AORTIC ENDOTHELIUM IN HIV-1 INFECTION - CHRONIC INJURY, ACTIVATION, AND INCREASED LEUKOCYTE ADHERENCE

Clinical and serological studies provide evidence for a pathogenetical ly relevant vasculopathy in acquired immune deficiency syndrome (AIDS) ; however, the morphological status of the endothelium under condition s of human immunodeficiency virus (HIV)-1 infection is only sparsely d ocumented In this study we adapted an en face preparation technique of endothelium for use in immunohistochemistry and investigated the aort ic endothelium of pre-AIDS and AIDS patients (n = 32) in comparison wi th an HIV-negative group (n = 17). The control group showed a regular pattern of evenly distributed aortic endothelial cells, whereas the en dothelial cell pattern in the HIV-1-infected patients was clearly dist urbed. Simultaneously, the degree of leukocyte adherence on the aortic endothelium increased significantly. These changes were accompanied b y an up-regulation of the vascular cell adhesion molecule-1 (VCAM-1) a nd E-selectin (ELAM-1). The endothelium turnover increased and one-hal f of the HIV-1-infected patients exhibited HLA-DR (major histocompatib ility complex class II) antigen in the aortic endothelium. Our results provide evidence for a profound and repeated injury With regeneration and activation of the endothelium in HIV-1 infection. Injury as well as activation of the endothelium impairs its normal regulatory propert ies. This could have consequences for the maintenance of the blood-bra in barrier; it might influence the immunologically important interacti on of the endothelium with T cells; and it might trigger Kaposi's sarc oma.