Journal of veterinary science · 2026
Swine TRIM25 inhibits vesicular stomatitis virus replication by activation of type I IFN signaling pathway and binding vRNA.
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Cao Ying, Zhang Jinxia, Yoo Dongwan, Zhang Haowen, Jiang Dandan, Hu Yue, Cong Xiaoyan, Li Juntong, Wu Xiangju, Du Yijun, Qi Jing, Huang Juan
Аннотация
IMPORTANCE: Vesicular 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.
OBJECTIVE: To define the mechanism by which swine TRIM25 restricts vesicular stomatitis virus replication.
METHODS: Porcine 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.
RESULTS: TRIM25 overexpression reduced viral RNA and infectious titers, whereas TRIM25 knockdown increased replication (p < 0.01). TRIM25 increased interferon-beta and interferon-stimulated gene expression and enhanced interferon-beta and interferon-stimulated response element promoter activity (p < 0.01). Mechanistically, TRIM25 promoted Lys63-linked ubiquitination of RIG-I and increased phosphorylation of TANK-binding kinase 1 and interferon regulatory factor 3. TRIM25 also bound vesicular stomatitis virus genomic RNA, and binding required the C-terminal region.
CONCLUSIONS AND RELEVANCE: Porcine TRIM25 restricts vesicular stomatitis virus replication by amplifying type I interferon signaling and directly binding viral RNA.
OBJECTIVE: To define the mechanism by which swine TRIM25 restricts vesicular stomatitis virus replication.
METHODS: Porcine 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.
RESULTS: TRIM25 overexpression reduced viral RNA and infectious titers, whereas TRIM25 knockdown increased replication (p < 0.01). TRIM25 increased interferon-beta and interferon-stimulated gene expression and enhanced interferon-beta and interferon-stimulated response element promoter activity (p < 0.01). Mechanistically, TRIM25 promoted Lys63-linked ubiquitination of RIG-I and increased phosphorylation of TANK-binding kinase 1 and interferon regulatory factor 3. TRIM25 also bound vesicular stomatitis virus genomic RNA, and binding required the C-terminal region.
CONCLUSIONS AND RELEVANCE: Porcine TRIM25 restricts vesicular stomatitis virus replication by amplifying type I interferon signaling and directly binding viral RNA.