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SARS-CoV-2 损害干扰素产生的机制。

Mechanisms of impairment of interferon production by SARS-CoV-2.

机构信息

Children's Hospital of Eastern Ontario Research Institute, Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON K1H 5B2, Canada.

Patrick G Johnston Centre for Cancer Research, Queen's University Belfast, Belfast, Northern Ireland BT9 7AE, U.K.

出版信息

Biochem Soc Trans. 2023 Jun 28;51(3):1047-1056. doi: 10.1042/BST20221037.

DOI:10.1042/BST20221037
PMID:37199495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10317165/
Abstract

Interferons (IFNs) are crucial components of the cellular innate immune response to viral infections. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has shown a remarkable capacity to suppress the host IFN production to benefit viral replication and spread. Thus far, of the 28 known virus-encoded proteins, 16 have been found to impair the host's innate immune system at various levels ranging from detection and signaling to transcriptional and post-transcriptional regulation of expression of the components of the cellular antiviral response. Additionally, there is evidence that the viral genome encodes non-protein-coding microRNA-like elements that could also target IFN-stimulated genes. In this brief review, we summarise the current state of knowledge regarding the factors and mechanisms by which SARS-CoV-2 impairs the production of IFNs and thereby dampens the host's innate antiviral immune response.

摘要

干扰素(IFNs)是细胞固有免疫应答病毒感染的关键组成部分。严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)表现出显著抑制宿主 IFN 产生的能力,以利于病毒复制和传播。迄今为止,在已知的 28 种病毒编码蛋白中,发现其中 16 种在不同层面上损害宿主固有免疫系统,包括检测和信号转导,以及细胞抗病毒反应组成部分的转录和转录后表达调控。此外,有证据表明,病毒基因组编码非蛋白编码的 miRNA 样元件,也可以靶向 IFN 刺激基因。在这篇简要综述中,我们总结了目前关于 SARS-CoV-2 如何损害 IFN 产生从而抑制宿主固有抗病毒免疫应答的相关因素和机制的知识状态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a49f/10317165/3d0ed4712ca0/BST-51-1047-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a49f/10317165/3d0ed4712ca0/BST-51-1047-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a49f/10317165/3d0ed4712ca0/BST-51-1047-g0001.jpg

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本文引用的文献

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J Cell Sci. 2023 Oct 1;136(19). doi: 10.1242/jcs.261286. Epub 2023 Oct 11.
2
SARS-CoV-2 ORF6 disrupts innate immune signalling by inhibiting cellular mRNA export.SARS-CoV-2 的 ORF6 通过抑制细胞 mRNA 输出来破坏先天免疫信号。
PLoS Pathog. 2022 Aug 25;18(8):e1010349. doi: 10.1371/journal.ppat.1010349. eCollection 2022 Aug.
3
SARS-CoV-2 impairs interferon production via NSP2-induced repression of mRNA translation.
严重急性呼吸综合征冠状病毒2与甲型流感病毒之间的病毒干扰
PLoS Pathog. 2024 Jul 22;20(7):e1012017. doi: 10.1371/journal.ppat.1012017. eCollection 2024 Jul.
4
Repression of mRNA translation initiation by GIGYF1 via disrupting the eIF3-eIF4G1 interaction.GIGYF1通过破坏eIF3-eIF4G1相互作用来抑制mRNA翻译起始。
Sci Adv. 2024 Jul 19;10(29):eadl5638. doi: 10.1126/sciadv.adl5638. Epub 2024 Jul 17.
SARS-CoV-2 通过 NSP2 诱导的 mRNA 翻译抑制来损害干扰素的产生。
Proc Natl Acad Sci U S A. 2022 Aug 9;119(32):e2204539119. doi: 10.1073/pnas.2204539119. Epub 2022 Jul 25.
4
Cap-independent translation and a precisely located RNA sequence enable SARS-CoV-2 to control host translation and escape anti-viral response.非依赖帽子翻译机制和一个精确定位的 RNA 序列使 SARS-CoV-2 能够控制宿主翻译并逃避抗病毒反应。
Nucleic Acids Res. 2022 Aug 12;50(14):8080-8092. doi: 10.1093/nar/gkac615.
5
Reovirus μ2 protein modulates host cell alternative splicing by reducing protein levels of U5 snRNP core components.呼肠孤病毒 μ2 蛋白通过降低 U5 snRNP 核心组件的蛋白水平来调节宿主细胞的可变剪接。
Nucleic Acids Res. 2022 May 20;50(9):5263-5281. doi: 10.1093/nar/gkac272.
6
SARS-CoV-2 NSP13 helicase suppresses interferon signaling by perturbing JAK1 phosphorylation of STAT1.严重急性呼吸综合征冠状病毒2(SARS-CoV-2)非结构蛋白13(NSP13)解旋酶通过干扰信号转导和转录激活因子1(STAT1)的Janus激酶1(JAK1)磷酸化来抑制干扰素信号传导。
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8
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Signal Transduct Target Ther. 2022 Jan 24;7(1):22. doi: 10.1038/s41392-022-00878-3.
9
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Nat Genet. 2022 Feb;54(2):125-127. doi: 10.1038/s41588-021-00996-8. Epub 2022 Jan 13.
10
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Front Immunol. 2021 Dec 23;12:767726. doi: 10.3389/fimmu.2021.767726. eCollection 2021.