Background: Chagas disease is caused by the protozoan parasite Trypanosoma cruzi, which exhibits a high genetic variability. TcI, TcII, or mixed TcI/TcII strains may be found during acute human infection while mainly TcII parasites are present at the chronic stage of disease. In a previously studied Chagas disease outbreak, we identified mixed TcI/TcII strains in the vector Triatoma tibiamaculata and only TcII strains in infected humans, indicating that T. cruzi populations may be selected within the human host.
Methods: Utilizing molecular typing and cell biology techniques, we investigated the interaction of TcI, TcII, and mixed TcI/TcII strains with macrophages, an important cell population implicated in controlling protozoan infection.
Results: TcII but not TcI strains were selected by both human and murine macrophages in vitro and by peritoneal cavity cells in vivo. Biological analysis revealed that, compared with TcI, TcII strains display higher infective and multiplicative ability as well as lower doubling time inside macrophages. However, TcI and TcII strains present similar susceptibility to interferon-γ-activated macrophages in vitro.
Conclusions: Taken together, our results reveal the existence of an intracellular selection process in macrophages that favors TcII, but not TcI, when infection occurs with vector-derived mixed TcI/TcII strains.