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Coronavirus infection induces ER stress and the interferon response, which reflects different adaptive cellular processes. An understanding of how coronavirus-elicited ER stress is actively involved in viral replication and manipulates the host IFN-I response has remained elusive. Here, TGEV inhibited host miR-30a-5p via the ER stress sensor IRE1\u03b1, which led to the increased expression of negative regulators of JAK-STAT signaling cascades, namely, SOCS1 and SOCS3. Increased SOCS1 or SOCS3 expression impaired the IFN-I antiviral response, promoting TGEV replication. These findings enhance our understanding of the strategies used by coronaviruses to antagonize IFN-I innate immunity via IRE1\u03b1-mediated manipulation of the miR-30a-5p\/SOCS axis, highlighting the crucial role of IRE1\u03b1 in innate antiviral resistance and the potential of IRE1\u03b1 as a novel target against coronavirus infection.<\/jats:p>","DOI":"10.1128\/jvi.00728-18","type":"journal-article","created":{"date-parts":[[2018,9,3]],"date-time":"2018-09-03T09:06:29Z","timestamp":1535965589000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":81,"title":["The Coronavirus Transmissible Gastroenteritis Virus Evades the Type I Interferon Response through IRE1\u03b1-Mediated Manipulation of the MicroRNA miR-30a-5p\/SOCS1\/3 Axis"],"prefix":"10.1128","volume":"92","author":[{"given":"Yanlong","family":"Ma","sequence":"first","affiliation":[{"name":"State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary 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