真核细胞应激颗粒的产生与病毒逃逸策略概述

Overview of production of eukaryotic stress granules and viral escape strategies

真核细胞受到氧化应激、热休克或病毒感染等外界不利因素刺激时,会迅速启动细胞应激反应,停滞自身翻译,导致大量应激颗粒(stress granules,SGs)的产生,使细胞处于自我保护的休眠状态。SGs是一种动态、无膜的蛋白-RNA聚集物,在维持细胞内环境稳态、调控宿主基因表达的过程中发挥重要作用。SGs在抵抗病毒复制过程中也发挥重要作用,既可以停滞宿主蛋白翻译系统避免病毒“劫持”,也能够招募天然免疫相关的宿主因子,共同抵抗病毒复制。然而,病毒在长期进化中已经具备多种逃逸SGs抗病毒的策略,以便为自身复制提供更好的细胞内环境。因此,对SGs产生、抗病毒机制以及病毒进化过程中逃逸SGs抗病毒的策略进行综述,以期为抗病毒药物的研发提供新的视角。

When eukaryotic cells are undergoing stimulations like oxidative stress,heat shock,or viral infection,cellular stress response will quickly initiate to stop translation,leading to the production of a large number of stress granules(SGs).SGs,as dynamic membraneless protein-RNA aggregates,play an important role in maintaining cellular homeostasis and regulating host gene expression.Upon viral invasion,the host halts translation to form SGs,thereby arresting the translation of viral proteins within host cells.This process recruits innate immune-related host factors,limiting the virus from exploiting host translation machinery to complete its life cycle.It activates the innate immune pathway.However,some viruses have evolved multiple mechanisms to counter SGs,in order to provide a better intracellular environment for viral replication.Here,we review the generation of SGs,antiviral mechanism of SGs,and the strategies for escaping SGs during virus evolution,in order to provide a new perspective for the development of antiviral drugs.