生物
病毒学
基因敲除
先天免疫系统
病毒
病毒复制
日本脑炎
RNA病毒
核糖核酸
免疫系统
基因
遗传学
脑炎
作者
Min Yao,Zhiyuan Cheng,Tongwen Xu,Yuexiang Li,Wei Ye,Hui Zhang,Lei He,Liang Zhang,Yingfeng Lei,Fanglin Zhang,Xin Lv
标识
DOI:10.1186/s12985-023-02275-w
摘要
Abstract N6-methyladenosine (m6A) is present in diverse viral RNA and plays important regulatory roles in virus replication and host antiviral innate immunity. However, the role of m6A in regulating JEV replication has not been investigated. Here, we show that the JEV genome contains m6A modification upon infection of mouse neuroblast cells (neuro2a). JEV infection results in a decrease in the expression of m6A writer METTL3 in mouse brain tissue. METTL3 knockdown by siRNA leads to a substantial decrease in JEV replication and the production of progeny viruses at 48 hpi. Mechanically, JEV triggered a considerable increase in the innate immune response of METTL3 knockdown neuro2a cells compared to the control cells. Our study has revealed the distinctive m6A signatures of both the virus and host in neuro2a cells infected with JEV, illustrating the positive role of m6A modification in JEV infection. Our study further enhances understanding of the role of m6A modification in Flaviviridae viruses.
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