Human immunodeficiency virus type 1 (HIV-1) promotes a generalized immune activation that alters the physiology of cells that are not sensitive to viral infection. Endothelial cells (ECs) display heavy dysfunctions in HIV-1-seropositive (HIV+) patients that persist even in patients under successful combined antiretroviral therapy (cART). In vivo studies failed to demonstrate the presence of replicating virus in ECs suggesting that a direct role of the virus in vascular dysfunction is unlikely. This finding paves the way to the hypothesis of a key role of molecules released in the microenvironment by HIV-1-infected cells in sustaining aberrant EC function. Here we review the current understanding regarding the contribution of HIV-1 infection to vascular dysfunction. In particular, we argue that different HIV-1 proteins may play a key role in driving and sustaining inflammation and EC dysregulation, thus underlining the need to target them for therapeutic benefit.
Part of the book: Endothelial Dysfunction