Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center - Shreveport, United States.
Curr Opin Virol. 2017 Oct;26:74-80. doi: 10.1016/j.coviro.2017.07.017. Epub 2017 Aug 4.
Like all herpesviruses, the ability of Epstein-Barr virus (EBV) to establish life-long persistent infections is related to a biphasic viral lifecycle that involves latency and reactivation/lytic replication. Memory B cells serve as the EBV latency compartment where silencing of viral gene expression allows maintenance of the viral genome, avoidance of immune surveillance, and life-long carriage. Upon viral reactivation, viral gene expression is induced for replication, progeny virion production, and viral spread. EBV uses the host epigenetic machinery to regulate its distinct viral gene expression states. However, epigenetic manipulation by EBV affects the host epigenome by reprogramming cells in ways that leave long-lasting, oncogenic phenotypes. Such virally-induced epigenetic alterations are evident in EBV-associated cancers.
与所有疱疹病毒一样,EB 病毒(EBV)建立终身持续性感染的能力与其双相病毒生命周期有关,该周期涉及潜伏期和再激活/裂解复制。记忆 B 细胞是 EBV 潜伏期所在的部位,其中病毒基因表达的沉默允许维持病毒基因组、避免免疫监视和终身携带。当病毒再次激活时,病毒基因表达被诱导以进行复制、产生子代病毒粒子和病毒传播。EBV 使用宿主表观遗传机制来调节其独特的病毒基因表达状态。然而,EBV 的表观遗传操作通过以留下持久致癌表型的方式重新编程细胞来影响宿主表观基因组。这种由病毒引起的表观遗传改变在 EBV 相关癌症中很明显。