Carriere Jessica, Rao Youliang, Liu Qizhi, Lin Xiaoxi, Zhao Jun, Feng Pinghui
Section of Infection and Immunity, Ostrow School of Dentistry, University of Southern California, Los Angeles, CA, United States.
Front Microbiol. 2019 Nov 14;10:2647. doi: 10.3389/fmicb.2019.02647. eCollection 2019.
Herpesviruses constitute a large family of disease-causing DNA viruses. Each herpesvirus strain is capable of infecting particular organisms with a specific cell tropism. Upon infection, pattern recognition receptors (PRRs) recognize conserved viral features to trigger signaling cascades that culminate in the production of interferons and pro-inflammatory cytokines. To invoke a proper immune response while avoiding collateral tissue damage, signaling proteins involved in these cascades are tightly regulated by post-translational modifications (PTMs). Herpesviruses have developed strategies to subvert innate immune signaling pathways in order to ensure efficient viral replication and achieve persistent infection. The ability of these viruses to control the proteins involved in these signaling cascades post-translationally, either directly virus-encoded enzymes or indirectly through the deregulation of cellular enzymes, has been widely reported. This ability provides herpesviruses with a powerful tool to shut off or restrict host antiviral and inflammatory responses. In this review, we highlight recent findings on the herpesvirus-mediated post-translational control along PRR-mediated signaling pathways.
疱疹病毒是一大类致病DNA病毒。每种疱疹病毒毒株都能够感染具有特定细胞嗜性的特定生物体。感染后，模式识别受体（PRR）识别保守的病毒特征，触发信号级联反应，最终导致干扰素和促炎细胞因子的产生。为了引发适当的免疫反应同时避免附带的组织损伤，参与这些级联反应的信号蛋白受到翻译后修饰（PTM）的严格调控。疱疹病毒已经开发出策略来颠覆先天免疫信号通路，以确保病毒的有效复制并实现持续感染。这些病毒通过病毒编码的酶直接或通过细胞酶的失调间接在翻译后控制参与这些信号级联反应的蛋白质的能力已被广泛报道。这种能力为疱疹病毒提供了一个强大的工具来关闭或限制宿主的抗病毒和炎症反应。在这篇综述中，我们重点介绍了疱疹病毒介导的沿PRR介导的信号通路的翻译后控制的最新发现。
