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Background
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A novel coronavirus has recently been identified as the causative agent of SARS (Severe Acute Respiratory Syndrome). Coronaviruses are a major cause of upper respiratory diseases in humans. The genomes of these viruses are positive-stranded RNA approximately 27-31kb in length. SARS infection can be mediated by the binding of the viral S (Spike) protein, a glycosylated 139 kDa protein and the major surface antigen of the virus, to the angiotensin-converting enzyme 2 (ACE2) on target cells. The M protein (Membrane protein, Matrix protein) is another major structural viral protein. It is an integral membrane protein involved in the budding of the viral particles and interacts with S protein and the nucleocapsid protein. The SARS E protein contains a short palindromic transmembrane helical hairpin that seems to deform lipid bilayers, which may explain its role in viral budding and virion envelope morphogenesis. ACE2, the SARS receptor, normally plays a central role in vascular, renal, and myocardial physiology. In contrast to its homolog ACE, ACE2 expression is restricted to heart, kidney, and testis.
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