“…This evidence is not unexpected, as platelet biology appears to be largely perturbed in patients with SARS-CoV-2 infection, and further contributes to magnify their risk of developing pulmonary or disseminated thrombosis. 24,25 Although a thoughtful discussion on the interplay between platelets and SARS-CoV-2 infection has already been provided in some previous articles, 24,25 a brief overview on the significance of these findings is perhaps advisable. SARS-CoV-2 can contribute to platelets activation via a variety of mechanisms and different pathways, such as direct binding to platelet surface, provoking endothelial injury, sustaining an inflammation-related release of von Willebrand factor (VWF) compounded by a concomitant decrease in the activity of ADAMTS-13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) which would then lead to impaired cleavage of ultralarge VWF, as well as by reducing heparan sulfates at blood vessel surface and impairing generation of vasoeffective mediators (e.g., nitric oxide, prostacyclin, and prostaglandin).…”