Background: Endothelial activation caused by HIV-1
infection leads to release of
von Willebrand factor (VWF), which enters the circulation or attaches to vessel walls and self-assembles into strings and fibers, enabling platelet adhesion; this adhesive activity is regulated by the
VWF-cleaving protease ADAMTS13. Our objective was to assess VWF adhesive activity and
ADAMTS13 protease activity in HIV-1
infection. Methods: We measured levels of VWF
antigen, VWF activation
factor (a measure of adhesive activity), ADAMTS13
antigen, ADAMTS13 activity, and
apolipoprotein A1 (which interferes with VWF self-association) in serum samples from HIV-1-infected men whose
infections were acute (n=10), chronic untreated (n=10), or chronic treated (n=10), compared to uninfected controls (n=10). Means across groups were compared using analysis of variance with contrasts, and Pearson correlations were calculated. Results: Plasma viral load was positively correlated with VWF adhesive activity, which was elevated in acute relative to chronic treated HIV-1
infection. ADAMTS13
antigen and activity were both positively correlated with plasma viral load, and ADAMTS13 activity was significantly higher in men with acute
HIV infection than in uninfected controls, and in both acute and chronic untreated
HIV infection relative to chronic treated
infection. Conclusion: These findings suggest that even in the setting of increased
ADAMTS13 protease activity, VWF in HIV-1
infection is hyperadhesive, which may favor development of microvascular and arterial
thromboses and thereby contribute to increased cardiovascular risk in HIV-1-infected individuals.