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Endothelial activation and dysfunction in the pathogenesis of influenza A virus infection

机译:甲型流感病毒感染的发病机制中的内皮激活和功能障碍

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摘要

The development of severe influenza has been attributed, in part, to a heightened innate immune response. Recent evidence suggests that endothelial activation, loss of barrier function, and consequent microvascular leak may also serve important mechanistic roles in the pathogenesis of severe influenza. The aim of this review is to summarize the current evidence in support of endothelial activation and dysfunction as a central feature preceding the development of severe influenza. We also discuss the effect of influenza on platelet- endothelial interactions.
机译:严重流感的发展部分归因于先天免疫应答的增强。最近的证据表明,在严重流感的发病机理中,内皮细胞的活化,屏障功能的丧失以及随之而来的微血管渗漏也可能起着重要的机械作用。这篇综述的目的是总结支持内皮活化和功能障碍的当前证据,将其作为重症流感发生之前的主要特征。我们还讨论了流感对血小板-内皮相互作用的影响。

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