【摘要】 轮状病毒是导致许多哺乳动物严重腹泻的主要病原,它的入侵会导致宿主细胞抗病毒状态的建立,如病毒核酸与RIG-Ⅰ、MDA5、LGP2、dsRNA依赖的蛋白激酶及NLR炎症小体作用,导致IFN的分泌和细胞焦亡等;非结构蛋白NSP4会激活NF-κB信号通路。但轮状病毒也进化出多种策略来对抗宿主的天然免疫,其中以非结构蛋白1(NSP1)研究较多,NSP1可抑制STAT-Y701磷酸化,降解干扰素调节因子、MAVS和β-TrCP等,进而阻止IFN-β和NF-κB信号通路的激活;VP3降解MAVS,拮抗OAS/RNase L通路激活阻止宿主细胞对病毒RNA的应答;VP2、NSP2、NSP3也发挥了一定拮抗天然免疫的作用。论文主要对轮状病毒各蛋白调控宿主天然免疫的机制进行综述,以期为轮状病毒感染防控、新型疫苗研制等提供参考。更多还原

【Abstract】 Rotavirus, a leading cause of severe diarrhoea in many mammals, and its infection will lead to the establishment of antiviral state of host cells.For example, viral nucleic acid interacts with RIG-Ⅰ,MDA5,LGP2,PKR and NOD-like receptor inflammasome, resulting in interferon secretion and pyroptosis, and the non-structural protein NSP4 activates NF-κB signal pathway.However, rotavirus has also evolved a variety of strategies to combat the host’s innate immunity.Among them, the non-structural protein NSP1 has been widely studied.NSP1 can inhibit STAT-Y701 phosphorylation, degrade interferon regulatory factors, MAVS and β-TrCP,and then block the activation of IFN-β and NF-κB signal pathways; VP3 degrades MAVS,antagonizes the activation of OAS/RNase L pathway to prevent host cells from responding to virus RNA; VP2,NSP2 and NSP3 also play an antagonistic role in innate immunity.This paper mainly reviewed the mechanism of rotavirus proteins regulating innate immunity in order to provide reference for rotavirus prevention and control and new vaccine development.更多还原