Abstract 2111 Allergy, and Rheumatology Poster Symposium, Sunday, 5/2

HIV-1 infection leads to death of CD4+ T cells in vitro although the mechanisms of this cell death are not well defined. We used flow cytometry to concurrently and analyze infection and apoptosis of the CD+ CEM T cell line and human PBMC. Surprisingly, T cells productively infected with HIV-1 IIIB showed less apoptosis than control, uninfected T cells. This relative paucity of apoptosis was a characteristic of IIIB, since a large number of cells infected with the viral clone, HIV-1 NL4-3, were apoptotic. The nef, vpr and vpu gene products were not responsible for apoptosis of NL4-3 infected cells, since NL4-3δV prδV puδNef, and HXB-2 (a nef, vpr and vpu triple mutant derived from IIIB) also killed infected cells. Moreover, only IIIB infected cells showed a resistance to background levels of apoptosis. Thus, the apoptotic (and anti-apoptotic) properties of HIV-1 do not map solely to mutations in nef, vpr, or vpu. We postulate that, in vivo, HIV variants that do not induce rapid apoptosis in the cells they infect may have a selective advantage.