SARS-CoV-2与宿主固有免疫系统的相互作用

Interaction between SARS-CoV-2 and Host Innate Immunity

2019冠状病毒病(coronavirus disease 2019,COVID-19,我国通称新型冠状病毒肺炎,简称新冠肺炎)是由严重急性呼吸综合征冠状病毒2(severe acute respiratory syndrome coronavirus 2,SARS-CoV-2)引起的一种以肺部病变为主的呼吸道传染病,自2019年暴发后引起全球性大流行,对公共卫生及民众健康造成严重威胁。Ⅰ型干扰素(interferon,IFN)是宿主固有免疫系统的重要组成部分,在抵御病毒感染过程中发挥着非常重要的作用。病毒和固有免疫系统的博弈,往往决定感染后的疾病进程。研究显示,SARS-CoV-2病毒能通过与宿主免疫系统之间相互作用,抑制IFN的产生及IFN通路的激活;而Ⅰ型IFN反应减弱或延迟,引起宿主免疫应答的紊乱,是造成SARS-CoV-2高发病率和高死亡率的重要原因之一。本文讨论了SARS-CoV-2编码的病毒蛋白与宿主固有免疫系统之间,特别是Ⅰ型IFN通路之间的相互作用,以期为病毒逃逸宿主免疫应答机制及临床上IFN治疗COVID-19提供新思路和新策略。

Coronavirus disease 2019(COVID-19),an infectious disease caused by severe acute respiratory syndrome coronavirus 2(SARS-CoV-2),has caused a global pandemic since its outbreak in 2019,presenting serious threats to public health and the health of the people.As one of the main components of the host innate immune system,type-Ⅰinterferon(IFN)plays a critical role in the defense against viral infections.The battle between the virus and the host innate immune system determines the disease progression.It has been reported that SARS-CoV-2 inhibits IFN production and suppresses the activation of IFN signaling pathway through its interactions with the host innate immune system.Then,the weakened or delayed response of type-Ⅰinterferon causes the disturbance of host immune responses,which is one of the important reasons why SARS-CoV-2 causes such high morbidity and mortality.Herein,we reviewed and discussed the interaction between SARS-CoV-2 viral proteins and the host innate immune system,especially the interaction with type-ⅠIFN pathway,to provide new insights into the mechanisms of viral evasion of host immune response and new perspectives and strategies for treating COVID-19 with IFN.