Toll-like Receptors as Pro-Thrombotic Drivers in Viral Infections: A Narrative Review

Toll-like receptors (TLRs) have a critical role in the pathogenesis and disease course of viral infections. The induced pro-inflammatory responses result in the disturbance of the endovascular surface layer and impair vascular homeostasis. The injury of the vessel wall further promotes pro-thrombotic and pro-coagulatory processes, eventually leading to micro-vessel plugging and tissue necrosis. Moreover, TLRs have a direct role in the sensing of viruses and platelet activation. TLR-mediated upregulation of von Willebrand factor release and neutrophil, as well as macrophage extra-cellular trap formation, further contribute to (micro-) thrombotic processes during inflammation. The following review focuses on TLR signaling pathways of TLRs expressed in humans provoking pro-thrombotic responses, which determine patient outcome during viral infections, especially in those with cardiovascular diseases.

Automated summary

Toll-like receptors (TLRs) play a critical role in viral infections by inducing pro-inflammatory responses and disrupting vascular homeostasis. The injury to the vessel wall leads to pro-thrombotic processes and eventually causes micro-vessel plugging and tissue necrosis. TLRs also directly contribute to virus sensing and platelet activation. Upregulation of von Willebrand factor release and extra-cellular trap formation by TLRs further enhance thrombotic processes during inflammation. This review focuses on TLR signaling pathways in humans, which provoke pro-thrombotic responses during viral infections, particularly in individuals with cardiovascular diseases.