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从流感保护性炎症向不利炎症转变:病毒决定因素和止血被视为罪魁祸首。

Switch from protective to adverse inflammation during influenza: viral determinants and hemostasis are caught as culprits.

机构信息

VirPath, EA4610 Virologie et Pathologie Humaine, Faculté de médecine RTH Laennec, Université Claude Bernard Lyon 1, Université de Lyon, 69008, Lyon, France.

出版信息

Cell Mol Life Sci. 2014 Mar;71(5):885-98. doi: 10.1007/s00018-013-1479-x. Epub 2013 Oct 4.

DOI:10.1007/s00018-013-1479-x
PMID:24091817
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11114008/
Abstract

Influenza viruses cause acute respiratory infections, which are highly contagious and occur as seasonal epidemic and sporadic pandemic outbreaks. Innate immune response is activated shortly after infection with influenza A viruses (IAV), affording effective protection of the host. However, this response should be tightly regulated, as insufficient inflammation may result in virus escape from immunosurveillance. In contrast, excessive inflammation may result in bystander lung tissue damage, loss of respiratory capacity, and deterioration of the clinical outcome of IAV infections. In this review, we give a comprehensive overview of the innate immune response to IAV infection and summarize the most important findings on how the host can inappropriately respond to influenza.

摘要

流感病毒引起急性呼吸道感染,具有高度传染性,可呈季节性流行和散发大流行。甲型流感病毒(IAV)感染后,固有免疫反应迅速被激活,为宿主提供有效的保护。然而,这种反应应受到严格调控,因为炎症不足可能导致病毒逃避免疫监视。相反,过度的炎症可能导致旁观者肺组织损伤、丧失呼吸能力,并使 IAV 感染的临床结局恶化。在这篇综述中,我们全面概述了对 IAV 感染的固有免疫反应,并总结了宿主对流感可能不适当反应的最重要发现。

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