Resolution of primary severe acute respiratory syndrome-associated coronavirus infection requires Stat1

J Virol. 2004 Oct;78(20):11416-21. doi: 10.1128/JVI.78.20.11416-11421.2004.


Intranasal inhalation of the severe acute respiratory syndrome coronavirus (SARS CoV) in the immunocompetent mouse strain 129SvEv resulted in infection of conducting airway epithelial cells followed by rapid clearance of virus from the lungs and the development of self-limited bronchiolitis. Animals resistant to the effects of interferons by virtue of a deficiency in Stat1 demonstrated a markedly different course following intranasal inhalation of SARS CoV, one characterized by replication of virus in lungs and progressively worsening pulmonary disease with inflammation of small airways and alveoli and systemic spread of the virus to livers and spleens.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bronchiolitis, Viral / virology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Immunohistochemistry
  • Lung / pathology
  • Lung / virology
  • Mice
  • STAT1 Transcription Factor
  • Severe Acute Respiratory Syndrome / immunology*
  • Severe Acute Respiratory Syndrome / pathology
  • Severe Acute Respiratory Syndrome / physiopathology*
  • Severe Acute Respiratory Syndrome / virology
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*


  • DNA-Binding Proteins
  • STAT1 Transcription Factor
  • Stat1 protein, mouse
  • Trans-Activators