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Epigenetic Repression of Herpes Simplex Virus Infection by the Nucleosome Remodeler CHD3

机译：核小体重塑剂CHD3对单纯疱疹病毒感染的表观遗传抑制。

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Upon infection, the genome of herpes simplex virus is rapidly incorporated into nucleosomes displaying histone modifications characteristic of heterochromatic structures. The initiation of infection requires complex viral-cellular interactions that ultimately circumvent this repression by utilizing host cell enzymes to remove repressive histone marks and install those that promote viral gene expression. The reversion of repression and activation of viral gene expression is mediated by the cellular coactivator HCF-1 in association with histone demethylases and methyltransferases. However, the mechanisms and the components that are involved in the initial repression remain unclear. In this study, the chromatin remodeler chromodomain helicase DNA binding (CHD3) protein is identified as an important component of the initial repression of the herpesvirus genome. CHD3 localizes to early viral foci and suppresses viral gene expression. Depletion of CHD3 results in enhanced viral immediate early gene expression and an increase in the number of transcriptionally active viral genomes in the cell. Importantly, CHD3 can recognize the repressive histone marks that have been detected in the chromatin associated with the viral genome and this remodeler is important for ultimately reducing the levels of accessible viral genomes. A model is presented in which CHD3 represses viral infection in opposition to the actions of the HCF-1 coactivator complex. This dynamic, at least in part, determines the initiation of viral infection. >IMPORTANCE Chromatin modulation of herpesvirus infection is a dynamic process involving regulatory components that mediate suppression and those that promote viral gene expression and the progression of infection. The mechanisms by which the host cell employs the assembly and modulation of chromatin as an antiviral defense strategy against an invading herpesvirus remain unclear. This study defines a critical cellular component that mediates the initial repression of infecting HSV genomes and contributes to understanding the dynamics of this complex interplay between host cell and viral pathogen.
机译：感染后，单纯疱疹病毒的基因组被迅速整合到核小体中，显示出异色结构特征的组蛋白修饰。感染的开始需要复杂的病毒-细胞相互作用，这些相互作用最终通过利用宿主细胞酶去除抑制性组蛋白标记并安装促进病毒基因表达的标记来绕过这种抑制。阻遏和病毒基因表达激活的逆转是由细胞共激活因子HCF-1与组蛋白脱甲基酶和甲基转移酶介导的。但是，尚不清楚初始抑制所涉及的机制和组件。在这项研究中，染色质重塑剂染色体域解旋酶DNA结合（CHD3）蛋白被确定为疱疹病毒基因组初始抑制的重要组成部分。 CHD3定位于早期病毒灶，并抑制病毒基因表达。 CHD3的减少导致病毒立即早期基因表达增强，并增加细胞中转录活性病毒基因组的数量。重要的是，CHD3可以识别在与病毒基因组相关的染色质中已检测到的阻遏性组蛋白标记，并且该重塑剂对于最终降低可及的病毒基因组水平非常重要。提出了一种模型，其中CHD3抑制病毒感染，与HCF-1共激活因子复合物的作用相反。这种动态至少部分地决定了病毒感染的开始。 >重要意义疱疹病毒感染的染色质调节是一个动态过程，涉及调节成分，这些成分介导抑制作用，并促进病毒基因表达和感染进程。宿主细胞利用染色质的组装和调节作为针对入侵性疱疹病毒的抗病毒防御策略的机制仍不清楚。这项研究确定了关键的细胞成分，该成分介导了感染HSV基因组的初始抑制，并有助于理解宿主细胞和病毒病原体之间这种复杂相互作用的动力学。

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