These include endothelial dysfunction from chronic inflammation or endothelial injury caused by shed HIV viral proteins and complement activation,9 direct infection of endothelial cells by the virus,10 and the development of autoantibodies to ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, type 13), an enzyme which exerts an antithrombotic effect through the cleavage of ultra-large von Willebrand factor (UL-vWF).11 Here, VWF is linked to infection.