Figure 2.

Aspects of Trypanosoma cruzi evasion and persistence in the vertebrate host. T. cruzi parasites develop different strategies to evade the host defenses and establish a persistent infection. T. cruzi parasites evade the host innate immune responses associated with macrophage and complement system (A). The trans-sialidase (TS), a T. cruzi-derived virulence factor, can also overcome the host resistance responses to optimize the invasion and parasite persistence in chronic infection (B). The development of anti-parasite immune response is coupled with the activation of neuroendocrine axes that may affect the course of disease (C). Adipose tissue can be considered as a parasite reservoir and may contribute to the establishment of persistent infections, playing a major role in T. cruzi burst during immunosuppression periods (D). The recognition of T. cruzi-derived antigens in the thymus may restrict the central tolerance to parasite infection, while the release of immature and potentially autoimmune T cells to the peripheral non-lymphoid tissues may be related with disease pathology in the chronic phase (E).