The dynamic nature of interactions between invading viral pathogens and their hosts has fascinated scientists for several decades. The well-known capacity of herpes simplex virus (HSV) to establish life-long infections in humans reflects a dynamic balance between maintaining a latent state in which viral genomes are silenced and re-entry into the lytic phase during reactivation. Silencing of the viral genome has been shown to be a function of innate immune signalling, intrinsic cellular antiviral mechanisms and epigenetic repression. Thus, although many important observations have been made identifying cellular processes that contribute to the repression of the viral genome and latency, the field has lacked an understanding of how these factors work together. In this issue of EMBO Reports, Suzich et al (2021) present convincing evidence that brings together individual observations into a cohesive model that explains many of these outstanding mysteries. Here, we will review the background data that lead to this outstanding piece of work.

中文翻译：

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新模型整合了先天反应、PML-NB 形成、表观遗传控制和潜伏期重新激活

几十年来，入侵病毒病原体与其宿主之间相互作用的动态特性一直让科学家们着迷。众所周知，单纯疱疹病毒 (HSV) 在人类中建立终身感染的能力反映了维持病毒基因组被沉默的潜伏状态与重新激活期间重新进入裂解阶段之间的动态平衡。病毒基因组的沉默已被证明是先天免疫信号、内在细胞抗病毒机制和表观遗传抑制的功能。因此，尽管已经进行了许多重要的观察，以确定有助于抑制病毒基因组和潜伏期的细胞过程，但该领域缺乏对这些因素如何协同工作的理解。在本期EMBO 报告中，Suzichet al (2021) 提出了令人信服的证据，将个人观察结果整合到一个有凝聚力的模型中，从而解释了其中许多未解之谜。在这里，我们将回顾导致这项杰出工作的背景数据。