PMC:7281546 / 27485-28644 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7281546","sourcedb":"PMC","sourceid":"7281546","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7281546","text":"Induction of IFN-α/β is the most rapid and effective mechanism for hosts to initiate antiviral innate immune responses. SARS-CoV, MHV and many other CoVs are sensitive to IFNs. A great number of viral dsRNAs intermediates are generated during CoVs infection that contribute to IFN production, but these CoVs remain highly pathogenic. As a matter of fact, CoVs have developed a set of elaborate mechanisms to evade or inhibit the host antiviral innate immune response during virus evolution [134,167]. The evasive strategies utilized by PEDV are classified into four major types: (1) inhibition of RLRs-mediated IFN production pathways, (2) inhibition of the activation of transcription factors responsible for IFN induction, (3) disruption of the signal cascades induced by IFN, and (4) hiding its viral RNA to avoid the exposure of viral RNA to immune sensors. In the past decade, accumulating evidence demonstrates that PEDV N protein, nsp1, PLP2, nsp5, nsp15, and nsp16 antagonize type I IFN or type III IFNs production [58,65,78,80,100,132,135,168]. This explains why only weak IFNs’ and cytokines’ expression is detected in PEDV-infected cells 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