Chagas' disease affects over 18 million people in Latin America. The agent responsible is a protozoan parasite, Trypanosoma cruzi, transmitted by haematophagous insects. For survival in the host's organism, it uses several strategies, but especially one of inhibiting the host's immune response. Research scientists from the IRD and INSERM (1) who are studying this trypanosome found that one of the proteins it secretes, Tc52, is a virulence factor that plays a pivotal role in the infection mechanism. Combining different invitro and in-vivo approaches, they brought into evidence its role in the development of infection and performed the molecular characterization by peptide analysis of the minimal sequence of Tc52 that carries immunosuppressive activity. Knowledge of the biological activity of this factor raises the prospects for developing vaccination strategies or drugs to combat T. cruzi.

Chagas' disease or American trypanosomiasis is a parasitic illness which affects nearly 20 million people mainly in tropical regions of Central and South America. The aetiological agent that causes it is a flagellate protozoan, Trypanosoma cruzi, transmitted to humans by haematophagous insects (Reduviidae). Research scientists from the IRD research unit "Pathognie des Trypanosomatidae" and co-workers from INSERM have studied the parasite's development cycle, its virulence and its involvement in the infection process, with a view to identifying possible prevention and control methods. Using techniques of cellular and molecular biology, and of biochemistry, they sought to identify the nature and function of T. cruzi genes which code for the factors responsible for the virulence, in particular a protein called Tc52.

As in any parasitic disease, the pathogen's ability to survive in its vertebrate host depends on many mechanisms, especially one which weakens the host's immune response. In Chagas' disease, during its life-cycle in humans T. cruzi takes on two forms,
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Contact: Bndicte Robert
presse@paris.ird.fr
33-1-48-03-75-19
Institut de Recherche Pour le Dveloppement
6-Jan-2004

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