Effects of key molecules in m6A methylation modification on the replication and proliferation of Japanese encephalitis virus
10.3969/j.issn.1002-2694.2025.00.023
- VernacularTitle:m6A甲基化修饰过程中关键分子对日本脑炎病毒复制增殖影响的研究
- Author:
Zhi-rong CHENG
1
;
Min YAO
;
Xue-yun LI
;
Chao-jie CHAI
;
Pin-xiang DANG
;
Si-yu WANG
;
Fang-lin ZHANG
;
Xin LYU
Author Information
1. 延安大学生命科学学院,延安 716000;空军军医大学基础医学院,微生物与病原生物学教研室,西安 710032
- Publication Type:Journal Article
- Keywords:
fat mass and obesity-associated protein(FTO);
methyltransferase like protein 3(METTL3);
N6-methylade-nosine(m6A);
Japanese encephalitis virus(JEV);
interferon(IFN)
- From:
Chinese Journal of Zoonoses
2025;41(2):150-157
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed at investigating the effects of demethylase fat mass and obesity-associated protein(FTO)and methyltransferase methyltransferase like protein 3(METTL3),key molecules in N6-methyladenosine(m6A)modification,on the replication and proliferation of Japanese encephalitis virus(JEV).Recombinant lentiviruses were generated by packaging the FTO and green fluorescent protein into lentiviral vectors.Neuro2a cells,a mouse neuroblastoma cell line,were infected with the lentivirus,and stable FTO-expressing cell lines were obtained through puromycin selection.Successful overexpression of FTO was confirmed through fluorescence microscopy,real-time quantitative PCR,and western blot analysis.When Neuro2a cells overexpressing FTO were infected with JEV,the overexpression of FTO decreased JEV replication in the cells,and increased the expression of interferon(IFN)and related molecules.Additionally,treatment of JEV-infected Neuro2a cells with the METTL3-specific inhibitor STM2457 resulted in a dose-dependent decrease in JEV replication and viral protein expression.These findings suggested that lowering m6A methylation levels inhibits JEV replication,thus shedding light on the regulatory role of methylation modification in JEV replication.
