An international outbreak of
severe acute respiratory syndrome, a recently recognized syndrome caused by the newly identified
severe acute respiratory syndrome-associated coronavirus, began in November 2002 and ended in July 2003. Since then, a large body of research on the syndrome has been published; the most updated developments are summarized here.
RECENT FINDINGS: Recent findings suggest that animal
severe acute respiratory syndrome-like coronaviruses may have been transmitted to humans without detection for years before the recent outbreak, and that such transmission may be continuing today. The 2002-2003 outbreak probably originated from similar animal-to-human transmission, but selection and purification of the animal
severe acute respiratory syndrome-like virus appears to have occurred, creating the more virulent
severe acute respiratory syndrome-associated coronavirus. Recent studies have documented that
severe acute respiratory syndrome-associated coronavirus is primarily transmitted via contact and/or respiratory droplets and that the combination of standard, contact, and droplet precautions is generally effective for its control. It has been shown that
severe acute respiratory syndrome-associated coronavirus is typically relatively inefficiently transmitted, with the notable exception of transmission during superspreading events. Insights into the pathogenesis of
severe acute respiratory syndrome have been made: one study suggests that
human leukocyte antigen HLA-B*4601 is a possible risk factor for more severe disease, while another identifies
angiotensin-converting enzyme 2 as a cellular receptor for
severe acute respiratory syndrome-associated coronavirus. Promising treatments have been identified, including
interferons, an anti-spike
monoclonal antibody, and fusion inhibitors. In addition, many promising
vaccines are currently in development.
SUMMARY: