The role of von Willebrand factor and its cleaving protease, ADAMTS13, in young patients with HIV-related stroke.

Abstract

The Human Immunodeficiency Virus (HIV) is neuro-invasive and neurological complications of HIV infection occur frequently through a variety of possible mechanisms. Stroke in the setting of HIV is not uncommonly seen in young adults. High levels of von Willebrand factor (VWF), a protein with key roles in platelet adhesion and aggregation, and low levels of A Disintegrin and Metalloproteinase with a Thrombospondin type 1 motif, member 13 (ADAMTS13), the protease that cleaves ultra large VWF multimers into smaller less haemostatically active multimers, have been associated with an increased propensity for thrombosis. Stroke is a potential complication of the aberrant activity of these two proteins. HIV infection has also been associated with endothelial dysfunction, and VWF is a marker of the latter. The investigation of VWF and ADAMTS13 may therefore provide new insights into the pathogenesis of HIV-related stroke.