CRYPTOCOCCUS-NEOFORMANS INFECTION IN MICE PREVIOUSLY INFECTED WITH LP-BM5 MULV, THE AGENT OF MURINE AIDS (MAIDS)

We studied susceptibility to experimental systemic cryptococcosis in m ice previously infected with the retroviral complex LP-BM5 (responsibl e for murine AIDS). LP-BM5 was inoculated to C57B1/6 mice by intraveno us (i.v.) injection 8 weeks before an i.v. challenge with 4x10(3) CFU of Cryptococcus neoformans. Uninfected and singly infected mice-were u sed as controls. LP-BM5 infection did not result in a significant incr ease in fungal burdens in the lungs or brains of co-infected animals c ompared to mice infected with C. neoformans alone. However, mortality was enhanced in the co-infected animals. The kinetics of splenocyte su bsets differed in co-infected mice and LP-BM5-infected mice; the incre ase in CD4(+), CD8(+) and Ly5(+) cells was only moderate in the former . Cytokine production by concanavalin A (Con A)-stimulated splenocytes from co-infefted mice showed a marked decrease in the Th1 response (I FN-gamma, IL-2) and an increase in the Th2 response (IL-4, IL-10). Fur thermore, cryptococcosis altered the course of MAIDS, inhibiting splen omegaly. This effect was not related to a decrease in ecotropic virus titres in the spleen or to improved in vitro responsiveness of spleen cells to Con A. The marked decrease in IFN-gamma production in co-infe cted animals could partly explain the inhibition of LP-BM5-induced spl enomegaly. This model of murine retroviral infection does not seem to be suitable for studying cryptococcosis in immunosuppressed animals, b ut remains valuable for investigating in vivo interactions between two pathogens.