Author Summary [PLoS NTDS] The Trypanosoma cruzi acute infections can be asymptomatic but approximately one third of the chronically infected cases may present Chagas disease. Parasite persistence and autoimmunity are theories trying to explain the clinical and pathological manifestations of Chagas disease in the heart and the digestive system. To clearly demonstrate roles played by parasite persistence and autoimmunity in Chagas disease we used a chicken model refractory to the T. cruzi. In this study we inoculated the invasive T. cruzi in the air chamber of embryonated eggs. The infection was eradicated by the innate immunity and the chicks were parasite-free at hatching, but they retained the parasitic mitochondrial kinetoplast DNA minicircle in their genome. We documented the kDNA minicircle integrated in the chicken genome by a targeted prime TAIL-PCR, Southern hybridizations, cloning and sequencing. The kDNA minicircles integrated in coding regions of various chromosomes, and mutated chickens developed an inflammatory cardiomyopathy hallmark of Chagas disease, whereby immune system mononuclear cells lyse parasite-free target heart fibers. Genotype alterations resulting from transfers of the parasitic DNA were associated with the tissue destruction carried out by effectors CD45⁺, CD8γδ⁺, CD8α lymphocytes. This research provides insights about a protozoan infection that can induce genetically driven autoimmune disease.

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Teixeira ARL, Gomes C, Nitz N, Sousa AO, Alves RM, et al. (2011) Trypanosoma cruzi in the Chicken Model: Chagas-Like Heart Disease in the Absence of Parasitism. PLoS Negl Trop Dis 5(3): e1000. doi:10.1371/journal.pntd.0001000