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Here, we identify the RNA\u2010binding protein RBM25 as a potent, broad\u2010spectrum host antiviral factor, independently of the type I interferon (IFN\u2010I) pathway. Viral infection downregulates RBM25 expression, and RBM25\u2010deficient mice exhibit enhanced susceptibility to multiple viruses and more aggravated tissue damage. In vitro, RBM25 inhibits the viral infection and replication across a spectrum of RNA and DNA viruses. Mechanistically, the antiviral activity of RBM25 is independent of IFN\u2010I signaling and is instead linked to an early blockade in the viral life cycle. RBM25 specifically impedes viral cell entry through the suppression of the host GTPase Rab22a, a well\u2010known facilitator of viral endocytosis. Virus infection\u2010elicited downregulation of RBM25 results in Rab22a upregulation, which consequently potentiates viral entry. Furthermore, we elucidate the post\u2010transcriptional mechanisms that RBM25 interacts with RC3H1 (ring finger and CCCH\u2010type domains 1) to form an RNA\u2010binding complex that binds and destabilizes\n                    <jats:italic>Rab22a<\/jats:italic>\n                    mRNA, thereby limiting its protein translation. Collectively, our work unveils the RBM25\/RC3H1\u2010Rab22a axis as an interferon\u2010independent post\u2010transcriptional pathway that governs viral entry by modulating the mRNA stability of a critical host endocytosis factor, which presents a potential target for developing broad\u2010spectrum antiviral strategies.\n                  <\/jats:p>","DOI":"10.1002\/advs.76160","type":"journal-article","created":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T10:23:42Z","timestamp":1781605422000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["RNA\u2010Binding Protein RBM25 Targets the mRNA Stability of GTPase Rab22a to Restrict Viral Entry and Infection"],"prefix":"10.1002","volume":"13","author":[{"given":"Yingying","family":"Ding","sequence":"first","affiliation":[{"name":"National Key Laboratory of Immunity &amp; Inflammation Department of Pathogen Biology Naval Medical University  Shanghai 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