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{{short description|species of virus causing severe acute respiratory syndrome}}
{{short description|species of virus causing severe acute respiratory syndrome}}
{{For|the virus strain belonging to this species implicated in the 2019–20 Wuhan coronavirus outbreak|2019 novel coronavirus}}
{{For|the virus strain belonging to this species implicated in the 2019–20 Wuhan coronavirus outbreak|2019 novel coronavirus}}

Revision as of 17:45, 15 February 2020

For the virus strain belonging to this species implicated in the 2019–20 Wuhan coronavirus outbreak, see 2019 novel coronavirus.
Severe acute respiratory syndrome-related coronavirus
Electron microscope image of a SARS-CoV virion
Virus classification Edit this 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
Strain:
Severe acute respiratory syndrome-related coronavirus
Synonyms
  • SARS coronavirus
  • SARS-related coronavirus
  • Severe acute respiratory syndrome coronavirus[1]

Severe acute respiratory syndrome-related coronavirus (SARS-CoV, SARSr-CoV) is the virus that causes severe acute respiratory syndrome (SARS).[2] On April 16, 2003, following the outbreak of SARS in Asia and secondary cases elsewhere in the world, the World Health Organization (WHO) issued a press release stating that the coronavirus identified by a number of laboratories was the official cause of SARS. Samples of the virus are held in laboratories in New York City, San Francisco, Manila, Hong Kong, and Toronto.

The Centers for Disease Control and Prevention (CDC) in the United States and National Microbiology Laboratory (NML) in Canada identified the SARS genome in April 2003.[3][4] Scientists at Erasmus University in Rotterdam, the Netherlands demonstrated that the SARS coronavirus fulfilled Koch's postulates thereby confirming it as the causative agent. In the experiments, macaques infected with the virus developed the same symptoms as human SARS victims.[5]

The SARS coronavirus is one of several viruses identified by WHO as a likely cause of a future epidemic in a new plan developed after the Ebola epidemic for urgent research and development before and during an epidemic towards diagnostic tests, vaccines and medicines.[6][7]

SARS

SARS, or severe acute respiratory syndrome, is the disease caused by SARS coronavirus. It causes an often severe illness marked initially by systemic symptoms of muscle pain, headache, and fever, followed in 2–14 days by the onset of respiratory symptoms,[8] mainly cough, dyspnea, and pneumonia. Another common finding in SARS patients is a decrease in the number of lymphocytes circulating in the blood.[9]

In the SARS outbreak of 2003, about 9% of patients with confirmed SARS infection died.[10] The mortality rate was much higher for those over 60 years old, with mortality rates approaching 50% for this subset of patients.[10]

History

On April 12, 2003, scientists working at the Michael Smith Genome Sciences Centre in Vancouver finished mapping the genetic sequence of a coronavirus believed to be linked to SARS. The team was led by Dr. Marco Marra and worked in collaboration with the British Columbia Centre for Disease Control and the National Microbiology Laboratory in Winnipeg, Manitoba, using samples from infected patients in Toronto. The map, hailed by the WHO as an important step forward in fighting SARS, is shared with scientists worldwide via the GSC website (see below). Dr. Donald Low of Mount Sinai Hospital in Toronto described the discovery as having been made with "unprecedented speed".[11] The sequence of the SARS coronavirus has since been confirmed by other independent groups.

In late May 2003, studies from samples of wild animals sold as food in the local market in Guangdong, China, found the SARS coronavirus could be isolated from masked palm civets (Paguma sp.), but the animals did not always show clinical signs. The preliminary conclusion was the SARS virus crossed the xenographic barrier from palm civet to humans, and more than 10,000 masked palm civets were killed in Guangdong Province. The virus was also later found in raccoon dogs (Nyctereuteus sp.), ferret badgers (Melogale spp.), and domestic cats. In 2005, two studies identified a number of SARS-like coronaviruses in Chinese bats.[12][13] Phylogenetic analysis of these viruses indicated a high probability that SARS coronavirus originated in bats and spread to humans either directly or through animals held in Chinese markets. The bats did not show any visible signs of disease, but are the likely natural reservoirs of SARS-like coronaviruses. In late 2006, scientists from the Chinese Centre for Disease Control and Prevention of Hong Kong University and the Guangzhou Centre for Disease Control and Prevention established a genetic link between the SARS coronavirus appearing in civets and humans, confirming claims that the disease had jumped across species.[14]

Virology

Scanning Electron Micrograph of SARS virions

The SARS coronavirus is a positive and single stranded RNA virus belonging to a family of enveloped coronaviruses. Its genome is about 29.7kb, which is one of the largest among RNA viruses. The SARS virus has 13 known genes and 14 known proteins. There are 265 nucleotides in the 5'UTR and 342 nucleotides in the 3'UTR. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs, 1a and 1b, both of which are polyproteins.

The functions of several of these proteins are known:[15] ORFs 1a and 1b encode the replicase and there are four major structural proteins: nucleocapsid, spike, membrane and envelope. It also encodes for eight unique proteins, known as the accessory proteins, all with no known homologues. The function of these accessory proteins remains unknown.[16]

Coronaviruses usually express pp1a (the ORF1a polyprotein) and the PP1ab polyprotein with joins ORF1a and ORF1b. The polyproteins are then processed by enzymes that are encoded by ORF1a. Product proteins from the processing includes various replicative enzymes such as RNA dependent polymerase, RNA helicase, and proteinase. The replication complex in coronavirus is also responsible for the synthesis of various mRNAs downstream of ORF 1b, which are structural and accessory proteins. Two different proteins, 3CLpro and PL2pro, cleave the large polyproteins into 16 smaller subunits.

SARS-Coronavirus follows the replication strategy typical of the Coronavirus genus.

The primary human receptor of the virus is angiotensin-converting enzyme 2 (ACE2), first identified in 2003.[17]

Morphology

The morphology of the SARS coronavirus is characteristic of the coronavirus family as a whole. These viruses have large pleomorphic spherical particles with bulbous surface projections that form a corona around particles, creating an inherent crown-shaped appearance. The envelope of the virus contains lipid and appears to consist of a distinct pair of electron dense shells.

The internal component of the shell is a single-stranded helical ribonucleoprotein. There are also long surface projections that protrude from the lipid envelope. The size of these particles is in the 80–90 nm range.

Some coronavirus virions have been found to range from 3.62-39.83 nm to as large 336-473 nm in length. This structure changes in the presence of hydroxyoctanoic acid which is a fatty acid that can act as an indicator for common mistakes of beta-hydroxy fatty acid metabolism inside the human body [18]. This acid creates conditions that cause the SARS-CoV to begin morphing its structure as if it were attacking an enzyme needed for reproduction.

[19]During this breakdown, it has been discovered that the outer shell of the SARS-CoV produces structures common in the coronavirus family such as spike and membrane proteins used for attaching to cellular structures in the host body and nucleocapsids which help create more infectious particles. No matter which strain of coronavirus, each of these spike structures consist of three different parts: an ectodomain, a transmembrane anchor, and a short tail that goes between cells. The ectodomain of the spike is a structure that contains the S1 receptor-binder which attaches itself to protein receptors. The membrane anchorage is carried out by a structure known as S2 that acts as a middle ground between the viral and host cell, creating a hospitable fusion between the two cell membranes that allows for the dissemination of viral genomes into the host organism.

Evolution

SARS-CoV is most closely related to group 2 coronaviruses (Betaconoravirus), meaning that it can evolve and spread only through mammalian species like its relative group known as Alphacoronaviruses. A theory has been proposed that bat coronaviruses have been coevolved with their hosts for a long time then jumped species from bats to humans.[20][21] Viral samples isolated during the time of the SARS epidemic (2003-2004) indicate a strong similarity between human strains and palm civets that were taken from animal markets surrounding infected areas.[22] The closest outgroup to the coronaviruses are the toroviruses, with which it has homology in the ORF 1b replicase and the two viron proteins of S and M. SARS was determined to be an early split off from the group 2 coronaviruses based on a set of conserved domains that it shares with group 2.

A main difference between other group 2 coronavirus and SARS is the nsp3 replicase subunit encoded by ORF1a. SARS does not have a papain-like proteinase 1.

[22]Another primary difference between the two species lies in their S1-CTD structures which help the virus bind to protein receptors. The human S1-CTD attaches to the protein receptors Asn479 and Thr487 while the animal species of the virus targets the receptors Lys479 and Ser487. Both strains of the virus seek out an enzyme that converts zinc peptidase known as ACE2, but the human SARS-CoV binds itself to this enzyme in a much stronger fashion than its animal counterpart. There are two areas on ACE2 specifically, Lys31 and Lys353, that both contain salt bridges which act as aids for this strengthened virus-receptor binding. Asn479 and Thr487 have a powerful reaction with these salt bridges that result in virus mutation, leading scientists to believe that the interspecies jump resulted from this interaction.

See also

Notes

  1. ^ "ICTV Taxonomy history: Severe acute respiratory syndrome-related coronavirus" (html). International Committee on Taxonomy of Viruses (ICTV). Retrieved 27 January 2019.
  2. ^ Thiel V (editor). (2007). Coronaviruses: Molecular and Cellular Biology (1st ed.). Caister Academic Press. ISBN 978-1-904455-16-5. {{cite book}}: |author= has generic name (help)
  3. ^ "Remembering SARS: A Deadly Puzzle and the Efforts to Solve It". Centers for Disease Control and Prevention. 11 April 2013. Archived from the original on 1 August 2013. Retrieved 3 August 2013.
  4. ^ "Coronavirus never before seen in humans is the cause of SARS". United Nations World Health Organization. 16 April 2006. Archived from the original on 12 August 2004. Retrieved 5 July 2006.
  5. ^ Fouchier RA, Kuiken T, Schutten M, et al. (2003). "Aetiology: Koch's postulates fulfilled for SARS virus". Nature. 423 (6937): 240. Bibcode:2003Natur.423..240F. doi:10.1038/423240a. PMID 12748632.
  6. ^ Kieny, Marie-Paule. "After Ebola, a Blueprint Emerges to Jump-Start R&D". Scientific American Blog Network. Archived from the original on 20 December 2016. Retrieved 13 December 2016.
  7. ^ "LIST OF PATHOGENS". World Health Organization. Archived from the original on 20 December 2016. Retrieved 13 December 2016.
  8. ^ Chan-Yeung M; Xu RH (November 2003). "SARS: epidemiology". Respirology (Carlton, Vic.). 8 (Suppl): S9–14. doi:10.1046/j.1440-1843.2003.00518.x. PMID 15018127.
  9. ^ Yang M; Li CK; Li K; Hon KL; Ng MH; Chan PK; Fok TF (August 2004). "Hematological findings in SARS patients and possible mechanisms (review)". International Journal of Molecular Medicine. 14 (2): 311–5. doi:10.3892/ijmm.14.2.311. PMID 15254784. Archived from the original on 2015-09-24.
  10. ^ a b Sørensen MD; Sørensen B; Gonzalez-Dosal R; Melchjorsen CJ; Weibel J; Wang J; Jun CW; Huanming Y; Kristensen P (May 2006). "Severe acute respiratory syndrome (SARS): development of diagnostics and antivirals". Annals of the New York Academy of Sciences. 1067 (1): 500–5. Bibcode:2006NYASA1067..500S. doi:10.1196/annals.1354.072. PMID 16804033.
  11. ^ "B.C. lab cracks suspected SARS code". CBCNews, Canada. April 2003. Archived from the original on 2007-11-26.
  12. ^ Li W, Shi Z, Yu M, et al. (2005). "Bats are natural reservoirs of SARS-like coronaviruses". Science. 310 (5748): 676–9. Bibcode:2005Sci...310..676L. doi:10.1126/science.1118391. PMID 16195424.
  13. ^ Lau SK, Woo PC, Li KS, et al. (2005). "Severe acute respiratory syndrome coronavirus-like virus in Chinese horseshoe bats". Proc. Natl. Acad. Sci. U.S.A. 102 (39): 14040–5. Bibcode:2005PNAS..10214040L. doi:10.1073/pnas.0506735102. PMC 1236580. PMID 16169905.
  14. ^ "Scientists prove SARS-civet cat link". China Daily. 23 November 2006. Archived from the original on 14 June 2011.
  15. ^ McBride R; Fielding BC (November 2012). "The role of severe syndrome (SARS)-coronavirus accessory proteins in virus pathogenesis". Viruses. 4 (11): 2902–23. doi:10.3390/v4112902. PMC 3509677. PMID 23202509.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  16. ^ McBride, Ruth; Fielding, Burtram C. (2012-11-07). "The Role of Severe Acute Respiratory Syndrome (SARS)-Coronavirus Accessory Proteins in Virus Pathogenesis". Viruses. 4 (11): 2902–2923. doi:10.3390/v4112902. ISSN 1999-4915. PMC 3509677. PMID 23202509.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ Li, Wenhui; Moore, Michael J.; Vasilieva, Natalya; Sui, Jianhua; Wong, Swee Kee; Berne, Michael A.; Somasundaran, Mohan; Sullivan, John L.; Luzuriaga, Katherine; Greenough, Thomas C.; Choe, Hyeryun (Nov 2003). "Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus". Nature. 426 (6965): 450–454. doi:10.1038/nature02145. ISSN 0028-0836. PMID 14647384.
  18. ^ PubChem. "3-Hydroxyoctanoic acid". pubchem.ncbi.nlm.nih.gov. Retrieved 2020-02-13.
  19. ^ Lin, Shiming; Lee, Chih-Kung; Lee, Shih-Yuan; Kao, Chuan-Liang; Lin, Chii-Wann; Wang, An-Bang; Hsu, Su-Ming; Huang, Long-Sun (2005). "Surface ultrastructure of SARS coronavirus revealed by atomic force microscopy". Cellular Microbiology. 7 (12): 1763–1770. doi:10.1111/j.1462-5822.2005.00593.x. ISSN 1462-5822.
  20. ^ Cui J; Han N; Streicker D; Li G; Tang X; Shi Z; Hu Z; Zhao G; Fontanet A; Guan Y; Wang L; Jones G; Field HE; Daszak P; Zhang S (Oct 2007). "Evolutionary relationships between bat coronaviruses and their hosts". Emerg. Infect. Dis. 13 (10): 1526–32. doi:10.3201/eid1310.070448. PMC 2851503. PMID 18258002.
  21. ^ Ge XY; Li JL; Yang XL; Chmura AA; Zhu G; Epstein JH; Mazet JK; Hu B; Zhang W; Peng C; Zhang YJ; Luo CM; Tan B; Wang N; Zhu Y; Crameri G; Zhang SY; Wang LF; Daszak P; Shi ZL (Nov 28, 2013). "Isolation and characterization of a bat SARS-like coronavirus that uses the ACE2 receptor". Nature. 503 (7477): 535–8. Bibcode:2013Natur.503..535G. doi:10.1038/nature12711. PMC 5389864. PMID 24172901.
  22. ^ a b Li, Fang (2016-09-29). "Structure, Function, and Evolution of Coronavirus Spike Proteins". Annual review of virology. 3 (1): 237–261. doi:10.1146/annurev-virology-110615-042301. ISSN 2327-056X. PMC 5457962. PMID 27578435.

References

External links

Wikimedia Commons has media related to Severe acute respiratory syndrome-related coronavirus.
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