期刊
ISCIENCE
卷 24, 期 5, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.isci.2021.102477
关键词
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资金
- Canadian Institutes of Health Research (CIHR)
- Natural Sciences and Engineering Research Council of Canada (NSERC)
- Canadian Foundation for Innovation
- Canada Research Chairs Program
- Ontario Early Career Researcher Award
- CIHR COVID-19 rapid response grant
- CIHR New Investigator Award
- Ontario Early Researcher Award
- Zhejiang University
Recent studies have shown that SARS-CoV-2 proteins can inhibit human type I interferon responses, and the timing and extent of interferon production are associated with COVID-19 severity. SARS-CoV-2 infection induces a type I interferon response in vitro and in moderate cases of COVID-19, with physiological levels of IFNa being sufficient to suppress SARS-CoV-2 replication in human airway cells.
Type I interferons (IFNs) are our first line of defense against virus infection. Recent studies have suggested the ability of SARS-CoV-2 proteins to inhibit IFN responses. Emerging data also suggest that timing and extent of IFN production is associated withmanifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wild-type SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are scarce. Here we demonstrate that SARS-CoV-2 infection induces a type I IFN response in vitro and inmoderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Furthermore, we show that physiological levels of IFNa detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.
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