APOPTOSIS INDUCED BY HIV-GP120 IN A TH1 CLONE INVOLVES THE GENERATIONOF REACTIVE OXYGEN INTERMEDIATES DOWNSTREAM CD95 TRIGGERING

HIV-gp120 sensitizes Th1 clones from seronegative donors to apoptosis, which occurs through two distinct events: expression of CD95L followe d by its interaction with CD95 to trigger cell death, gp120-apoptosis of the Th1 clone 103 was inhibited by Cyclosporin A, the PTK inhibitor s Genistein and PNU152518, as well as the anti-oxidants Ascorbic Acid and Glutathione. Cyclosporin A interfered with CD95L expression, Ascor bic Acid and Glutathione inhibited cell death triggered by CD95/CD95L interaction; Genistein and PNU152518 acted on both steps, The occurren ce of oxidative stress during CD95-dependent apoptosis was supported b y the direct evidence of ROI production, (C) 1997 Federation of Europe an Biochemical Societies.