PMC:7281546 / 51016-52413 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":"5. Conclusions\nPEDV has caused epidemic and endemic infections in pig populations in many countries and has become a major economic threat to the swine industry. Previous studies have identified viral factors that target key signaling molecules in the RLRs’ pathways, as well as viral factors that target the downstream signaling pathways responsible for ISGs induction. Of the 23 PEDV-encoded proteins, at least 10 viral proteins have been identified as type I IFN antagonists [65,78]. The mechanisms utilized by PEDV nsp1, PLP2, nsp5, and N protein to antagonize type I IFN production have been clarified (Figure 3, [58,65,78,80,129]). However, the specific mechanisms of other viral proteins to inhibit type I IFN production remain largely unknown. At present, 11 PEDV proteins have been identified as type III IFNs’ antagonists. The suppression of type III IFN signaling by N protein, nsp1, as well as nsp15, has been reported, while the mechanisms utilized by these viral proteins need to be further investigated. In addition, the CoVs replication cycle may induce the changes of ER stress, cell apoptosis, autophagy pathways, which contain intricate virus-host interactions and cross-talk relationships. Thus, more researches for PEDV are needed to truly reflect viral evasions from innate immune defenses. The findings of PEDV-host interactions will help prevent and control PEDV 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