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干扰 SARS-CoV-2:干扰素在 COVID-19 中是敌是友?

Interfering with SARS-CoV-2: are interferons friends or foes in COVID-19?

机构信息

Harvard Medical School, and Division of Immunology, Division of Gastroenterology, Boston Children's Hospital, United States.

出版信息

Curr Opin Virol. 2021 Oct;50:119-127. doi: 10.1016/j.coviro.2021.08.004. Epub 2021 Aug 17.

DOI:10.1016/j.coviro.2021.08.004
PMID:34454352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8367741/
Abstract

Type I and type III interferons are among the most potent anti-viral cytokines produced by the immune system. The recent outbreak of SARS-CoV-2, which causes COVID-19, underscores the vital role of these cytokines in controlling the virus and dictating disease severity. Here we delineate the pathways that lead to interferon production in response to SARS-CoV-2 encounter, and elucidate how this virus hinders the production and action of these cytokines; we also highlight that these interferon families serve protective as well as detrimental roles in patients with COVID-19, and conclude that a better understanding of the time, dose, localization, and activity of specific members of the interferon families is imperative for designing more efficient therapeutic interventions against this disease.

摘要

I 型和 III 型干扰素是免疫系统产生的最有效的抗病毒细胞因子之一。最近爆发的导致 COVID-19 的 SARS-CoV-2 病毒凸显了这些细胞因子在控制病毒和决定疾病严重程度方面的重要作用。在这里,我们描述了 SARS-CoV-2 感染后诱导干扰素产生的途径,并阐明了该病毒如何阻碍这些细胞因子的产生和作用;我们还强调了这些干扰素家族在 COVID-19 患者中具有保护和有害作用,并得出结论,更好地了解干扰素家族特定成员的时间、剂量、定位和活性对于设计针对这种疾病的更有效的治疗干预措施至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7756/8367741/16c3b996cbdc/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7756/8367741/a5bf1ad9ceef/fx1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7756/8367741/16c3b996cbdc/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7756/8367741/a5bf1ad9ceef/fx1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7756/8367741/16c3b996cbdc/gr1_lrg.jpg

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本文引用的文献

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Proc Natl Acad Sci U S A. 2022 Feb 22;119(8). doi: 10.1073/pnas.2111600119.
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SARS-CoV-2 infection induces a pro-inflammatory cytokine response through cGAS-STING and NF-κB.SARS-CoV-2 感染通过 cGAS-STING 和 NF-κB 诱导促炎细胞因子反应。
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The interferon landscape along the respiratory tract impacts the severity of COVID-19.
广泛的基因-环境相互作用塑造了住院COVID-19患者对SARS-CoV-2感染的免疫反应。
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Am J Respir Cell Mol Biol. 2025 Mar;72(3):308-319. doi: 10.1165/rcmb.2024-0213OC.
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IFN-λ uniquely promotes CD8 T cell immunity against SARS-CoV-2 relative to type I IFN.IFN-λ 相对于 I 型 IFN ,特异性地促进 CD8 T 细胞对 SARS-CoV-2 的免疫应答。
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Reduced IFNL1 and/or IFNL2, but not IFNL3 is associated with worse outcome in patients with COVID-19.IFNL1 和/或 IFNL2 减少与 COVID-19 患者的不良结局相关,但 IFNL3 则不然。
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