TRIM25 inhibits Japanese encephalitis virus replication in U251 cells by up-regulation of the IFN-β and degrading the viral capsid protein
10.3760/cma.j.cn112309-20240418-00136
- VernacularTitle:TRIM25通过上调IFN-β和降解病毒衣壳蛋白抑制乙型脑炎病毒在U251细胞中的复制
- Author:
Chen CHEN
1
;
Kui XU
1
;
Zhuang ZHU
1
;
Rong HUANG
1
;
Yalan FENG
1
;
Ning TAN
1
;
Yajing HE
1
;
Yue LUO
1
;
Jian YANG
1
;
Lei YUAN
1
Author Information
1. 川北医学院，基础医学与法医学院，基础医学研究中心，南充 637100
- Publication Type:Journal Article
- Keywords:
Japanese encephalitis virus;
Tripartite motif-containing protein 25;
Innate immunity;
Antiviral activity
- From:
Chinese Journal of Microbiology and Immunology
2025;45(2):99-107
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the inhibitory effect of tripartite motif-containing 25 (TRIM25) on the replication of Japanese encephalitis virus (JEV) in cells and its molecular mechanism.Methods:Human glioma cells (U251 cells) and Kunming mice were infected with JEV, and then the cells and brain tissue samples were collected. The transcription levels of six TRIM genes were detected by real-time PCR, and the expression of TRIM25 in cells was detected by Western blot. U251 and A549 cells overexpressed with TRIM25 and U251 cells knocked out with TRIM25 gene were constructed. Cells were infected with JEV, and the replication of JEV was detected by viral plaque assay, real-time PCR and Western blot. The interaction of TRIM25 with viral proteins was investigated by co-immunoprecipitation (Co-IP) and indirect immunofluorescence assay. The expression of IFN-β in overexpressed TRIM25 cells was detected by real-time PCR and ELISA.Results:JEV infection promoted the expression of TRIM25 in cells and mouse brain tissues. TRIM25 overexpression restricted JEV replication in U251 and A549 cells, while TRIM25 knockout enhanced JEV replication. TRIM25 overexpression upregulated the level of IFN-β in cells. TRIM25 interacted with JEV capsid protein and promoted the degradation of capsid protein.Conclusion:TRIM25 can inhibit the replication of JEV in cells by upregulating IFN-β and promoting the degradation of JEV C protein.
