The Epstein–Barr Virus (EBV) is a double-stranded DNA-based human tumor virus that was first isolated in 1964 from lymphoma biopsies. Since its initial discovery, EBV has been identified as a major contributor to numerous cancers and chronic autoimmune disorders. The virus is particularly efficient at infecting B-cells but can also infect epithelial cells, utilizing an array of epigenetic strategies to establish long-term latent infection. The association with histone modifications, alteration of DNA methylation patterns in host and viral genomes, and microRNA targeting of host cell factors are core epigenetic strategies that drive interactions between host and virus, which are necessary for viral persistence and progression of EBV-associated diseases. Therefore, understanding epigenetic regulation and its role in post-entry viral dynamics is an elusive area of EBV research. Here, we present current outlooks of EBV epigenetic regulation as it pertains to viral interactions with its host during latent infection and its propensity to induce tumorigenesis. We review the important epigenetic regulators of EBV latency and explore how the strategies involved during latent infection drive differential epigenetic profiles and host-virus interactions in EBV-associated cancers.
爱泼斯坦-巴尔病毒（EBV）是一种双链DNA人类肿瘤病毒，于1964年首次从淋巴瘤活检组织中分离获得。自发现以来，该病毒已被证实是多种癌症及慢性自身免疫性疾病的重要致病因子。EBV对B细胞具有高效感染能力，同时也能感染上皮细胞，通过一系列表观遗传策略建立长期潜伏感染。其核心表观遗传机制包括组蛋白修饰、宿主与病毒基因组DNA甲基化模式改变，以及通过microRNA靶向宿主细胞因子，这些机制驱动宿主与病毒间的相互作用，对病毒持续感染及EBV相关疾病进展至关重要。因此，理解表观遗传调控及其在病毒侵入后动态变化中的作用，已成为EBV研究中亟待深入探索的领域。本文系统阐述了EBV潜伏感染期间病毒与宿主相互作用的表观遗传调控机制，及其诱导肿瘤发生的倾向性，重点综述了EBV潜伏期的重要表观遗传调控因子，并探讨潜伏感染相关策略如何驱动EBV相关癌症中差异化的表观遗传特征与宿主-病毒相互作用。
Epigenetic Mechanisms in Latent Epstein-Barr Virus Infection and Associated Cancers
肿瘤(癌症)患者之家