Fig. 2.

Overview of the intracellular life cycle of Trypanosoma cruzi in the mammalian host. (1) The metacyclic trypomastigote binds to receptors on the host cell surface resulting in the parasite being taken up into a parasitophorous vacuole. This occurs regardless of whether or not the host cell is phagocytic. (2) The parasite undergoes an asymmetric cell division following replication of the kinetoplast (red circle) and flagellum, but not the nucleus (Kurup and Tarleton, 2014). (3) This results in one daughter cell being a replication competent amastigote with a short flagellum, and the other being a dysnuclear flagellated cytoplasmic fragment. (4) The amastigote escapes into the cytoplasm and begins replication by binary fission. (5) The remaining parasite component is degraded by the proteasome and its antigens are presented on the surface. (6) Some amastigotes may become metabolically quiescent, although this is yet to be proven. Such amastigotes could reside long term in chronically infected tissue. (7) The amastigotes continue to replicate. (8) Amastigotes differentiate into an intracellular epimastigote-like form. It is not clear whether this is an obligate stage, or if they can go straight from amastigotes to trypomastigotes (dashed arrow). (9) The parasites finally differentiate into the flagellated bloodstream trypomastigotes, lyse the host cell and escape into the bloodstream or tissue fluids (10).