DIFFERENT PROLIFERATIVE RESPONSE OF HUMAN AND CHIMPANZEE LYMPHOCYTES AFTER CONTACT WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120

T cell functional defects are a common aspect of human immunodeficienc y virus (HIV) infection. Moreover, it has been suggested that indirect mechanisms are involved in CD4(+) cell depletion. Unresponsiveness to proliferative stimuli of lymphocytes incubated with HIV particles or with viral proteins is well documented. Nevertheless, drawing a clear picture of the anergy phenomenon is difficult because of several unres olved and controversial questions. Here we report that recombinant gp1 20 induces anergy in T helper lymphocytes cultured with different stim uli. The proliferative responses to interleukin (IL)-2, IL-4, IL-6, an ti-CD2, anti-CD3 and phorbol 12-myristate 13-acetate are inhibited. Mo reover, anergic cells show a different distribution in cell cycle phas es as compared to control cells, leading us to suggest that the progre sion in the cell cycle is hampered and that a pre-mitotic block takes place. Furthermore, since chimpanzees are susceptible to HIV-1 infecti on without showing immunodeficiency signs, we analyzed the proliferati on of chimpanzee lymphocytes without observing anergy in cells preincu bated with gp120. Taken together, these results support the hypothesis that anergy plays an important role in HIV infection in vivo.