Min Yuan-Qin, Huang Mengzhuo, Sun Xiulian, Deng Fei, Wang Hualin, Ning Yun-Jia
State Key Laboratory of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071/430207, China.
Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan 430071/430207, China.
Comput Struct Biotechnol J. 2021;19:4217-4225. doi: 10.1016/j.csbj.2021.07.023. Epub 2021 Jul 26.
The on-going pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to unprecedented medical and socioeconomic crises. Although the viral pathogenesis remains elusive, deficiency of effective antiviral interferon (IFN) responses upon SARS-CoV-2 infection has been recognized as a hallmark of COVID-19 contributing to the disease pathology and progress. Recently, multiple proteins encoded by SARS-CoV-2 have been shown to act as potential IFN antagonists with diverse possible mechanisms. Here, we summarize and discuss the strategies of SARS-CoV-2 for evasion of innate immunity (particularly the antiviral IFN responses), understanding of which will facilitate not only the elucidation of SARS-CoV-2 infection and pathogenesis but also the development of antiviral intervention therapies.
由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的2019冠状病毒病(COVID-19)大流行已导致前所未有的医学和社会经济危机。尽管病毒发病机制仍不清楚,但严重急性呼吸综合征冠状病毒2感染后有效的抗病毒干扰素(IFN)反应不足已被认为是COVID-19的一个标志,这有助于疾病的病理和进展。最近,严重急性呼吸综合征冠状病毒2编码的多种蛋白质已被证明可作为潜在的干扰素拮抗剂,其机制可能多种多样。在这里,我们总结并讨论了严重急性呼吸综合征冠状病毒2逃避先天免疫(特别是抗病毒干扰素反应)的策略,了解这些策略不仅将有助于阐明严重急性呼吸综合征冠状病毒2的感染和发病机制,还将有助于开发抗病毒干预疗法。