Interferon antagonists encoded by SARS-CoV-2 at a glance.

IF 5.5 3区 医学 Q1 IMMUNOLOGY Medical Microbiology and Immunology Pub Date : 2023-04-01 Epub Date: 2022-04-02 DOI:10.1007/s00430-022-00734-9
Jung-Hyun Lee, Lennart Koepke, Frank Kirchhoff, Konstantin M J Sparrer
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Abstract

The innate immune system is a powerful barrier against invading pathogens. Interferons (IFNs) are a major part of the cytokine-mediated anti-viral innate immune response. After recognition of a pathogen by immune sensors, signaling cascades are activated that culminate in the release of IFNs. These activate cells in an autocrine or paracrine fashion eventually setting cells in an anti-viral state via upregulation of hundreds of interferon-stimulated genes (ISGs). To evade the anti-viral effect of the IFN system, successful viruses like the pandemic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) evolved strategies to counteract both IFN induction and signaling. In fact, more than half of the about 30 proteins encoded by SARS-CoV-2 target the IFN system at multiple levels to escape IFN-mediated restriction. Here, we review recent insights into the molecular mechanisms used by SARS-CoV-2 proteins to suppress IFN production and the establishment of an anti-viral state.

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SARS-CoV-2 编码的干扰素拮抗剂一览。
先天免疫系统是抵御病原体入侵的强大屏障。干扰素(IFNs)是细胞因子介导的抗病毒先天性免疫反应的主要组成部分。免疫传感器识别病原体后,信号级联被激活,最终释放 IFNs。它们以自分泌或旁分泌的方式激活细胞,最终通过上调数百个干扰素刺激基因(ISGs)使细胞处于抗病毒状态。为了逃避 IFN 系统的抗病毒作用,大流行病严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)等成功的病毒进化出了对抗 IFN 诱导和信号传导的策略。事实上,在 SARS-CoV-2 编码的约 30 种蛋白质中,有一半以上在多个水平上以 IFN 系统为目标,以逃避 IFN 介导的限制。在此,我们回顾了 SARS-CoV-2 蛋白用于抑制 IFN 生成和建立抗病毒状态的分子机制的最新研究成果。
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来源期刊
CiteScore
10.60
自引率
0.00%
发文量
29
审稿时长
1 months
期刊介绍: Medical Microbiology and Immunology (MMIM) publishes key findings on all aspects of the interrelationship between infectious agents and the immune system of their hosts. The journal´s main focus is original research work on intrinsic, innate or adaptive immune responses to viral, bacterial, fungal and parasitic (protozoan and helminthic) infections and on the virulence of the respective infectious pathogens. MMIM covers basic, translational as well as clinical research in infectious diseases and infectious disease immunology. Basic research using cell cultures, organoid, and animal models are welcome, provided that the models have a clinical correlate and address a relevant medical question. The journal also considers manuscripts on the epidemiology of infectious diseases, including the emergence and epidemic spreading of pathogens and the development of resistance to anti-infective therapies, and on novel vaccines and other innovative measurements of prevention. The following categories of manuscripts will not be considered for publication in MMIM: submissions of preliminary work, of merely descriptive data sets without investigation of mechanisms or of limited global interest, manuscripts on existing or novel anti-infective compounds, which focus on pharmaceutical or pharmacological aspects of the drugs, manuscripts on existing or modified vaccines, unless they report on experimental or clinical efficacy studies or provide new immunological information on their mode of action, manuscripts on the diagnostics of infectious diseases, unless they offer a novel concept to solve a pending diagnostic problem, case reports or case series, unless they are embedded in a study that focuses on the anti-infectious immune response and/or on the virulence of a pathogen.
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