Biology:Severe acute respiratory syndrome coronavirus 2

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Short description: Virus that causes COVID-19


Severe acute respiratory syndrome coronavirus 2
Electron micrograph of SARS-CoV-2 virions with visible coronae
Colourised transmission electron micrograph of SARS-CoV-2 virions with visible coronae
Illustration of a SARS-CoV-2 virion
Atomic model of the external structure of the SARS-CoV-2 virion. Each "ball" is an atom.[1]
● Blue: envelope
● Turquoise: spike glycoprotein (S)
● Red: envelope proteins (E)
● Green: membrane proteins (M)
● Orange: glycan
Virus classification e
(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
  • B.1.1.7 (Alpha)
  • B.1.351 (Beta)
  • P.1 (Gamma)
  • B.1.617.2 (Delta)
  • Full list
Synonyms
  • 2019-nCoV

Severe acute respiratory syndrome coronavirus 2 (SARS‑CoV‑2),[2] also known as the coronavirus, is the virus that causes COVID-19 (coronavirus disease 2019), the respiratory illness responsible for the ongoing COVID-19 pandemic.[3] The virus was previously referred to by its 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 declared the outbreak a Public Health Emergency of International Concern on 30 January 2020, and a pandemic on 11 March 2020.[12][13] SARS‑CoV‑2 is a positive-sense single-stranded RNA virus[14] that is contagious in humans.[15] As described by the US National Institutes of Health, it is the successor to SARS-CoV-1, the virus that caused the 2002–2004 SARS outbreak.[16]

SARS‑CoV‑2 is a virus of the species severe acute respiratory syndrome–related coronavirus (SARSr-CoV).[2] It is believed to have zoonotic origins and has close genetic similarity to bat coronaviruses, suggesting it emerged from a bat-borne virus.[9][17] Research is ongoing as to whether SARS‑CoV‑2 came directly from bats or indirectly through any intermediate hosts.[18] 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.[19]

Epidemiological studies estimate that each infection results in an average of 2.4 to 3.4 new ones when no members of the community are immune and no preventive measures are taken.[20] The virus 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 or sneezes.[21][22] It mainly enters human cells by binding to angiotensin converting enzyme 2 (ACE2), a membrane protein that regulates the renin-angiotensin system.[23][24]

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".[25][26] In January 2020, the World Health Organization recommended "2019 novel coronavirus" (2019-nCov)[5][27] as the provisional name for the virus. This was in accordance with WHO's 2015 guidance[28] against using geographical locations, animal species, or groups of people in disease and virus names.[29][30]

On 11 February 2020, the International Committee on Taxonomy of Viruses adopted the official name "severe acute respiratory syndrome coronavirus 2" (SARS‑CoV‑2).[31] To avoid confusion with the disease SARS, the WHO sometimes refers to SARS‑CoV‑2 as "the COVID-19 virus" in public health communications[32][33] and the name HCoV-19 was included in some research articles.[8][9][10]

Infection and transmission

Human-to-human transmission of SARS‑CoV‑2 was confirmed on 20 January 2020 during the COVID-19 pandemic.[15][34][35][36] Transmission was initially assumed to occur primarily via respiratory droplets from coughs and sneezes within a range of about 1.8 metres (6 ft).[37][38] Laser light scattering experiments suggest that speaking is an additional mode of transmission[39][40] and a far-reaching[41] and under-researched[42] one, indoors, with little air flow.[43][44] Other studies have suggested that the virus may be airborne as well, with aerosols potentially being able to transmit the virus.[45][46][47] During human-to-human transmission, between 200 and 800 infectious SARS‑CoV‑2 virions are thought to initiate a new infection.[48][49][50] 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.[51] Indirect contact via contaminated surfaces is another possible cause of infection.[52] 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.[53][54] Viral RNA has also been found in stool samples and semen from infected individuals.[55][56]

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[57][58] or in the first week of symptoms and declines thereafter.[59] The duration of SARS-CoV-2 RNA shedding is generally between 3 and 46 days after symptom onset.[60]

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.[61] 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.[61]

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.[62][63][64] Some institutions have advised that those infected with SARS‑CoV‑2 restrict their contact with animals.[65][66]

Asymptomatic transmission

On 1 February 2020, the World Health Organization (WHO) indicated that "transmission from asymptomatic cases is likely not a major driver of transmission".[67] One meta-analysis found that 17% of infections are asymptomatic, and asymptomatic individuals were 42% less likely to transmit the virus.[68]

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.[69] 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.[70] Similarly, a study of ninety-four patients hospitalized in January and February 2020 estimated patients shed the greatest amount of virus two to three days before symptoms appear and that "a substantial proportion of transmission probably occurred before first symptoms in the index case".[71]

Reinfection

There is uncertainty about reinfection and long-term immunity.[72] It is not known how common reinfection is, but reports have indicated that it is occurring with variable severity.[72]

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.[73] 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.[73]

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.[74] The man's second infection was symptomatically more severe than the first infection, but the mechanisms that could account for this are not known.[74]

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

The first known infections from SARS‑CoV‑2 were discovered in Wuhan, China.[17] The original source of viral transmission to humans remains unclear, as does whether the virus became pathogenic before or after the spillover event.[9][19][75] Because many of the early infectees were workers at the Huanan Seafood Market,[76][77] it has been suggested that the virus might have originated from the market.[9][78] However, other research indicates that visitors may have introduced the virus to the market, which then facilitated rapid expansion of the infections.[19][79] 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.[80]

For a virus recently acquired through a cross-species transmission, rapid evolution is expected.[81] The mutation rate estimated from early cases of SARS-CoV-2 was of 6.54×10−4 per site per year.[80] Coronaviruses in general have high genetic plasticity,[82] but SARS-CoV-2's viral evolution is slowed by the RNA proofreading capability of its replication machinery.[83] For comparison, the viral mutation rate in vivo of SARS-CoV-2 has been found to be lower than that of influenza.[84]

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. Phylogenetic analysis indicates that samples taken from Rhinolophus sinicus show a resemblance of 80% to SARS‑CoV‑2.[85][86][87] Phylogenetic analysis also indicates that a virus from Rhinolophus affinis, collected in Yunnan province and designated RaTG13, has a 96.1% resemblance to SARS‑CoV‑2.[17][88] This sequence was the closest known to SARS-CoV-2 at the time of its identification,[80] but it is not its direct ancestor.[89] Other closely-related sequences were also identified in samples from local bat populations.[90]

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.[80][91] Differences between the bat coronavirus and SARS‑CoV‑2 suggest that humans may have been infected via an intermediate host;[78] although the source of introduction into humans remains unknown.[92][93]

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[94][95]), subsequent studies have not substantiated their contribution to the spillover.[80] 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[96]). In addition, despite similarities in a few critical amino acids,[97] pangolin virus samples exhibit poor binding to the human ACE2 receptor.[98]

Phylogenetics and taxonomy

Genomic information
SARS-CoV-2 genome.svg
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.[26] 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.[99] 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.[100]

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).[101][102] Coronaviruses undergo frequent recombination.[103] 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.[104] SARS-CoV-2 RNA sequence is approximately 30,000 bases in length,[105] relatively long for a coronavirus (which in turn carry the largest genomes among all RNA families)[106] Its genome consists nearly entirely of protein-coding sequences, a trait shared with other coronaviruses.[103]

A distinguishing feature of SARS‑CoV‑2 is its incorporation of a polybasic site cleaved by furin,[97] which appears to be an important element enhancing its virulence.[107] 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.[108] 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.[109][110] 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 PRRA.[111] This sequence is upstream of an arginine and serine which forms the S1/S2 cleavage site (PRRAR↓S) of the spike protein.[112] Although such sites are a common naturally-occurring feature of other viruses within the Subfamily Orthocoronavirinae,[111] it appears in few other viruses from the Beta-CoV genus,[113] and it is unique among members of its subgenus for such a site.[97]

Viral genetic sequence data can provide critical information about whether viruses separated by time and space are likely to be epidemiologically linked.[114] 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;[105][115] the number of genomes increased to 42 by 30 January 2020.[116] 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.[116] Examination of the topology of the phylogenetic tree at the start of the pandemic also found high similarities between human isolates.[117] (As of August 2021) 3,422 SARS‑CoV‑2 genomes, belonging to 19 strains, sampled on all continents except Antarctica were publicly available.[118]

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.[119]

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.[120][121]

Coronavirus genomes and subgenomes encode six open reading frames (ORFs).[122] 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.[123][124]

Phylogenetic tree

Variants

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.[125] 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).[126]

Several notable variants of SARS-CoV-2 emerged in late 2020. The World Health Organization has currently declared four variants of concern, which are as follows:[127]

  • 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.

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.[128]

Virology

Structure

Figure of a spherical SARSr-CoV virion showing locations of structural proteins forming the viral envelope and the inner nucleocapsid
Structure of a SARSr-CoV virion

Each SARS-CoV-2 virion is 50–200 nanometres (2.0×10−6–7.9×10−6 in) in diameter.[77] 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.[129] Coronavirus S proteins are glycoproteins and also type I membrane proteins (membranes containing a single transmembrane domain oriented on the extracellular side).[108] They are divided into two functional parts (S1 and S2).[99] In SARS-CoV-2, the spike protein, which has been imaged at the atomic level using cryogenic electron microscopy,[130][131] is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell;[129] specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion.[132]

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

Genome

SARS-CoV-2 has a linear, positive-sense, single-stranded RNA genome about 30,000 bases long.[99] Its genome has a bias against cytosine (C) and guanine (G) nucleotides like other coronaviruses.[133] 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%).[134] The nucleotide bias arises from the mutation of guanines and cytosines to adenosines and uracils, respectively.[135] The mutation of CG dinucleotides is thought to arise to avoid the zinc finger antiviral protein related defense mechanism of cells,[136] 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).[135] 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).[134] A similar codon usage bias trend is seen in other SARS–related coronaviruses.[137]

Replication cycle

Virus infections start when viral particles bind to host surface cellular receptors.[138] 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.[139] 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.[17][140][141][142] Studies have shown that SARS‑CoV‑2 has a higher affinity to human ACE2 than the original SARS virus.[130][143] SARS‑CoV‑2 may also use basigin to assist in cell entry.[144]

Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS‑CoV‑2.[23] The host protein neuropilin 1 (NRP1) may aid the virus in host cell entry using ACE2.[145] 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.[132] 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.[132] The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells.[146]

SARS‑CoV‑2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response.[129] Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).[147]

SARS-CoV-2 emerging from a human cell
SARS-CoV-2 virions emerging from a human cell
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.[148]

Epidemiology

Micrograph of SARS‑CoV‑2 virus particles isolated from a patient
Transmission electron micrograph of SARS‑CoV‑2 virions (red) isolated from a patient during the 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.[80]

A meta-analysis from November 2020 estimated the basic reproduction number ([math]\displaystyle{ R_0 }[/math]) of the virus to be between 2.39 and 3.44.[20] 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.[149] Many forms of preventive efforts may be employed in specific circumstances to reduce the propagation of the virus.[122]

There have been about 96,000 confirmed cases of infection in mainland China.[150] While the proportion of infections that result in confirmed cases or progress to diagnosable disease remains unclear,[151] 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.[152] Before 24 February 2020, over 95% of all deaths from COVID-19 worldwide had occurred in Hubei province, where Wuhan is located.[153][154] As of 30 December 2021, the percentage had decreased to 0.059%.[150]

As of 30 December 2021, there have been 285,043,163 total confirmed cases of SARS‑CoV‑2 infection in the ongoing pandemic.[150] The total number of deaths attributed to the virus is 5,425,817.[150]

See also

References

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  148. ↑ "Masitinib is a broad coronavirus 3CL inhibitor that blocks replication of SARS-CoV-2". Science 373 (6557): 931–936. August 2021. doi:10.1126/science.abg5827. PMID 34285133. 
  149. ↑ "COVID-19 outbreak on the Diamond Princess cruise ship: estimating the epidemic potential and effectiveness of public health countermeasures". Journal of Travel Medicine 27 (3). May 2020. doi:10.1093/jtm/taaa030. PMID 32109273. 
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  154. ↑ "Coronavirus: China to repay Africa in safeguarding public health". The Sun. 25 February 2020. https://www.sunnewsonline.com/coronavirus-china-to-repay-africa-in-safeguarding-public-health/. 

Further reading

External links

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Classification

Wikidata ☰ Q82069695 entry




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