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Marek's disease virus-encoded microRNA-M6-5p facilitates viral latent infection by targeting histone demethylase KDM2B

文献类型： 外文期刊

作者： Zhou, Linyi 1 ; Zhu, Runan 1 ; Jiang, Bo 1 ; Cheng, Jing 1 ; Liu, Wenxiao 1 ; Yao, Yongxiu 5 ; Li, Yongqing 1 ;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing, Peoples R China

2.Beijing Key Lab Prevent & Control Infect Dis Lives, Beijing, Peoples R China

3.Sino UK Joint Lab Prevent & Control Infect Dis Liv, Beijing, Peoples R China

4.Beijing Univ Agr, Coll Anim Sci & Technol, Beijing, Peoples R China

5.Pirbright Inst, Pirbright, England

6.UK China Ctr Excellence Res Avian Dis, Pirbright, England

关键词： MDV; latent infection; miRNAs; epigenetic regulation; KDM2B

期刊名称：JOURNAL OF VIROLOGY （ 影响因子：3.8； 五年影响因子：3.9 ）

ISSN： 0022-538X

年卷期： 2025 年 99 卷 2 期

页码：

收录情况： SCI

摘要： Marek's disease virus (MDV), a highly contagious and oncogenic avian alphaherpesvirus, establishes a latent infection primarily in CD4+ T cells. Latent infec tions are necessary for both persistent lifelong MDV infection and viral tumorigene sis. MicroRNAs (miRNAs) play critical roles as post-transcriptional regulators of viral infections. However, the role of miRNAs in regulating MDV latency remains unclear. In this study, we found that an MDV-encoded miRNA, miR-M6-5p, inhibited viral lytic replication in vitro by functional screening and that infection with an MDV mutant lacking miR-M6-5p resulted in impaired MDV latency, proliferation, and tumor formation in vivo. Importantly, we identified lysine-specific demethylase 2b (KDM2B), an important epigenetic factor, as a target of miR-M6-5p. Furthermore, KDM2B knockdown increased the level of the transcriptionally repressive histone mark H3K27me3 on the key lytic gene pp38 promoter, accompanied by suppression of pp38 expression and reduced latentto-lytic switch in MDV-latently infected cells, while treatment of cells with H3K27me3 inhibitors (GSK126 and Tazemetostat) markedly promoted the expression of pp38 and MDV reactivation from latency. Thus, miR-M6-5p facilitates MDV latency by epigenet ically suppressing pp38 expression by targeting KDM2B. These findings unravel the mechanism by which a virus-encoded miRNA plays a critical role in the regulation of latent MDV infection.

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