Abstract
Trypanosoma cruzi, the agent of Chagas disease, is a paradigmatic case of the predominant clonal evolution (PCE) model, which states that the impact of genetic recombination in pathogens’ natural populations is not sufficient to suppress a persistent phylogenetic signal at all evolutionary scales. In spite of indications for occasional recombination and meiosis, recent genomics and high-resolution typing data in T. cruzi reject the counterproposal that PCE does not operate at lower evolutionary scales, within the evolutionary units (=near-clades) that subdivide the species. Evolutionary patterns in the agent of Chagas disease at micro- and macroevolutionary scales are strikingly similar (“Russian doll pattern”), suggesting gradual, rather than saltatory evolution.
Highlights
Trypanosoma cruzi, the agent of Chagas disease, is a paradigmatic case of the predominant clonal evolution (PCE) model, which states that the impact of genetic recombination in pathogens’
The definition of clonality in PCE is based on severe restriction to genetic recombination, a definition that is shared by many authors working on pathogen population genetics
Which makes it possible to definitely and challenge the PCE hypothesis is the absence of a stable phylogenetic signal at any evolutionary scale and a population structure that meets panmictic expectations, lack of a statistically significant linkage disequilibrium [7]
Summary
Trypanosoma cruzi is the parasite responsible for Chagas disease in the New World. It has been the object of early, pioneering studies dealing with its isoenzyme variability, making it possible to characterize its strains [9]. The PCE model in T. cruzi has been challenged with two lines of arguments, namely—(i) it is based on outdated markers that lack resolution [13] This is not a valid argument—markers that lack resolution should favor the null hypothesis of panmixia (random genetic exchange) through a mechanism of statistical type II error (impossibility to reject the null hypothesis, not because this null hypothesis is true, but because of a lack of resolution of the used means to test it) rather than the working hypothesis of clonality (Figure 1). High-resolution genomic typing will show that similar patterns of obstacles to genetic exchange are not recorded at lower evolutionary scales, under the level of the near-clades [14]. This last argument aims at challenging the “Russian doll model” [15], which states that. II resolution error (see Figure wrong hypothesis of panmixia due to a statistical type II error (see Figure 1)
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