Abstract
An understanding of endothelial cell function both systemically and in the central nervous system is relevant to many aspects of HIV1 associated disease. Endothelial cells produce a variety of biologically active factors (e.g., NO, prostacyclin, chemokines) that control vascular permeability, vessel tone, coagulation, fibrinolysis, and inflammatory responses. These factors can be generated by other vascular cells, as well as nonvascular cells. Alterations of normal endothelial cell biology have critical significance in the development of vascular and neurovascular pathology during HIV1 infection. For example, such alterations can contribute to disruption of the BBB, to HIV1 entry into the brain, to the development of vasculopathies, and to atherosclerosis. The underlying mechanisms appear to be related to induction of oxidative stress and alterations of redoxrelated signaling. Vascular toxicity may be induced by HIV1 itself or it can be mediated by a variety of HIV1specific proteins, as well as by antiretroviral drugs. \