Function on Peyer patch in mother to infant infection with MAIDS virus

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We have found that MAIDS virus infection through mother to infant causes persistent infection in infant. They developed immunodeficiency with general lymphadenopathy and splenomegaly after long carrier state. In contrast to infant, adult mice develop immediately murin AIDS in 4-5 weeks. We analyzed the mechanism of chronic infection in mother to infant infection in MAIDS virus. We found spleen cells derived from infant showed very weak reaction for ConcanavarineA or anti-CD3 antibody stimulation. Furthermore examination demonstrated poor reactivity owed not antigen presenting cells but T cells. The cytokine production by anti-CD3 antibody stimulation was measured by ELISA.The production dose of gamma-IFN and IL2 war very low, these were parallel to the spleen cells proliferation. But, IL4 was equal to adult. These facts show Th2 is dominant in neonate, contrast to Th1 in adult. We analyzed the effect of the reactivity to the MAIDS virus antigen on adult, when mice had been exposured to them at infant. In adult mice, being Th1 dominant, MAIDS virus antigen can induce the proliferation on naive T cells. But, exposured mice at infant period can not do. Th2 dominant state may induce not acute infection but persistent infection.