Epstein-Barr Virus-host epigenetic interplay: mechanisms of regulation and therapeutic potential.

IF 4.4 2区医学 Q1 GENETICS & HEREDITY

Clinical Epigenetics Pub Date : 2026-07-06 DOI:10.1186/s13148-026-02181-2

Sanaz Baghban Rahimi, Ahmad Hosseinzadeh Adli, Hossein Bannazadeh Baghi, Vahdat Poortahmasebi, Jamal Sarvari

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引用次数: 0

Abstract

The Epstein-Barr virus (EBV) has evolved complex mechanisms to manipulate the host immune system and epigenetic machinery, enabling it to establish lifelong latent infection within host cells. Emerging evidence strongly indicates that the EBV acts as a main epigenetic manipulator by silencing host regulatory genes, altering host chromatin landscapes and exploiting B-cell biology. Key mechanisms include viral-mediated recruitment of host DNA methyltransferases and histone-modifying enzymes; modulation of host non-coding RNAs and chromatin architectural factors; and targeted disruption of interferon signaling through RNA methylation and restructuring of host chromatin. These integrated processes allow EBV to maintain a lifelong infection in humans, evade both innate and adaptive immunity, and respond to reactivation signals. Understanding the virus-host epigenetic interplay offers new opportunities for therapeutic interventions targeting epigenetic regulators in EBV-associated diseases.

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eb病毒-宿主表观遗传相互作用：调控机制和治疗潜力。

eb病毒（EBV）已经进化出复杂的机制来操纵宿主免疫系统和表观遗传机制，使其能够在宿主细胞内建立终身潜伏感染。新出现的证据有力地表明，EBV通过沉默宿主调控基因、改变宿主染色质景观和利用b细胞生物学，作为一个主要的表观遗传操纵者。主要机制包括病毒介导的宿主DNA甲基转移酶和组蛋白修饰酶的募集；宿主非编码rna和染色质结构因子的调控；以及通过RNA甲基化和宿主染色质重组靶向干扰素信号的破坏。这些综合过程使EBV在人类中维持终身感染，逃避先天免疫和适应性免疫，并对再激活信号作出反应。了解病毒-宿主表观遗传相互作用为针对ebv相关疾病的表观遗传调控因子的治疗干预提供了新的机会。

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来源期刊

Clinical Epigenetics ONCOLOGY-

自引率

5.30%

发文量

150

期刊介绍： Clinical Epigenetics, the official journal of the Clinical Epigenetics Society, is an open access, peer-reviewed journal that encompasses all aspects of epigenetic principles and mechanisms in relation to human disease, diagnosis and therapy. Clinical trials and research in disease model organisms are particularly welcome.