CLONAL EXPANSION BUT LACK OF SUBSEQUENT CLONAL DELETION OF BACTERIAL SUPERANTIGEN-REACTIVE T-CELLS IN MURINE RETROVIRAL INFECTION

Several studies have suggested that activation-induced apoptosis of Ag -specific CD4(+) T cells leads to depletion of this subset during HIV infection. The bacterial superantigen, staphylococcal enterotoxin A (S EA), is known to induce activation-induced apoptosis in the TCR V beta -bearing CD4(+) T cells in the periphery after clonal expansion of the se cells. The murine retroviral model of AIDS (MAIDS), which is induce d by LP-BM5 murine leukemia virus, shares many common features with HI V infection in humans, except that CD4(+) T cells increase progressive ly in susceptible strains. In this study, we challenged SEA to MAIDS m ice and examined whether this retrovirus affects the fate of the SEA-r eactive CD4(+) T cells in vivo. At 4 wk post-infection with LP-BM5 mur ine leukemia virus, clonal expansion and subsequent deletion of SEA-re active CD4(+)V beta 3(+) T cells occurred normally after SEA administr ation, whereas in vitro proliferative responses were severely impaired . At 8 wk postinfection, the in vivo expansion of CD4(+)V beta 3(+) T cells was evident, but not followed by clonal deletion, as late as 14 days after SEA administration. This expanding subset in the infected m ice expressed the Fas Ag in the same amount as the same subset in unin fected controls. These findings suggest that activation-induced apopto sis of superantigen-reactive CD4(+) T cells is interfered with in vivo during the course of MAIDS, which is not attributable to underexpress ion of the Fas Ag by the CD4(+) T cells.