SARS coronavirus pathogenesis: host innate immune responses and viral antagonism of interferon

Curr Opin Virol. 2012 Jun;2(3):264-75. doi: 10.1016/j.coviro.2012.04.004. Epub 2012 May 7.

Abstract

SARS-CoV is a pathogenic coronavirus that emerged from a zoonotic reservoir, leading to global dissemination of the virus. The association SARS-CoV with aberrant cytokine, chemokine, and Interferon Stimulated Gene (ISG) responses in patients provided evidence that SARS-CoV pathogenesis is at least partially controlled by innate immune signaling. Utilizing models for SARS-CoV infection, key components of innate immune signaling pathways have been identified as protective factors against SARS-CoV disease, including STAT1 and MyD88. Gene transcription signatures unique to SARS-CoV disease states have been identified, but host factors that regulate exacerbated disease phenotypes still remain largely undetermined. SARS-CoV encodes several proteins that modulate innate immune signaling through the antagonism of the induction of Interferon and by avoidance of ISG effector functions.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Disease Models, Animal
  • Humans
  • Immune Evasion*
  • Immunity, Innate*
  • Interferons / antagonists & inhibitors*
  • Severe acute respiratory syndrome-related coronavirus / immunology
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*
  • Signal Transduction
  • Virulence
  • Virulence Factors / metabolism*

Substances

  • Virulence Factors
  • Interferons