RNA病毒感染对应激颗粒的调控作用  

REGULATION OF STRESS GRANULES DURING RNA VIRUS INFECTION

作　　者：王晓旭[1] 孙英杰[2] 丁云磊[3] 王桂军[1] 丁铲[2] 

机构地区：[1]安徽农业大学动物科技学院,合肥223006 [2]中国农业科学院上海兽医研究所,上海200241 [3]南京农业大学动物医学院,南京210095

出　　处：《中国动物传染病学报》2014年第4期72-80,共9页Chinese Journal of Animal Infectious Diseases

基　　金：863计划(2011AA10A209);公益性行业(农业)科研专项(201003012)

摘　　要：哺乳动物细胞受到热休克、氧化应激、营养缺乏或者病毒感染等环境压力时,能够迅速启动细胞的压力应答机制,终止细胞内的蛋白翻译,在这个过程中,往往会形成应激颗粒。应激颗粒作为胞浆中终止活动的翻译起始复合物的聚集产物,在细胞的基因表达和内平衡中发挥着重要的作用。尤其是当病毒感染细胞时,应激颗粒的形成可以使细胞的蛋白翻译水平大大降低,从而抑制病毒的复制。然而在病毒的长期进化过程中,也衍生出了对抗细胞压力应答的相应机制,有些病毒甚至可以利用应激颗粒中包裹的沉默的转录本促进自身的复制。本文将着重就RNA病毒对应激颗粒的调控以及最近提出的压力应激与先天性免疫之间的关系做一综述。Stress granules （SGs） are reversible dynamic structures that rapidly form when mammalian cells encounter environmental stress like heat shock, oxidative, nutrient deprivation, or viral infection, which can reduce global translation rates. As the complexes of stalled translation factor, SGs play major roles in gene expression and homeostasis. When virus infects host cells, the formation of SGs can greatly reduce the level of protein translation, thereby inhibit viral replication. Yet simple viruses have evolved efficient means to resist the stress responses, some of them even can use the silent transcripts involved in SGs to increase their replication. This review covers the range of interactions between RNA viruses and SGs and discusses the newly described interactions between stress responses and innate immune responses.

关 键 词：应激颗粒 RNA病毒 调控机制 先天性免疫 

分 类 号：S852.42[农业科学—基础兽医学]