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Trypanosoma cruzi, the etiological agent of Chagas disease, presents a high degree of intraspecific genetic variability, with possible implications for the clinical forms of the disease, like the development of cardiopathy, megaesophagus, and megacolon, alone or in combination. This tissue tropism involved in the pathogenesis of Chagas disease has still not been totally elucidated. Thus, the current review approaches key aspects of T. cruzi genetic diversity, the clinical forms of Chagas disease, and the infection of the host cell by the parasite and the immune response. Other aspects discussed here include the release of immunosuppressive factors by the parasite, acting in the host's immune response pathways; host cell apoptosis inhibition; the pathogenesis of chagasic megaesophagus, which can be related to host-parasite interaction; and finally the association between megaesophagus and increased risk for the development of squamous-cell esophageal carcinoma. However, despite great advances in the understanding of this disease, it is still not possible to establish the true relationship between the parasite's genetic variability and the clinical form of Chagas disease.

Implications of genetic variability of Trypanosoma cruzi for the pathogenesis of Chagas disease