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病毒感染后通过信号转导引发机体免疫反应。环鸟苷酸-腺苷酸合成酶(c GAS)识别病毒DNA,与干扰素基因刺激蛋白(STING)相互作用,介导产生1型干扰素(IFN1)。维甲酸诱导基因1(RIG-1)受体识别病毒RNA,通过线粒体抗病毒信号蛋白(MAVS)引发RIG-1信号通路,激活IFN1。STING不仅可以作为DNA病毒信号通路蛋白,还可与MAVS相互作用,参与RNA病毒信号通路。然而,登革病毒、丙型肝炎病毒等RNA病毒的蛋白酶通过与STING相互作用逃逸免疫系统监视,抑制IFN产生。本文对STING与MAVS的相互作用机制,以及RNA病毒通过STING逃逸免疫系统监视进行综述,以期为研究病毒逃逸天然免疫调节机制提供新思路。
Virus infection through the signal transduction triggered the body’s immune response. Cyclic guanylate-adenylate synthase (cGAS) recognizes viral DNA and interacts with STING to mediate the production of type 1 interferon (IFN-1). The RIG-1 receptor recognizes the viral RNA and triggers the RIG-1 signaling pathway through mitochondrial antiviral signaling protein (MAVS), activating IFN1. STING acts not only as a DNA viral signaling pathway protein but also interacts with MAVS to participate in RNA viral signaling pathways. However, proteases of RNA viruses such as dengue virus and hepatitis C virus evade immune system surveillance by interfering with IFN production by interacting with STING. This review summarizes the mechanism of interaction between STING and MAVS, as well as the surveillance of RNA viruses by the STING escape immune system, with a view to providing new ideas for the study of the natural immunomodulatory mechanisms of virus escape.