The Th1 to Th2 shift induced by Schistosoma mansoni does not exacerbate murine aids (MAIDS)

Schistosoma mansoni infection in mice is associated with a switch from a Th 1 to a Th2-type cytokine response. The role of Th1 and Th2 responses in imm une dysregulations associated with AIDS and murine AIDS (MAIDS) is controve rsial, bur a Th2 bias could be associated with disease progression, raising the hypothesis that helminth infections might accelerate the retroviral di sease progression. Here, we used the murine model of AIDS to evaluate the c ourse of the viral disease during co-infection with S. mansoni, C57BL/6 mic e were infected with S. mansoni cercariae S weeks before intravenous challe nge with the LP-BM5 retroviral complex. MAIDS did not progress faster in co -infected mice, in terms of spleen and inguinal lymphadenopathy size, ecotr opic vine titres in the spleen, or in vitro proliferative responses to mito gen. Th2 cytokine production was not enhanced in co-infected animals, excep t for an isolated increase in IL-4 production 21 weeks after LP-BM5 injecti on. Co-infected animals had significantly lower lymph node and spleen weigh ts than mice infected with LP-BM5 only. MAIDS did not influence the granulo matous response to S. mansoni in the liver of co-infected mice. Finally, in fection with S. mansoni neither enhanced Th2 cytokine production nor accele rated MAIDS progression in animals subsequently challenged with LP-BM5,