Swine TRIM25 inhibits vesicular stomatitis virus replication by activation of type I IFN signaling pathway and binding vRNA
10.4142/jvs.25139
- Author:
Ying CAO
;
Jinxia ZHANG
;
Dongwan YOO
;
Haowen ZHANG
;
Dandan JIANG
;
Yue HU
;
Xiaoyan CONG
;
Juntong LI
;
Xiangju WU
;
Yijun DU
;
Jing QI
;
Juan HUANG
- Publication Type:Research Report
- From:Journal of Veterinary Science
2026;27(3):e25-
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 interferonstimulated 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.
