{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T05:36:50Z","timestamp":1789105010408,"version":"build-2803163510"},"update-to":[{"DOI":"10.1371\/journal.ppat.1014032","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T00:00:00Z","timestamp":1772755200000}}],"reference-count":39,"publisher":"Public Library of Science (PLoS)","issue":"3","license":[{"start":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T00:00:00Z","timestamp":1772496000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Fund of China","doi-asserted-by":"crossref","award":["32373000"],"award-info":[{"award-number":["32373000"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Shandong Provincial Key Research and Development Program","award":["2022CXGC020711-2"],"award-info":[{"award-number":["2022CXGC020711-2"]}]},{"name":"Jinan Innovation Team","award":["202228060"],"award-info":[{"award-number":["202228060"]}]},{"name":"Jinan Research Pioneer Workshop","award":["202333059"],"award-info":[{"award-number":["202333059"]}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>The activation of type I interferon (IFN-I) signaling is crucial for defending host cells against viral infections. A comprehensive IFN-I response necessitates the activation of several cellular factors, among them Interferon Regulator Factor 7 (IRF7). Nonetheless, the mechanisms governing IRF7 inactivation in response to viral infection remain largely unknown. Here, we illustrate that Cluster of differentiation 97 (CD97), a G protein-coupled receptor, interacts with PPM1G via intracellular Arg-819 and Arg-822 residues. PPM1G then recruits and dephosphorylates IRF7, leading to its inhibition. CD97-mediated inactivation of IRF7 impedes its translocation into the nucleus and subsequent activation of IFN-I, ultimately promoting the viral replication. Moreover, mice lacking CD97 display heightened resistance to viral infection. The compound sanguinarine (SANG) hinders viral replication by dampening CD97 expression. This study provides a basis for CD97 as a potential antiviral target and SANG as a candidate antiviral small molecule drug.<\/jats:p>","DOI":"10.1371\/journal.ppat.1014032","type":"journal-article","created":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T18:32:42Z","timestamp":1772562762000},"page":"e1014032","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":3,"title":["The CD97-PPM1G axis dampens antiviral immunity by dephosphorylating IRF7 in type I interferon 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