Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.

Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.
复制标题

与VP16或VP16诱导的复合体相关的宿主因素不同地影响HSV-1裂解感染。

DOI:
10.1002/rmv.2394
复制
发表时间:
2022-11
影响因子:
11.1
通讯作者:
Zhu, Liqian
Zhu, Liqian
中科院分区:
医学2区
文献类型:
--
作者:
Ding, Xiuyan;Neumann, Donna M.;Zhu, Liqian

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单纯疱疹病毒1型(HSV-1)是一种重要的人类嗜神经性病原体。粘膜或皮肤上皮细胞裂解感染后,主要在感觉神经元中建立终生潜伏期,应激可周期性地重新激活感觉神经元,导致疾病复发和病毒传播。在病毒的生产性感染过程中,被膜蛋白VP16是HSV-1病毒粒子的组成部分,与宿主细胞因子-1(HCF-1)和POU结构域蛋白OCT-1物理上结合,构建VP16诱导的复合体,这是刺激即刻早期(IE)基因转录和启动裂解程序所必需的。除了HCF-1和Oct-1外,VP16还与一系列其他宿主因子结合,使VP16诱导的调控开关激活或失活病毒基因转录。此外,VP16通过与多种宿主分子结合而影响不同的信号通路,这些宿主分子主要与先天免疫反应、RNA聚合酶、分子伴侣以及病毒感染诱导的宿主关闭有关。VP16还对给定的寄主因子进行功能补偿,如ppar-γ和ç-catenin。在这篇综述中,我们提供了关于VP16和协调病毒感染的宿主因素之间相互作用的最新见解的概述。
Herpes simplex virus type 1 (HSV‐1) is an important human pathogen with neurotropism. Following lytic infection in mucosal or skin epithelium, life‐long latency is established mainly in sensory neurons, which can periodically reactivate by stress, leading to recurrent disease and virus transmission. During the virus's productive infection, the tegument protein VP16, a component of HSV‐1 virion, is physically associated with two cellular factors, host cell factor‐1 (HCF‐1), and POU domain protein Oct‐1, to construct the VP16‐induced complex, which is essential to stimulate immediate early (IE)‐gene transcription as well as initiate the lytic programme. Apart from HCF‐1 and Oct‐1, VP16 also associates with a series of other host factors, making a VP16‐induced regulatory switch to either activate or inactivate virus gene transcription. In addition, VP16 has effects on distinct signalling pathways via binding to various host molecules that are essentially related to innate immune responses, RNA polymerases, molecular chaperones, and virus infection‐induced host shutoff. VP16 also functionally compensates for given host factors, such as PPAR‐γ and ß‐catenin. In this review, we provide an overview of the updated insights on the interplay between VP16 and the host factors that coordinate virus infection.
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