Procoagulant activity during viral infections
Procoagulant activity during viral infections
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DOI：
10.2741/4633
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发表时间：
2018-01-01
影响因子：
3.1
通讯作者：
Scharrer, Inge
中科院分区：
文献类型：
--
作者：
Subramaniam, Saravanan;Scharrer, Inge
大量证据表明，免疫和非免疫细胞的炎症可能导致病毒感染期间促凝和抗凝状态的不平衡。在全身感染期间，内皮在调节止血方面起关键作用，内皮功能和活化的严重失衡可导致器官衰竭。病毒感染可升高促凝血标志物如达特和D-二聚体TF阳性MP以及血管性血友病因子（vWF）的血浆水平。尽管多项临床研究显示病毒感染与血栓前风险增加相关，但大多数病毒感染的病理机制尚未完全确定。病毒感染介导的TLR活化是细胞类型和物种特异性的，并解释了将鼠模型数据与人数据相关联的困难。本文就TF依赖的凝血激活、Toll样受体（TLRs）信号转导及其在病毒感染中的促凝作用作一综述。
The abundance of evidence suggest that inflammation of immune and non-immune cells may lead to an imbalance of the pro- and anti-coagulant state during viral infections. During systemic infections, the endothelium plays a critical role in regulating hemostasis, and severe imbalances of endothelial function and activation can contribute to organ failure. Viral infections may elevate plasma levels of procoagulant markers such as TAT and D-dimer TF-positive MPs as well as von Willebrand factor (vWF). Although multiple clinical studies are showing the association of viral infection and increased prothrombotic risk, the pathological mechanisms have not been fully identified for most viral infections. Viral infection mediated TLRs activation is both cell type and species-specific and explains the difficulties in correlating murine model data with the human data. In this review, we briefly discuss the TF-dependent coagulation activation, Toll-like receptors (TLRs) signaling during viral infections, and their contributions to the procoagulant response.