existing rules that compute hierarchical relationships among coronaviruses based on five conserved sequences of nucleic acids the differences between what was then called 2019 nCoV and the virus from the 2003 SARS outbreak were insufficient to make them separate viral species Therefore they identified 2019 nCoV as a virus of Severe acute respiratory syndrome related coronavirus 127 In July 2020 scientists reported that a more infectious SARS CoV 2 variant with spike protein variant G614 has replaced D614 as the dominant form in the pandemic 128 129 Coronavirus genomes and subgenomes encode six open reading frames ORFs 130 In October 2020 researchers discovered a possible overlapping gene named ORF3d in the SARS CoV 2 genome It is unknown if the protein produced by ORF3d has any function but it provokes a strong immune response ORF3d has been identified before in a variant of coronavirus that infects pangolins 131 132 Phylogenetic tree A phylogenetic tree based on whole genome sequences of SARS CoV 2 and related coronaviruses is 133 134 SARS CoV 2 related coronavirus Bat Rc o319 81 to SARS CoV 2 Rhinolophus cornutus Iwate Japan 135 Bat SL ZXC21 88 to SARS CoV 2 Rhinolophus pusillus Zhoushan Zhejiang 136 Bat SL ZC45 88 to SARS CoV 2 Rhinolophus pusillus Zhoushan Zhejiang 136 Pangolin SARSr CoV GX 85 3 to SARS CoV 2 Manis javanica smuggled from Southeast Asia 137 Pangolin SARSr CoV GD 90 1 to SARS CoV 2 Manis javanica smuggled from Southeast Asia 138 Bat RshSTT182 92 6 to SARS CoV 2 Rhinolophus shameli Steung Treng Cambodia 139 Bat RshSTT200 92 6 to SARS CoV 2 Rhinolophus shameli Steung Treng Cambodia 139 Bat RacCS203 91 5 to SARS CoV 2 Rhinolophus acuminatus Chachoengsao Thailand 134 Bat RmYN02 93 3 to SARS CoV 2 Rhinolophus malayanus Mengla Yunnan 140 Bat RpYN06 94 4 to SARS CoV 2 Rhinolophus pusillus Xishuangbanna Yunnan 133 Bat RaTG13 96 1 to SARS CoV 2 Rhinolophus affinis Mojiang Yunnan 141 Bat BANAL 52 96 8 to SARS CoV 2 Rhinolophus malayanus Vientiane Laos 142 SARS CoV 2SARS CoV 1 79 to SARS CoV 2 Variants Main article Variants of SARS CoV 2 This section needs to be updated Please help update this article to reflect recent events or newly available information April 2023 nbsp False colour transmission 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 larger clades 143 Several different clade nomenclatures have been proposed Nextstrain divides the variants into five clades 19A 19B 20A 20B and 20C while GISAID divides them into seven L O V S G GH and GR 144 Several notable variants of SARS CoV 2 emerged in late 2020 The World Health Organization has currently declared five variants of concern which are as follows 145 Alpha Lineage B 1 1 7 emerged in the United Kingdom in September 2020 with evidence of increased transmissibility and virulence Notable mutations include N501Y and P681H An E484K mutation in some lineage B 1 1 7 virions has been noted and is also tracked by various public health agencies Beta Lineage B 1 351 emerged in South 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 include K417N E484K and N501Y Gamma Lineage P 1 emerged in Brazil 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 in India in October 2020 There is also evidence of increased transmissibility and changes to antigenicity Omicron Lineage B 1 1 529 emerged in Botswana in November 2021 Other notable variants include 6 other WHO designated variants under investigation and Cluster 5 which emerged among mink in Denmark and resulted in a mink euthanasia campaign rendering it virtually extinct 146 VirologyVirus structure nbsp Structure of a SARSr CoV virionEach SARS CoV 2 virion is 60 140 nanometres 2 4 10 6 5 5 10 6 in in diameter 106 84 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 the viral envelope 148 Coronavirus S proteins are glycoproteins and also type I membrane proteins membranes containing a single transmembrane domain oriented on the extracellular side 115 They are divided into two functional parts S1 and S2 105 In SARS CoV 2 the spike protein which has been imaged at the atomic level using cryogenic electron microscopy 149 150 is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell 148 specifically its S1 subunit catalyzes attachment the S2 subunit fusion 151 nbsp SARS CoV 2 spike homotrimer with one protein subunit highlighted The ACE2 binding domain is magenta Genome 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 the GISAID 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 105 Its genome has a bias against cytosine C and guanine G nucleotides like other coronaviruses 154 The genome has the highest composition of U 32 2 followed by A 29 9 and a similar composition of G 19 6 and C 18 3 155 The nucleotide bias arises from the mutation of guanines and cytosines to adenosines and uracils respectively 156 The mutation of CG dinucleotides is thought to arise to avoid the zinc finger antiviral protein related defense mechanism of cells 157 and to lower the energy to unbind the genome during replication and translation adenosine and uracil base pair via two hydrogen bonds cytosine and guanine via three 156 The depletion of CG dinucleotides in its genome has led the virus to have a noticeable codon usage bias For instance arginine s six different codons have a relative 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 receptor angiotensin converting enzyme 2 ACE2 on human cells to use them as a mechanism of cell entry 160 By 22 January 2020 a group in China working with the full virus genome and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS CoV 2 81 161 162 163 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 use basigin to assist in cell entry 165 Initial spike protein priming by transmembrane protease serine 2 TMPRSS2 is essential for entry of SARS CoV 2 26 The host protein neuropilin 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 a fusion peptide in the S2 subunit and the host receptor ACE2 151 After fusion an endosome forms around the virion separating it from the rest of the host cell The virion escapes when the pH of the endosome drops or when cathepsin a host cysteine protease cleaves it 151 The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus which infect more cells 167 SARS CoV 2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response 148 Whether they include downregulation of ACE2 as seen in similar coronaviruses remains under investigation as of May 2020 168 nbsp nbsp Digitally colourised scanning electron micrographs of SARS CoV 2 virions yellow emerging from human cells cultured in a laboratoryTreatment and drug developmentVery few drugs are known to effectively inhibit SARS CoV 2 Masitinib is a clinically safe drug and was recently found to inhibit its main protease 3CLpro and showed gt 200 fold reduction in viral titers in the lungs and nose in mice However it is not approved for the treatment of COVID 19 in humans as of August 2021 169 needs update In December 2021 the United States granted emergency use authorization to Nirmatrelvir ritonavir for the treatment of the virus 170 the European Union United Kingdom and Canada followed suit with full authorization soon after 171 172 173 One study found that Nirmatrelvir ritonavir reduced the risk of hospitalization and death by 88 174 COVID Moonshot is an international collaborative open science project started in March 2020 with the goal of developing an un patented oral antiviral drug for treatment of SARS CoV 2 175 EpidemiologyMain article COVID 19 pandemic 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 87 A meta analysis from November 2020 estimated the basic reproduction number R 0 displaystyle R 0 nbsp of the virus to be between 2 39 and 3 44 22 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 are immune and no preventive measures are taken The reproduction number may be higher in densely populated conditions such as those found on cruise 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 Reproductive value R0 of SARS CoV 2 variants 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century Molecular Medicine Reports Review 22 4 3035 3048 doi 10 3892 mmr 2020 11393 PMC 7453598 PMID 32945405 External links nbsp Scholia has a profile for SARS CoV 2 Q82069695 Coronavirus Disease 2019 COVID 19 Centers for Disease Control and Prevention CDC 11 February 2020 Coronavirus disease COVID 19 Pandemic World Health Organization WHO SARS CoV 2 Severe acute respiratory syndrome coronavirus 2 Sequences National Center for Biotechnology Information NCBI COVID 19 Resource Centre The Lancet Coronavirus Covid 19 The New England Journal of Medicine Covid 19 Novel Coronavirus Outbreak Wiley Archived from the original on 24 September 2020 Retrieved 13 February 2020 SARS CoV 2 Virus Pathogen Database and Analysis Resource SARS CoV 2 related protein structures Protein Data Bank Portals nbsp COVID 19 nbsp Medicine nbsp VirusesSARS CoV 2 at Wikipedia s sister projects nbsp Definitions from Wiktionary nbsp Media from Commons nbsp News from Wikinews nbsp Quotations from Wikiquote nbsp Texts from Wikisource nbsp Textbooks from Wikibooks nbsp Resources from Wikiversity nbsp Travel guides from Wikivoyage nbsp Taxa from Wikispecies nbsp Data from Wikidata Retrieved from https en wikipedia org w index php title SARS CoV 2 amp oldid 1187112430, wikipedia, wiki, book, books, library,

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