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Genetic Diversity of Trypanosoma cruzi and the Epidemiology of Chagas Disease

This chapter appears in the following book:

Molecular Mechanisms of Pathogenesis in Chagas Disease

Edited by: JohnM. Kelly
ISBN: 0-306-47849-8
» Get more information about this book at landesbioscience.com «

Chapter authors:
Michael A Miles, Matthew Yeo and Michael Gaunt

The complex epidemiology of Chagas disease is not fully understood. It has been suggested that distinct genotypes of Trypanosoma cruzi may cause the severe (megasyndromes)
and benign forms of chronic Chagas disease, which appear to differ in geographical distribution. Multi-locus enzyme electrophoresis (MLEE) and analyses of DNA polymorphisms with several targets have demonstrated that T. cruzi has a remarkable degree of genetic diversity. Both isoenzyme and DNA analyses define two major subdivisions within the species, T. cruzi I and T. cruzi II, with marked heterogeneity and five subdivisions within T. cruzi II (II a-e). Population genetic analyses have indicated that T. cruzi is predominantly clonal, although the isolates studied have mainly been sporadically collected over vast geographical distances. However, T. cruzi IId and IIe display putatively hybrid phenotypes in the form of multiple heterozygous isoenzyme phenotypes. Phylogenetics analyses have confirmed the hybrid nature of T. cruzi IId and IIe and indicate that genetic exchange has contributed to the evolution of genetic diversity in T. cruzi. The T. cruzi strain selected for the genome sequencing project is a hybrid (IIe) strain. We have proved experimentally that T. cruzi I has an active capacity for genetic exchange using parental isolates taken from a single locality where parents and hybrids were sympatric. Experimentally derived hybrid clones displayed a combination of parental phenotypes and genotypes, indicating that T. cruzi may evolve via hybridisation, aneuploidy and genome erosion. We propose tentative associations for T. cruzi I, with the maruspial Didelphis (common opossum), the triatomine genus Rhodnius and the palm tree ecotope, and for T. cruzi II with edentates (armadillos), rodents, the triatomine genus Triatoma and the terrestrial ecotope. We conclude that there must be a link between T. cruzi genotype and outcome of infection but the nature of the link in terms of disease pathogenesis remains to be defined.

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