单纯疱疹病毒Ⅰ型ICP0蛋白的E3泛素连接酶活性在抑制宿主免疫反应中的作用

单纯疱疹病毒Ⅰ型(herpes simplex virus type 1,HSV-1)编码的具有泛素连接酶(ubiquitin-ligase enzymes 3,E3)活性的ICP0(infected cell protein 0)蛋白是病毒由潜伏期进入裂解复制期的关键作用蛋白。作为E3泛素连接酶,ICP0能够直接降解多种细胞组分,阻碍细胞多种固有免疫和先天性免疫反应。本文综述了ICP0的E3泛素连接活性在对抗宿主免疫反应中的作用。重点阐述了ICP0在裂解性复制中靶向降解宿主SUMO(small ubiquitin-like modifier)化修饰的抗病毒蛋白、阻碍宿主干扰素抗病毒途径和DNA损伤反应的相关机制。

Suppressive roles of E3 ubiquitin ligase of HSV-1 protein ICP0 in host immune response

E3 ubiquitin ligase infected cell protein 0(ICP0), encoded by herpes simplex virus type 1(HSV-1),regulates the switch between the lytic and latent states of HSV-1. As an E3 ubiquitin ligase, ICP0 directs the degradation of several cellular targets, allowing the virus counteract different cellular intrinsic and innate immune responses. In this review, we focus on how ICP0’s E3 ubiquitin ligsase inactivates the host defenses to help the virus to survive. We put emphasis on the mechanisms of ICP0 in targeting degradation of the antiviral protein modified by SUMOs modified antiviral proteins, blocking host interferon antiviral pathway and DNA damage response.