T. cruzi infection and Chagas' disease is a major public health problem in Latin America. The disease shows three distinct phases of development, acute, indeterminate and chronic, with great geographical diversity in its severity and prevalence. The initial events of infection produce direct tissue damage due to host cell invasion but can eventually progress to a pathogenesis which seems no longer to require the parasite. The host's own anti-parasite immune response has been implicated in the pathology seen during late acute- and chronic-phase disease. Parasite antigens have the potential to modify the surface of both infected and uninfected host cells, thus exposing them to the host's own anti-parasite immune response in late acute phase. Autoimmunity develops during the chronic phase and could act to sustain the parasite-initiated pathogenesis. These observations have obvious implications for immunoprophylaxis—an effective vaccine must prevent or cure infection, but must not produce autoimmunization.
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Hudson et al. (1985) studied this question.