• Media type: E-Article
  • Title: Combined action of type I and type III interferon restricts initial replication of severe acute respiratory syndrome coronavirus in the lung but fails to inhibit systemic virus spread
  • Contributor: Mahlakõiv, Tanel; Ritz, Daniel; Mordstein, Markus; DeDiego, Marta L.; Enjuanes, Luis; Müller, Marcel A.; Drosten, Christian; Staeheli, Peter
  • Published: Microbiology Society, 2012
  • Published in: Journal of General Virology, 93 (2012) 12, Seite 2601-2605
  • Language: English
  • DOI: 10.1099/vir.0.046284-0
  • ISSN: 0022-1317; 1465-2099
  • Origination:
  • Footnote:
  • Description: STAT1-deficient mice are more susceptible to infection with severe acute respiratory syndrome coronavirus (SARS-CoV) than type I interferon (IFN) receptor-deficient mice. We used mice lacking functional receptors for both type I and type III IFN (double knockout, dKO) to evaluate the possibility that type III IFN plays a decisive role in SARS-CoV protection. We found that viral peak titres in lungs of dKO and STAT1-deficient mice were similar, but significantly higher than in wild-type mice. The kinetics of viral clearance from the lung were also comparable in dKO and STAT1-deficient mice. Surprisingly, however, infected dKO mice remained healthy, whereas infected STAT1-deficient mice developed liver pathology and eventually succumbed to neurological disease. Our data suggest that the failure of STAT1-deficient mice to control initial SARS-CoV replication efficiently in the lung is due to impaired type I and type III IFN signalling, whereas the failure to control subsequent systemic viral spread is due to unrelated defects in STAT1-deficient mice.
  • Access State: Open Access