Original research

Chagas disease and HIV co-infection: genetic analyses of two Trypanosoma cruzi strains under experimental immunosuppression

Célia M Marques de Brito¹, Marize Q Pires² and Raquel S Pacheco²

¹  Departamento de Ciências Biológicas, Escola Nacional de Saúde Publica, Fundação Oswaldo Cruz-FIOCRUZ, Rua Leopoldo Bulhões, 1480/6° andar, 21041-210, Rio de Janeiro, RJ, Brazil

²  Departamento de Bioquímica e Biologia Molecular, Instituto Oswaldo Cruz, FIOCRUZ, RJ, Brazil

Kinetoplastid Biology and Disease 2003, 2:17doi:10.1186/1475-9292-2-17

Published:	28 October 2003

Abstract

Background

Recently new aspects of the immunopathology of Chagas disease have been described in patients infected with HIV and unusual clinical manifestations such as cutaneous lesions, involvement of central nervous system and/or serious cardiac lesions related to the reactivation of the parasite have been reported. Two uncloned Trypanosoma cruzi strains previously isolated from chronic chagasic patients with HIV co-infection were studied in order to evaluate the impact of the immunosuppression on the genetic diversity of the parasite.

Results

We have exploited an experimental model to determine whether genetically distinct populations appear after immunosuppression as a consequence of in vivo selection or in vitro propagation. The in vitro and in vivo conditions have allowed us to study the selected populations. The first strain was isolated from a case of reactivation of Chagas disease in a patient which presented four cerebral lesions. It was possible to demonstrate that the patient was infected with at least three distinct populations of T. cruzi. The population, recovered after immunosuppression, in mice was genetically divergent from the primary human isolate. The second strain, isolated from a hemophiliac/HIV positive patient presenting cardiac manifestation of Chagas disease showed no marked genetic difference after experimental immunosuppression.

Conclusion

The immunological condition of the patient, associated or not to the reactivation of the infection, and also the strain of the parasite may have an important role during the course of the disease. The in vivo mechanism that generates parasite genetic variability or the participation of the selection under stress conditions will require further investigation.