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Epigenetic lifestyle of Epstein-Barr virus.
Seminars in Immunopathology ( IF 9 ) Pub Date : 2020-03-30 , DOI: 10.1007/s00281-020-00792-2
Alexander Buschle 1 , Wolfgang Hammerschmidt 1
Affiliation  

Epstein-Barr virus (EBV) is a model of herpesvirus latency and epigenetic changes. The virus preferentially infects human B-lymphocytes (and also other cell types) but does not turn them straight into virus factories. Instead, it establishes a strictly latent infection in them and concomitantly induces the activation and proliferation of infected B cells. How the virus establishes latency in its target cells is only partially understood, but its latent state has been studied intensively by many. During latency, several copies of the viral genome are maintained as minichromosomes in the nucleus. In latently infected cells, most viral genes are epigenetically repressed by cellular chromatin constituents and DNA methylation, but certain EBV genes are spared and remain expressed to support the latent state of the virus in its host cell. Latency is not a dead end, but the virus can escape from this state and reactivate. Reactivation is a coordinated process that requires the removal of repressive chromatin components and a gain in accessibility for viral and cellular factors and machines to support the entire transcriptional program of EBV’s ensuing lytic phase. We have a detailed picture of the initiating events of EBV’s lytic phase, which are orchestrated by a single viral protein – BZLF1. Its induced expression can lead to the expression of all lytic viral proteins, but initially it fosters the non-licensed amplification of viral DNA that is incorporated into preformed capsids. In the virions, the viral DNA is free of histones and lacks methylated cytosine residues which are lost during lytic DNA amplification. This review provides an overview of EBV’s dynamic epigenetic changes, which are an integral part of its ingenious lifestyle in human host cells.

中文翻译:

爱泼斯坦-巴尔病毒的表观遗传生活方式。

爱泼斯坦巴尔病毒(EBV)是疱疹病毒潜伏期和表观遗传变化的模型。该病毒优先感染人类B淋巴细胞(以及其他细胞类型),但不会直接将其转变为病毒工厂。相反,它在它们中建立了严格的潜伏感染,并同时诱导了受感染B细胞的活化和增殖。病毒如何在其靶细胞中建立潜伏期还只有部分了解,但是许多人已深入研究了其潜伏状态。在潜伏期中,病毒基因组的几个副本被保留为核中的微染色体。在潜伏感染的细胞中,大多数病毒基因受到细胞染色质成分和DNA甲基化的表观遗传抑制,但是某些EBV基因被保留下来并保持表达以支持病毒在其宿主细胞中的潜伏状态。延迟不是死胡同,但是病毒可以从此状态逃脱并重新激活。重新激活是一个协调的过程,需要去除抑制性染色质成分,并需要增加病毒和细胞因子以及机器的可及性,以支持EBV随后裂解阶段的整个转录程序。我们详细了解了EBV裂解阶段的启动事件,这些事件是由一种病毒蛋白BZLF1精心策划的。它的诱导表达可以导致所有裂解性病毒蛋白的表达,但最初它促进了掺入预先形成的衣壳中的病毒DNA的未经许可的扩增。在病毒体中,病毒DNA不含组蛋白,并且缺少甲基化的胞嘧啶残基,这些残基在裂解DNA扩增过程中会丢失。
更新日期:2020-03-30
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