CAJ | 학술논문

病毒感染哺乳动物细胞过程中，病毒复制产生的基因组或病毒蛋白激活先天性免疫信号通路后，产生干扰素的同时诱导干扰素下游基因表达，促进细胞的抗病毒反应。与此同时，病毒感染宿主细胞还能引起胞质颗粒的聚集，其成份大多为核糖核蛋白，RNA结合蛋白、翻译起始因子等，这个聚集区域被称之为应激颗粒（stress granules，SG）。先天性免疫通路和SG都是宿主细胞对病毒感染的一种抵抗性反应，而与之相对，一些病毒却通过抑制SG和先天性免疫通路的形成来促进自身复制。由于SG中包含RNA结合蛋白以及一系列病毒或宿主的RNA，而先天性免疫中识别病毒RNA的模式识别分子也能特异性结合病毒RNA，那SG如何协同先天性免疫在宿主抗病毒中发挥一定的作用，本文就SG在病毒感染诱导的先天性免疫中的作用进行简要综述。
병독감염포유동물세포과정중，병독복제산생적기인조혹병독단백격활선천성면역신호통로후，산생간우소적동시유도간우소하유기인표체，촉진세포적항병독반응。여차동시，병독감염숙주세포환능인기포질과립적취집，기성빈대다위핵당핵단백，RNA결합단백、번역기시인자등，저개취집구역피칭지위응격과립（stress granules，SG）。선천성면역통로화SG도시숙주세포대병독감염적일충저항성반응，이여지상대，일사병독각통과억제SG화선천성면역통로적형성래촉진자신복제。유우SG중포함RNA결합단백이급일계렬병독혹숙주적RNA，이선천성면역중식별병독RNA적모식식별분자야능특이성결합병독RNA，나SG여하협동선천성면역재숙주항병독중발휘일정적작용，본문취SG재병독감염유도적선천성면역중적작용진행간요종술。
In the course of virus infection, virus genome and protein produced by virus replication initiate innate immunity signaling pathway, leading to interferon secretion and interferon stimulate gene expression and ultimately establish an antiviral state. Meanwhile, virus infection also induced stress granule (SG) containing ribonucleoprotein, RNA binding protein and eukaryotic initiated factors, etc. Innate immunity and SG are both cellular antiviral response. Correspondingly, virus promotes its own replication through inhibit SG forma-tion and innate immunity. SG contains RNA binding protein and a series of virus or host RNA, while the molecular associated to innate immunity such as pattern recognition receptor also specifically recognize virus RNA, indicating their close relationship. This review will focus on the strategies how SG and innate immunity collaboratively exert antiviral function.