PMC:7281546 / 38457-40562
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7281546","sourcedb":"PMC","sourceid":"7281546","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7281546","text":"CoV nsp5 is called 3C-like protease (3CLpro), that resembles the 3Cpro of other RNA viruses. For CoV, the polyprotein precursors (pp1a and pp1b) are mainly processed to generate mature nonstructural proteins by 3CLpro. To date, the 3CLpro of CoVs, including PEDV and PDCoV, have been confirmed to antagonize type I IFN production by the cleavage of NF-κB essential modulator (NEMO) and STAT2 [100,207,208]. NEMO is essential for RNA virus-induced activation of NF-κB, IRF3, and IRF7 [209]. NEMO is required for MAVS-induced IKKα/β activation and is also crucial for the activation of TBK1/IKKε [149]. To establish successful infections, PEDV targets NEMO to subvert host innate immune responses. PEDV nsp5 significantly inhibits Sendai virus (SeV)-induced IFN-β synthesis and the process depends on its protease activity [100]. Further experiments show that PEDV nsp5 inhibits RIG-I/MDA5 signaling and targets the upstream of TBK1. The cleavage of NEMO by nsp5 is identified as responsible for this inhibitive effect. The PEDV nsp5-mediated cleavage of NEMO efficiently blocks NEMO-mediated downstream signaling. The cleavage site within NEMO that is grasped by nsp5 has been determined. Of these reported immune evasion strategies employed by CoVs, the cleavage of innate immune adaptors is a particularly effective manner to disrupt antiviral responses. Nsp5 is essential for the life cycle of PEDV and other CoVs [210,211]. It is a potential target for the development of anti-coronaviral therapeutics. Although PEDV nsp5 does not target STAT2 mediated type Ⅰ IFN signaling pathway, PEDV nsp7 has been reported to inhibit the STAT1 and STAT2 induced activation of ISRE [212]. Nsp7 competes with Karyopherin α (KPNA1), which is an adaptor mediating nuclear translocation of ISGF3, in combination with STAT1, to block ISGF3 nuclear transport. However, the expression and phosphorylation of STAT1 and STAT2 are not affected by PEDV nsp7. In fact, PEDV infection degrades STAT1, leading to the inhibition of IFN signaling [170]. 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