爱泼斯坦巴尔是人类第一个致癌病毒,与许多淋巴增生和恶性疾病密切相关,包括HL,BL,NPC,和GC。EBV建立了描绘双相病毒生命周期的终身持续性感染:潜伏期和裂解复制。B细胞是EBV潜伏基因的关键区域,其中病毒基因表达被抑制,促进病毒基因组维持和免疫识别逃避。裂解液重新激活后,病毒基因表达诱导其复制,后代生产,和传输。TSG表达中表观遗传调控的失调导致癌变。一些研究表明,EBV与异常的病毒DNA和宿主基因组甲基化模式有关。促进免疫监测,识别规避和宿主细胞持久性。在其他表观遗传修饰中,DNA甲基化抑制大多数病毒潜伏基因启动子,保留一些,并作为激活EBV裂解周期的先决条件,产生病毒后代。它通过将细胞重编程为致癌基因来影响宿主的表观基因组,持久的表型,在一些恶性肿瘤中很明显。在其生命周期的每个阶段,EBV利用表观遗传调控的细胞机制,暗示其独特的宿主-病原体关系。本文综述了DNA甲基化在几个EBV相关启动子区的调控作用。以及病理条件下的宿主基因组,突出涉及潜伏的病毒基因,EBV感染的裂解期和潜伏裂解期。此外,它提供了对EBV中基于甲基化的途径的图解见解。
Epstein Barr is the first-in-human oncogenic virus, closely related to numerous lymphoproliferative and malignant diseases, including HL, BL, NPC, and GC. EBV establishes life-long persistence infection portraying a biphasic viral life cycle: latent period and lytic replication. B-cells serve as critical regions for EBV latent genes, wherein viral gene expression is suppressed, promoting viral genome maintenance and immune recognition evasion. Upon its lytic reactivation, viral gene expression induces its replication, progeny production, and transmission. Dysregulations of epigenetic regulation in expressions of TSGs lead to carcinogenesis. Several studies reveal that EBV is associated with aberrant viral DNA and host genome methylation patterns, promoting immune monitoring, recognition evasiveness and host cell persistence. Among other epigenetic modifications, DNA methylation suppresses the majority of viral latent gene promoters, sparing a few, and acts as a prerequisite for activating EBV\'s lytic cycle, giving rise to viral progeny. It affects the host\'s epigenome via reprogramming cells to oncogenic, long-lasting phenotypes, as evident in several malignancies. At each phase of its life cycle, EBV exploits cellular mechanisms of epigenetic regulation, implying its unique host-pathogen relationship. This review summarized the DNA methylation\'s regulatory roles on several EBV-related promoter regions, along with the host genome in pathological conditions, highlights viral genes involved in a latent, lytic and latent-lytic phase of EBV infection. Moreover, it provides diagrammatic insights into methylation-based pathways in EBV.