Mahlakõiv, Tanel;
Ritz, Daniel;
Mordstein, Markus;
DeDiego, Marta L.;
Enjuanes, Luis;
Müller, Marcel A.;
Drosten, Christian;
Staeheli, Peter
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
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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.