Endothelial cells (EC) participate in inflammatory and immune reactions by
producing and responding to soluble mediators. Human immunodeficiency virus
(HIV)-1 profoundly alters the features of EC. In some anatomical districts
, they are infected by the virus and may represent a relevant reservoir. Du
ring lymphomononuclear cell diapedesis, EC activate virus replication in cr
ossing cells. Direct or indirect damage of EC is particularly relevant in c
entral nervous system, where blood-brain barrier perturbation is pivotal in
neuronal degeneration. The observed alterations of EC adhesive properties
contribute in altered leukocyte traffic from blood to lymphoid organs and t
issues and play a role in the onset of immune surveillance alteration. Thes
e alterations of EC functions are relevant for the general vasculopathy, wh
ich marks the acquired immunodeficiency syndrome, and in particular are ins
trumental in the pathogenesis of Kaposi's sarcoma. Here we discuss the biol
ogical and molecular activation of EC in HIV-1 infection that represents th
e basis to understand the pathogenesis of HIV-1 associated vascular disease
s. (C) 2001 Elsevier Science Ltd. All rights reserved.