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| VWF & platelet reactivity with inflammation and infection (dengue) Martha Eva Viveros. |
Abstract
VWF & PLATELET REACTIVITY WITH INFLAMMATION AND INFECTION (DENGUE)
Dengue virus (DENV) infection is a re-emerging disease responsible of 50-100 million clinical cases and 10,000 deaths every year worldwide. It is characterized by a wide spectrum of clinical manifestations ranging from mild febrile illness to severe dengue with hemorrhage and shock.
Platelets play a fundamental role in dengue virus infection, as they are not only involved in hemostasis, but also in the immune response and the pathogenesis of the disease. During dengue infection, there is significant thrombocytopenia which contributes to the risk of bleeding. In addition, the activation and destruction of platelets is associated with the release of inflammatory mediators that exacerbate the immune response, as well as increased interaction with leucocytes promoting NETosis.
In this context, the von Willebrand factor (vWF) becomes relevant, as it has been shown that its levels increase during dengue infection, mostly due to endothelial damage and release from Weibel Palade bodies. vWF can enhance platelet adhesion to the vascular endothelium and promote the formation of microthrombi, which contributes to both vascular alterations and the hemorrhagic complications characteristic of severe dengue. Therefore, the interaction between platelets and vWF is key to understanding the clinical manifestations and severity of the disease.
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