RESISTANCE TO MURINE AIDS IN OFFSPRING OF MICE INFECTED WITH LP-BM5 -ROLE OF CD8 T-CELLS

The murine-acquired immunodeficiency syndrome (MAIDS) is caused by a m ixture of murine leukemia viruses (LP-BM5 MuLV). The influence of peri natal contact with retroviruses or their Ags on the response to infect ion was tested by infecting with LP-BM5 (MuLV) the adult offspring of mice with MAIDS. These offspring were resistant to disease after virus challenge. Most of them were free of defective viral DNA, and even th ose with molecular evidence of infection had lymphoid cells with a low er infectious capacity to cause MAIDS in naive recipients. No ecotropi c, xenotropic, or mink cell focus-forming (MCF) virus expression was f ound at the age of 5 wk, which is the time of LP-BM5 (MuLV) challenge. However, at 22 wk of age, one-half of the offspring from MAIDS mother s had ecotropic virus-expressing cells in their spleens, At the time o f suckling, offspring from infected mothers had enhanced percentages o f B cells and CD4 and CD8 T cells in the spleen, possibly followed by a slight persistent splenomegaly. These results suggest that immune re activity, rather than tolerance to the virus, is responsible for resis tance to disease after challenge. The offspring of MAIDS mice could cl ear the virus after challenge, This clearance was mediated by CD8 T ce lls, as continuous CD8 T cell depletion initiated at the time of viral challenge abrogated the resistance of these mice to MAIDS.