Abstract

In terms of control of Chagas disease, it is important to reexamine the association of T. cruzi genotypes with drug susceptibility, virulence, and pathogenesis, all of which are traits that may be rapidly spread by genetic exchange within and between lineages. Given the high level of genetic diversity within T. cruzi and the complexity of its population structure, new drugs should be tested against representatives of all the lineages, including hybrid strains. The concept that genetic exchange is of little importance to T. cruzi is no longer tenable. Experimental work has demonstrated that T. cruzi has an extant capacity for genetic exchange, albeit by a somewhat unusual mechanism of fusion of diploids and genome erosion. Interlineage genetic exchange, though infrequent, has clearly shaped the evolution of the species, giving rise to at least two of the principal DTUs, TcV, and TcVI. Furthermore, this has had a profound epidemiological impact: TcV and TcVI are widespread and probably recently dispersed agents of severe Chagas disease. Mitochondrial introgression suggests additional interlineage recombination events. Mechanisms of genetic exchange in natural populations may be more varied and distinct from fusion of diploids and genome erosion discovered in the laboratory. The extent of intralineage genetic exchange is still not clear, and demands improved intensive multiclonal sampling, and genetic analysis of populations from single hosts, vectors, and communities. Ideally, further experimental crosses combined with genome–scale sequence analysis of parents and resulting hybrids, as well as higher resolution analysis of natural hybrids and their putative parents, would give rapid and incisive insights into mechanisms of genetic exchange in T. cruzi.

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