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Contact: Patrick Reilly
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Public Library of Science

Parasite-induced genetically driven autoimmune chagas disease

Researchers have shown that the Trypanosoma cruzi agent of Chagas Disease (CD) invades host embryo cells and spreads its mitochondrial DNA (kDNA) minicircles into the host's genome. Dr. Antonio Teixeira and associates at the University of Brasília, Brazil, inoculated virulent typanosomes in fertile chicken eggs and documented the heritability and fixation of the kDNA mutations in the chicks and their progeny. The results, published in the open-access journal PLoS Neglected Tropical Diseases on March 29th, show that kDNA-mutated chickens undergo genotype alterations, developing an inflammatory heart condition similar to Chagas disease in humans.

Chagas is one of the most lethal endemic infectious diseases in the Western Hemisphere, and although initially restricted to South America, it is now present in many parts of the world. This insect-born infection can also be transmitted from mother to child and via blood transfusion, and while acute infections are usually acquired in infancy or childhood, chronic Chagas disease kills many of those infected after they reach 40 years of age. The disease attacks the heart and is the most frequent cause of heart failure in endemic regions. While the treatment of Chagas disease with anti-trypanosomal nitroderivatives curtails the parasitic infection, it does not abrogate the destructive heart lesions which can lead to death.

An earlier study by Santos-Buch and Teixeira (1974) showed that immune lymphocytes from chagasic rabbits destroy embryo heart cells in vitro, and that this accelerated rejection of target cells occurred within 10 hours. Control, non-immune lymphocytes adhered to target heart cells 72 hours after incubation. Now, Dr Teixeira's research team describes the origin of the autoimmune rejection of the target heart cells in Chagas disease: "This chicken model was necessary to eliminate any residual active infection, because the birds are resistant to T. cruzi infection upon hatching. The kDNA-mutated chickens develop clinical signs of the heart disease and failure - their hearts are grossly enlarged and microscopic exams reveal that immune lymphocytes adhere to the target cells and lyses."

As Dr. Teixeira explains, this is "the first time that an autoimmune disease has been experimentally reproduced in an animal model, showing specific parasite induced kDNA modifications in coding regions of the host's genome".

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FINANCIAL DISCLOSURE: This work was supported by the National Research Council-CNPq and by the Foundation for Science Development of the Federal District, Brazil. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

COMPETING INTERESTS: The authors have declared that no competing interests exist.

PLEASE ADD THIS LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.plos.org/10.1371/journal.pntd.0001000 (link will go live upon embargo lift)

CITATION: 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

CONTACT:

Prof. Antonio Teixeira
University of Brasilia
55+61 3349 4987
ateixeir@unb.br

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