PMC:7200337 / 6033-7178 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7200337","sourcedb":"PMC","sourceid":"7200337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7200337","text":"As these cytokines represent a major barrier to viral infection, CoVs have evolved several mechanisms to inhibit IFN-I induction and signaling. Numerous studies have demonstrated that SARS-CoV-1 suppresses IFN release in vitro and in vivo (Cameron et al., 2012, Minakshi et al., 2009, Siu et al., 2009, Wathelet et al., 2007). SARS-CoV-2 likely achieves a similar effect, as suggested by the lack of robust type I/III IFN signatures from infected cell lines, primary bronchial cells, and a ferret model (Blanco-Melo et al., 2020). In fact, patients with severe COVID-19 demonstrate remarkably impaired IFN-I signatures as compared to mild or moderate cases (Hadjadj et al., 2020). As is often the case, there are multiple mechanisms of evasion for CoVs, with viral factors antagonizing each step of the pathway from PRR sensing and cytokine secretion to IFN signal transduction (Figure 1 ).\nFigure 1 Mechanisms of Host Innate Immune Response and Coronaviruses Antagonism\nOverview of innate immune sensing (left) and interferon signaling (right), annotated with the known mechanisms by which SARS-CoV-1 and MERS-CoV antagonize the pathways 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