Severe acute respiratory syndrome: an update : Current Opinion in Infectious Diseases (original) (raw)

Nosocomial and hospital-related infections

aToronto Medical Laboratories and Mount Sinai Hospital Department of Microbiology, Toronto, Ontario, Canada, bDepartments of Laboratory Medicine and Pathobiology and cMedicine, University of Toronto, Toronto, Ontario, Canada

Correspondence to Donald E. Low MD, FRCPC, Mount Sinai Hospital, 600 University Avenue, Room 1485, Toronto, Ontario, Canada M5G 1X5 Tel: +1 416 586 4435; fax: +1 416 586 8746; e-mail: [email protected]

Abbreviations

ACE2: angiotensin-converting enzyme 2

CoV: coronavirus

SARS: severe acute respiratory syndrome

SARS-CoV: severe acute respiratory syndrome-associated coronavirus

Abstract

Purpose of review

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

New findings regarding severe acute respiratory syndrome are continuing to be discovered at an unprecedented pace, permitting a better understanding of the disease and enabling better preparation for its possible return.