Release 5.6

Published August 2, 2005

Headlines

The dramatic outbreak of Severe Acute Respiratory Syndrome virus may be due to two mutations in the virus spike protein

The SARS coronavirus is a new human pathogen that emerged in Asia in 2002-2003. The animal reservoir of the virus is presumably palm civet, whose meat is a delicacy in Southern China.

The virus induces an acute respiratory distress in human and is deadly in 10% of all cases. It enters pulmonary cells through binding of the viral spike protein (human isolate Tor2 and palm civet isolate SZ3: P59594) to angiotensin-converting enzyme 2 (ACE2) (palm civet: Q56NL1; human: Q9BYF1). These proteins have recently been annotated or updated in UniProtKB/Swiss-Prot.

It has been recently shown that two amino acid mutations on palm civet SARS spike protein, Lys-479 and Ser-487, are sufficient for the virus to acquire the ability to bind efficiently human ACE2 (see EMBO J. 24:1634-1643(2005); PubMed: 15791205).

The severity of the 2002-2003 epidemic was presumably due to those two amino-acid mutations, giving opportunity to an animal virus to cause a major infection in the human species.

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