The effects of HIV infection on endothelial function

Endothelial dysfunction and/or injury is pivotal to the development of card iovascular and inflammatory pathology. Endothelial dysfunction and/or injur y has been described in Human Immunodeficiency Virus (HIV) infection. Elabo ration of circulating markers of endothelial activation, such as soluble ad hesion molecules and procoagulant proteins, occurs in HIV infection. Certai n endothelial cells, such as those lining liver sinusoids, human umbilical vein endothelial cells, bone marrow stromal endothelial cells or brain micr ovascular endothelial cells, have been shown to be variably permissive for HIV infection. Entry of virus into endothelial cells may occur via CD4 anti gen or galactosyl-ceramide receptors. Other mechanisms of entry including c hemokine receptors have been proposed. Nevertheless, endothelial activation may also occur in HIV infection either by cytokines secreted in response t o mononuclear or adventitial cell activation by virus or else by the effect s of the secreted HIV-associated proteins, gp 120 (envelope glycoprotein:) and Tat (transactivator of viral replication) on endothelium. Enhanced adhe siveness of endothelial cells, endothelial cell proliferation and apoptosis as well as activation of cytokine secretion have all been demonstrated. Sy nergy between select inflammatory cytokines and viral proteins in inducing endothelial injury has been shown. In HIV infection, dysfunctional or injur ed endothelial cells potentiate tissue injury, inflammation and remodeling, and accelerate the development of cardiovascular disease.