School of Medicine of Ribeirao Preto, University of Sao Paulo, Federal University of Bahia School of Medicine, Seattle Biomedical Research Institute, Department of Medicine, Division of International Medicine, Cornell University Medical College, Ribeirao Preto, Brazil
Given the dissemination of acquired immunodeficiency syndrome (AIDS) in Latin America, where Chagas' disease is endemic, there is a present and increasing risk of concurrent infections with human immunodeficiency virus (HIV) and Trypanosoma cruzi. We used the model of murine acquired immunodeficiency syndrome (MAIDS) caused by a murine leukemia virus (MuLV) that induces immunologic alterations with similarities to those accompanying human HIV infection to study aspects of concomitant infections. The MuLV infection was found to reactivate T. cruzi infection in C57BI/10 mice, as indicated by elevated parasitemia and lymphocytic infiltration in the myocardium. The T cells from these animals did not respond to T. cruzi antigens (lymphocyte proliferation, interferon-gamma, or interleukin-2 [IL-2] production) but had increased levels of IL-10. Trypanosoma cruzi-specific antibody was decreased but not absent in dually infected animals. In a second set of experiments, we infected MAIDS-resistant B6D2 mice with MuLV, followed by infection with T. cruzi. These animals had higher parasitemia than those infected with T. cruzi alone. More interestingly, only dually infected animals developed MAIDS. The present report describes the activation of T. cruzi infection by MuLV as well as the aggravation of MuLV infection by T. cruzi. These results may be relevant to coinfections with retrovirus and protozoan parasites in humans.