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Updated: Aug 11, 2026

Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
Published on: July 29, 2012
Induction of cardiac autoimmunity in Chagas heart disease: a case for molecular mimicry
Edecio Cunha-Neto1, Angelina M Bilate, Kenneth V Hyland
1Heart Institute (InCor), Laboratory of Immunology, São Paulo, Brazil. edecunha@usp.br
Insights
Chagas disease cardiomyopathy (CCC) may stem from an autoimmune response, not just the parasite Trypanosoma cruzi. Molecular mimicry is a key factor in this post-infectious autoimmune process.
Area of Science:
- Immunology
- Infectious Diseases
- Cardiology
Background:
- Chagas disease affects millions in Latin America, with a third developing chronic cardiomyopathy.
- Cardiomyocyte destruction in Chagas disease cardiomyopathy (CCC) involves inflammation and fibrosis, with few parasites present.
- The pathogenesis of CCC suggests a potential post-infectious autoimmune mechanism.
Purpose of the Study:
- To review evidence supporting an autoimmune basis for CCC.
- To emphasize the role of molecular mimicry in CCC pathogenesis.
Main Methods:
- Review of scientific literature on Chagas disease cardiomyopathy.
- Analysis of autoimmune and molecular mimicry phenomena in human and experimental models.
Main Results:
- Significant reports indicate autoimmune phenomena and molecular mimicry in CCC over the last two decades.
- Evidence supports an autoimmune basis for CCC pathogenesis.
Conclusions:
- Autoimmunity, particularly molecular mimicry, is a fundamental mechanism in Chagas disease cardiomyopathy.
- Understanding these autoimmune processes is crucial for developing effective treatments for CCC.
Abstract:
Up to 18 million of individuals are infected by the protozoan parasite Trypanosoma cruzi in Latin America, one third of whom will develop chronic Chagas disease cardiomyopathy (CCC) up to 30 years after infection. Cardiomyocyte destruction is associated with a T cell-rich inflammatory infiltrate and fibrosis. The presence of such lesions in the relative scarcity of parasites in the heart, suggested that CCC might be due, in part, to a postinfectious autoimmune process. Over the last two decades, a significant amount of reports of autoimmune and molecular mimicry phenomena have been described in CCC. The authors will review the evidence in support of an autoimmune basis for CCC pathogenesis in humans and experimental animals, with a special emphasis on molecular mimicry as a fundamental mechanism of autoimmunity.
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