SARS coronavirus

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SARS coronavirus
Virus classification
Group: Group IV ((+)ssRNA)
Order: Nidovirales
Family: Coronaviridae
Genus: Coronavirus
Species: SARS coronavirus

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Overview

The SARS coronavirus 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 labratories 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." [1]

The sequence of the SARS coronavirus has since been confirmed by other independent groups.

Viral Replication

Coronavirus (CoV) genome replication takes place in the cytoplasm in a membrane-protected microenvironment and starts with the translation of the genome to produce the viral replicase. CoV transcription involves a discontinuous RNA synthesis (template switch) during the extension of a negative copy of the subgenomic mRNAs. The requirement for basepairing during transcription has been formally demonstrated in arteriviruses and CoVs. CoV N protein is required for coronavirus RNA synthesis and has RNA chaperone activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. CoVs initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after CoV infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation and immune and stress responses. The balance between genes up- and down-regulated could explain the pathogenesis caused by these viruses. Coronavirus expression systems based on single genome constructed by targeted recombination, or by using infectious cDNAs, have been developed. The possibility of expressing different genes under the control of transcription regulating sequences (TRSs) with programmable strength and engineering tissue and species tropism indicates that CoV vectors are flexible. CoV based vectors have emerged with high potential vaccine development and possibly for gene therapy.[2]

References

  1. Thiel V (editor). (2007). Coronaviruses: Molecular and Cellular Biology (1st ed. ed.). Caister Academic Press. ISBN 978-1-904455-16-5 .
  2. Enjuanes L; et al. (2008). "Coronavirus Replication and Interaction with Host". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6.

Scientific and medical journal articles

See also

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