Pathogenesis of severe acute respiratory syndrome

Curr Opin Immunol. 2005 Aug;17(4):404-10. doi: 10.1016/j.coi.2005.05.009.

Abstract

Severe acute respiratory syndrome (SARS) is a zoonotic infectious disease caused by a novel coronavirus (CoV). The tissue tropism of SARS-CoV includes not only the lung, but also the gastrointestinal tract, kidney and liver. Angiotensin-converting enzyme 2 (ACE2), the C-type lectin CD209L (also known L-SIGN), and DC-SIGN bind SARS-CoV, but ACE2 appears to be the key functional receptor for the virus. There is a prominent innate immune response to SARS-CoV infection, including acute-phase proteins, chemokines, inflammatory cytokines and C-type lectins such as mannose-binding lectin, which plays a protective role against SARS. By contrast there may be a lack of type 1 interferon response. Moreover, lymphopenia with decreased numbers of CD4+ and CD8+ T cells is common during the acute phase. Convalescent patients have IgG-class neutralizing antibodies that recognize amino acids 441-700 of the spike protein (S protein) as the major epitope.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Genetic Predisposition to Disease
  • Humans
  • Immunity, Innate / immunology
  • Lung / immunology
  • Lung / pathology
  • Lung / virology
  • Severe Acute Respiratory Syndrome / genetics
  • Severe Acute Respiratory Syndrome / immunology*
  • Severe Acute Respiratory Syndrome / pathology
  • Severe Acute Respiratory Syndrome / virology*
  • Severe acute respiratory syndrome-related coronavirus / immunology*
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*
  • Severe acute respiratory syndrome-related coronavirus / physiology