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The results: how does T. cruzi evolve?

Having performed evolutionary analysis based on the principles recalled above, the results presented hereafter have emerged.

Is T. cruzi a "good" species?

This is the first question to arise from a medical and epidemiological point of view, especially when studying molecular epidemiology (strain typing). Defining what a good species is refers to the very definition of what a species is. Briefly, species are generally defined as: (1) a community of sexual reproduction (the biological species concept); (2) a clade (a monophyletic lineage with only one ancestor; the phylogenetic species concept); or (3) a set of organisms that share specific phenotypic traits (the phenotypic species concept). The biological species concept is not easy to handle and inadequate in those organisms in which sexual reproduction is not a constant and mandatory process, which it is the case for the agent of Chagas disease. On the other hand, there is no doubt that T. cruzi meets the criteria for (2) and (3) (phylogenetic and phenotypic species concepts). All phylogenetic studies have brought all T. cruzi strains into a single clade that is distinguishable from closely

related taxa (T. cruzi marenkellei, a close relative of T. cruzi, a bat parasite, is the best choice of such an outgroup). Moreover, all T. cruzi strains share a set of specific phenotypic characteristics (morphological aspect, vectorial transmission by triatomine bugs, potential host range extended to all mammal species, but restricted to them, geographical distribution limited to the New World, potential pathogenic power all point to Chagas disease). Consequently, according to the phylogenetic and phenotypic concepts, T. cruzi is a so-called good species. The fact that T. cruzi is a unique clade makes it possible to design various molecular markers that will be specifically shared by all strains of the taxon and only by them (in the cladistic jargon, synapomorphic characteristics).

T. cruzi undergoes PCE

It can actually be said that the agent of Chagas disease is a paradigmatic case of this evolutionary model. Recurrent observations have been made of multilocus genotypes that have persisted unchanged for more than 30 years over vast geographical areas. Moreover, the linkage disequilibrium in T. cruzi is considerable and has been verified for a large set of genetic markers, including MLEE,1,53 restriction-fragment length polymorphism of kinetoplast DNA,54 RAPD,55,56 and microsatellites.57 Linkage disequilibrium is so strong in T. cruzi that it also involves the polymorphism of expressed genes surveyed by random amplified differentially expressed sequences (RADES)58 and genes that undergo strong natural selection.59

Again, clonality and clonal evolution are taken here in the genetic sense and the precise cytological mechanism of PCE in T. cruzi continues to be debated. Homogamy and self-fertilization10 could play a role in some cycles, as suggested by results obtained with microsatellite markers.60 Nevertheless, the important result remains: genetically homogeneous lines isolated from each other (genetic clones by definition) persist over long periods of time and vast geographical areas in natural populations of T. cruzi.

Other evidence for PCE in T. cruzi comes from the existence of stable genetic subdivisions, within which PCE is also verified (see further).

 
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