As a parasite with a potentially decades-long intracellular stage, Trypanosoma cruzi could
represent a case study for extreme mechanisms for the maintenance of mitochondrial sequence
integrity. While an intact mitochondrial repertoire of membrane-associated cytochromes and NADH
dehydrogenases are required for passage through the insect forms, within the vertebrate host many of
these products may be dispensable, as in vertebrate-exclusive relatives. The degeneration seen in
maxicircle genomes from clinical isolates and from culture indicates that the maintenance of intact
maxicircles and a complete library of minicircles is an uphill battle that the parasite manages actively.
Both the maxicircle and minicircle have been implicated in the clinical manifestation of Chagas
disease. The implications of both these scenarios on the biology of the parasite relative to the host are
discussed.