Human immunodeficiency virus 1 (HIV-1) replicates through the integration of its viral DNA into the genome of human immune target cells. Chronically infected individuals thus carry a genomic burden of virus-derived sequences that persists through antiretroviral therapy. This burden consists of a small fraction of intact, but transcriptionally silenced, i.e. latent, viral genomes and a dominant fraction of defective sequences. Remarkably, all viral-derived sequences are subject to interaction with host cellular physiology at various levels. In this review, we focus on epigenetic aspects of this interaction. We provide a comprehensive overview of how epigenetic mechanisms contribute to establishment and maintenance of HIV-1 gene repression during latency. We furthermore summarize findings indicating that HIV-1 infection leads to changes in the epigenome of target and bystander immune cells. Finally, we discuss how an improved understanding of epigenetic features and mechanisms involved in HIV-1 infection could be exploited for clinical use.

中文翻译：

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HIV-1慢性感染的表观遗传串扰。

人类免疫缺陷病毒1（HIV-1）通过将其病毒DNA整合到人类免疫靶细胞的基因组中而复制。因此，慢性感染的个体携带了病毒衍生序列的基因组负担，并通过抗逆转录病毒疗法持续存在。该负担由一小部分完整但转录沉默的病毒基因组和缺陷序列的主要部分组成。值得注意的是，所有病毒来源的序列都在不同水平上与宿主细胞生理学相互作用。在这篇综述中，我们集中于这种相互作用的表观遗传方面。我们提供了有关后代过程中表观遗传机制如何有助于建立和维持HIV-1基因抑制的全面概述。我们进一步总结发现，表明HIV-1感染会导致靶标和旁观者免疫细胞的表观基因组发生变化。最后，我们讨论如何更好地理解与HIV-1感染有关的表观遗传学特征和机制，以用于临床。