Abstract

After the horizontal transference of kDNA minicircle sequences into the genome of chagasic mammals it was possible to show the heritage of the kDNA mutation into those rabbits breed. However, mammals are permissive to infection by T. cruzi, which may persist through the animal life. To ensure that the kDNA mutation was not only a noise produced by the cryptic infection it was necessary to dismiss this possibility. This was possible through experiments using birds that are refractory to T. cruzi infection but are permissive to infection only in the first 10 days of embryonic life. When the fertile eggs were inoculated with T. cruzi the breed was born without infection but presenting the kDNA mutation. In this regard, rabbits and birds with kDNA mutation presented typical Chagas disease lesions: minimal rejection unit which is characteristic of the pathology of this disease where the non-parasitized target cell was destroyed by the cells from the vertebrate host´s immune system. These experiments showed that the minimal rejection unit is the common denominator of the pathogenesis of Chagas disease in vertebrate animals. In the chicken model refractory to T. cruzi the cardiomegaly was linked to the minimal rejection unit’s inflammatory infiltration. Therefore the parasite-free chicken heart pathology seen in kDNA-mutated chickens could be linked to the genotype and phenotype alterations. The mechanism whereby these alterations induce the immune rejection of the chicken’s heart requires further investigation.