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血小板与 SARS-CoV-2 在 COVID-19 中的作用:免疫、血栓形成及其他。

Platelets and SARS-CoV-2 During COVID-19: Immunity, Thrombosis, and Beyond.

机构信息

Department of Medicine, Divisions of Cardiovascular Medicine (A.S., H.C., M.K.), University of Massachusetts Chan Medical School, Worcester, MA.

Innate Immunity (F.H.). University of Massachusetts Chan Medical School, Worcester, MA.

出版信息

Circ Res. 2023 May 12;132(10):1272-1289. doi: 10.1161/CIRCRESAHA.122.321930. Epub 2023 May 11.

DOI:10.1161/CIRCRESAHA.122.321930
PMID:37167360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10171305/
Abstract

COVID-19 is characterized by dysregulated thrombosis and coagulation that can increase mortality in patients. Platelets are fast responders to pathogen presence, alerting the surrounding immune cells and contributing to thrombosis and intravascular coagulation. The SARS-CoV-2 genome has been found in platelets from patients with COVID-19, and its coverage varies according to the method of detection, suggesting direct interaction of the virus with these cells. Antibodies against Spike and Nucleocapsid have confirmed this platelet-viral interaction. This review discusses the immune, prothrombotic, and procoagulant characteristics of platelets observed in patients with COVID-19. We outline the direct and indirect interaction of platelets with SARS-CoV-2, the contribution of the virus to programmed cell death pathway activation in platelets and the consequent extracellular vesicle release. We discuss platelet activation and immunothrombosis in patients with COVID-19, the effect of Spike on platelets, and possible activation of platelets by classical platelet activation triggers as well as contribution of platelets to complement activation. As COVID-19-mediated thrombosis and coagulation are still not well understood in vivo, we discuss available murine models and mouse adaptable strains.

摘要

新型冠状病毒肺炎的特征是血栓形成和凝血功能紊乱,这会增加患者的死亡率。血小板对病原体的存在反应迅速,向周围免疫细胞发出警报,并有助于血栓形成和血管内凝血。已经在新型冠状病毒肺炎患者的血小板中发现了 SARS-CoV-2 基因组,其覆盖率因检测方法而异,这表明病毒与这些细胞直接相互作用。针对 Spike 和 Nucleocapsid 的抗体证实了血小板与病毒的相互作用。本文综述了新型冠状病毒肺炎患者血小板的免疫、促血栓形成和促凝特性。我们概述了血小板与 SARS-CoV-2 的直接和间接相互作用、病毒对血小板程序性细胞死亡途径激活的贡献以及由此导致的细胞外囊泡释放。我们讨论了新型冠状病毒肺炎患者的血小板激活和免疫血栓形成、Spike 对血小板的影响,以及经典的血小板激活触发物对血小板的可能激活作用,以及血小板对补体激活的贡献。由于新型冠状病毒肺炎介导的血栓形成和凝血功能紊乱在体内尚未得到很好的理解,我们讨论了现有的鼠模型和可适应于小鼠的品系。

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