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It is produced through programmed \u22121 ribosomal frameshift in NS2A. Our previous study demonstrated that JEV NS1\u2032 could antagonize type I IFN (IFN-I) production, but the mechanism is still unclear. In the current study, we found that JEV NS1\u2032 inhibits the expression of MAVS, and knockdown of MAVS hampers inhibition of IFN-\u03b2 induction by NS1\u2032, suggesting that JEV NS1\u2032 inhibits IFN-I production by targeting MAVS. This finding is further supported by the result of the in vivo assay that showed the similar mortality caused by NS1\u2032-deficient virus and its wild type virus in MAVS-deficient mice. Based on our previous sequencing results of noncoding RNA in JEV-infected cells, microRNA-22 (miR-22) was identified to be a key regulator for MAVS expression during JEV infection. Furthermore, we demonstrated that JEV NS1\u2032 could induce the expression of miR-22 by increasing the binding of transcriptional factors, CREB and c-Rel, to the promoter elements of miR-22. Taken together, our results reveal a novel mechanism by which JEV NS1\u2032 antagonizes host MAVS by regulating miR-22, thereby inhibiting the IFN-I production and facilitating viral replication.<\/jats:p>","DOI":"10.4049\/jimmunol.1900946","type":"journal-article","created":{"date-parts":[[2020,1,29]],"date-time":"2020-01-29T20:35:13Z","timestamp":1580330113000},"page":"1287-1298","source":"Crossref","is-referenced-by-count":50,"title":["The Japanese Encephalitis Virus NS1\u2032 Protein Inhibits Type I IFN Production by Targeting MAVS"],"prefix":"10.1093","volume":"204","author":[{"given":"Dengyuan","family":"Zhou","sequence":"first","affiliation":[{"name":"State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University , Wuhan 430070, Hubei ,","place":["People\u2019s Republic of China"]},{"name":"Laboratory of Animal Virology, College of Veterinary Medicine, Huazhong Agricultural University , Wuhan 430070, Hubei ,","place":["People\u2019s Republic of 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