| SARS coronavirus Urbani | |
|---|---|
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| Virus classification | |
| Group: | Group IV ((+)ssRNA) |
| Order: | Nidovirales |
| Family: | Coronaviridae |
| Genus: | Coronavirus |
| Species: | SARS coronavirus |
The SARS coronavirus, sometimes shortened to SARS-CoV, is the virus that causes severe acute respiratory syndrome (SARS).[1] 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 being held in laboratories in New York, San Francisco, Manila, Hong Kong, and Toronto.
On April 12, 2003, scientists working at the Michael Smith Genome Sciences Centre in Vancouver, British Columbia 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."[2]
The sequence of the SARS coronavirus has since been confirmed by other independent groups.
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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. SARS is similar to other coronaviruses in that its genome expression starts with translation of two large ORFs 1a and 1b, which are two polyproteins. The SARS virus has 13 known genes and 14 known proteins. There are 265bp in the 5'UTR and 342bp in the 3'UTR. 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.
The life cycle of the SARS coronavirus starts when it enters a host cell by membrane fusion. The viral nucleic acid is then replicated, and proteins are synthesized. Assembly of the nucelocapsid is done in the rough ER by putting together N (nucleocapsid proteins) proteins and genomic RNA. The golgi apparatus swells to form smooth vesicles containing the nucleocapsides, which then bud from the golgi. The last step of forming the complete virus is the assembling of the envelop with the nucleocapsids. The smooth vesicles fuse with the cell membrane to release the viruses.
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. The envelop 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 envelop. The size of these particles are about 80-90nm.
Virons first attached themselves to the surface of the host and their envelops fused with the cell membrane and the nucleocapsides enter the cell. The virus does not enter the cell via endocytosis, which is the mechanism employed by other coronaviruses. The viruses replicate their RNA inside the host cells.
The SARS coronavirus infects type 2 pneumocytes, which are important for secreting pulmonary surfactants that reduce surface tension and preserves the integrity of alveolar space. SARS also infects type 1 pneumocytes, which are the primary targets early on in the infection. The spike protein also plays an important role in the pathogenesis of SARS. The S protein increases ER stress and the unfolded protein response (UPR).
SARS is most closely related to group 2 coronaviruses, but it does not segregate into any of the other three groups of coronaviruses. 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 group 2 coronovirus and SARS is the nsp3 replicase subunit encoded by ORF1a. SARS does not have a papain-like proteinase 1.
Engineering of SARS virus has been done. In a paper published in 2006, a new transcription circuit was engineered to make recombinant SARS viruses. The recombination allowed for efficient expression of viral transcripts and proteins. The engineering of this transcription circuit reduces the RNA recombinant progeny viruses. The TRS (transcription regulatory sequences) circuit regulates efficient expression of SARS-CoV subgenomic mRNAs. The wild type TRS is ACGAAC. A double mutation results in TRS-1 (ACGGAT) and a triple mutation results in TRS-2 (CCGGAT). When the remodeled TRS circuit containing viruses are genetically recombined with wild type TRS circuits, the result is a circuit reduced in production of subgenomic mRNA. The goal of modifying the SARS virus with this approach is to produce chimeric progeny that have reduced viability due to the incompatibility of the WT and engineered TRS circuits.
See also
Notes
- ^ Thiel V (editor). (2007). Coronaviruses: Molecular and Cellular Biology (1st ed.). Caister Academic Press. ISBN 978-1-904455-16-5.
- ^ B.C. lab cracks suspected SARS code - CBCNews, Canada, April 2003
References
- J S M Peiris et al. (5 April 2003). "Coronavirus as a possible cause of severe acute respiratory syndrome" (PDF). The Lancet 361 (9364). http://image.thelancet.com/extras/03art3477web.pdf.
- Paul A. Rota et al. (30 May 2003). "Characterization of a Novel Coronavirus Associated with Severe Acute Respiratory Syndrome". Science 300 (5624): 1394–1399. doi:. PMID 12730500. http://www.sciencemag.org/cgi/content/full/300/5624/1394.. Published online 1 May 2003; doi:10.1126/science.1085952
- Marco A. Marra et al. (30 May 2003). "The Genome Sequence of the SARS-Associated coronavirus". Science 300 (5624): 1399–1404. doi:. PMID 12730501. http://www.sciencemag.org/cgi/content/full/300/5624/1399.. Published online 1 May 2003; doi:10.1126/science.1085953
- Snijder EJ et al. (29 August 2003). "Unique and conserved features of genome and proteome of SARS-coronavirus, an early split-off from the coronavirus group 2 lineage". J Mol Biol 331 (5): 991-1004. http://www.ncbi.nlm.nih.gov/pubmed/12927536.
- Yount B et al. (15 August 2006). "Rewiring the severe acute respiratory syndrome coronavirus (SARS-CoV) transcription circuit: engineering a recombination-resistant genome". Proc Natl Acad Sci U S A 103 (33): 12546-51. http://www.ncbi.nlm.nih.gov/sites/entrez.
- Thiel V (editor). (2007). Coronaviruses: Molecular and Cellular Biology (1st ed.). Caister Academic Press. ISBN 978-1-904455-16-5.
- Enjuanes L, et al. (2008). "Coronavirus Replication and Interaction with Host". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6.
External links
- WHO press release identifying and naming the SARS virus
- The SARS virus genetic map
- Science special on the SARS virus (free content: no registration required)
- McGill University SARS Resources (From web archive)
- U.S. Centers for Disease Control and Prevention (CDC) SARS home
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