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严重急性呼吸综合征冠状病毒 2 型对 I 型干扰素的拮抗作用。

Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2.

机构信息

Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas, USA.

Institute for Human Infections and Immunity, University of Texas Medical Branch, Galveston, Texas, USA.

出版信息

J Interferon Cytokine Res. 2020 Dec;40(12):543-548. doi: 10.1089/jir.2020.0214.

DOI:10.1089/jir.2020.0214
PMID:33337934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7757701/
Abstract

The coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), warranting urgent study of the molecular mechanisms of SARS-CoV-2 infection and host immune response. Type I interferon (IFN-I) is a key component of host innate immune system responsible for eliminating the virus at the early stage of infection. In contrast, SARS-CoV-2 has evolved multiple strategies to evade innate immune response to facilitate viral replication, transmission, and pathogenesis. This review summarizes the recent progresses on SARS-CoV-2 proteins that antagonize host IFN-I production and/or signaling. These progresses have provided knowledge for new vaccine and antiviral development to prevent and control COVID-19.

摘要

新型冠状病毒病(COVID-19)大流行是由严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起的,迫切需要研究 SARS-CoV-2 感染和宿主免疫反应的分子机制。I 型干扰素(IFN-I)是宿主固有免疫系统的关键组成部分,负责在感染的早期阶段消除病毒。相比之下,SARS-CoV-2 已经进化出多种策略来逃避固有免疫反应,以促进病毒复制、传播和发病机制。这篇综述总结了 SARS-CoV-2 蛋白拮抗宿主 IFN-I 产生和/或信号转导的最新进展。这些进展为预防和控制 COVID-19 的新型疫苗和抗病毒药物的开发提供了知识。

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