ArticleJournal of veterinary science2026
Swine TRIM25 inhibits vesicular stomatitis virus replication by activation of type I IFN signaling pathway and binding vRNA.
Article in Journal of veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
importanceVesicular stomatitis virus is a zoonotic rhabdovirus that infects livestock and can cause economically important disease. Tripartite motif-containing 25 (TRIM25) is an E3 ubiquitin ligase involved in innate antiviral signaling, but its role in pigs during vesicular stomatitis virus infection is unclear.
objectiveTo define the mechanism by which swine TRIM25 restricts vesicular stomatitis virus replication.
methodsPorcine 3D4/21 cells with TRIM25 overexpression or knockdown were infected with vesicular stomatitis virus. Viral replication was quantified by immunoblotting, quantitative reverse transcription polymerase chain reaction, and 50% tissue culture infectious dose assays. Type I interferon signaling was assessed by transcript quantification, interferon-beta and interferon-stimulated response element reporter assays, and co-immunoprecipitation. Viral RNA binding was tested by RNA immunoprecipitation.
resultsTRIM25 overexpression reduced viral RNA and infectious titers, whereas TRIM25 knockdown increased replication ( CONCLUSIONS AND RELEVANCE: Porcine TRIM25 restricts vesicular stomatitis virus replication by amplifying type I interferon signaling and directly binding viral RNA.
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