摘要：SummaryType 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 with manifestation 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 responsein vitroand in moderate cases of COVID-19.In vitrostimulation 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 IFNα detected in patients with moderate COVID-19 is sufficient to suppress SARS-CoV-2 replication in human airway cells.Graphical abstractDisplay OmittedHighlights•SARS-CoV-2 induces the expression of type I IFNs in human lung cells•Moderate cases of COVID-19 have higher serum levels of IL-10 and IFNα•Severe cases of COVID-19 have higher serum levels of IL-6, TNFα and IL-8•Physiological levels of IFNα reduces SARS-CoV-2 replication in human airway cellsImmunology; Virology
