生物
N6-甲基腺苷
病毒复制
基因敲除
柯萨奇病毒
基因组
甲基转移酶
细胞生物学
遗传学
病毒
病毒学
基因
肠道病毒
甲基化
作者
Hainian Zhao,Zhiyun Gao,Jiawen Sun,Hongxiu Qiao,Yan Zhao,Yan Cui,Baoxin Zhao,Weijie Wang,Sandra Chiu,Xia Chuai
出处
期刊:Viruses
[Multidisciplinary Digital Publishing Institute]
日期:2024-09-11
卷期号:16 (9): 1448-1448
被引量:1
摘要
Enteroviruses such as coxsackievirus B3 are identified as a common cause of viral myocarditis, but the potential mechanism of its replication and pathogenesis are largely unknown. The genomes of a variety of viruses contain N6-methyladenosine (m6A), which plays important roles in virus replication. Here, by using the online bioinformatics tools SRAMP and indirect immunofluorescence assay (IFA), we predict that the CVB3 genome contains m6A sites and found that CVB3 infection could alter the expression and cellular localization of m6A-related proteins. Moreover, we found that 3-deazaadenosine (3-DAA), an m6A modification inhibitor, significantly decreased CVB3 replication. We also observed that the m6A methyltransferases methyltransferase-like protein 3 (METTL3) and METTL14 play positive roles in CVB3 replication, whereas m6A demethylases fat mass and obesity-associated protein (FTO) or AlkB homolog 5 (ALKBH5) have opposite effects. Knockdown of the m6A binding proteins YTH domain family protein 1 (YTHDF1), YTHDF2 and YTHDF3 strikingly decreased CVB3 replication. Finally, the m6A site mutation in the CVB3 genome decreased the replication of CVB3 compared with that in the CVB3 wild-type (WT) strain. Taken together, our results demonstrated that CVB3 could exploit m6A modification to promote viral replication, which provides new insights into the mechanism of the interaction between CVB3 and the host.
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