Abstract
Acquisition of detailed knowledge of the structure and evolution of Trypanosoma cruzi populations is essential for control of Chagas disease. We profiled 75 strains of the parasite with five nuclear microsatellite loci, 24Sα RNA genes, and sequence polymorphisms in the mitochondrial cytochrome oxidase subunit II gene. We also used sequences available in GenBank for the mitochondrial genes cytochrome B and NADH dehydrogenase subunit 1. A multidimensional scaling plot (MDS) based in microsatellite data divided the parasites into four clusters corresponding to T. cruzi I (MDS-cluster A), T. cruzi II (MDS-cluster C), a third group of T. cruzi strains (MDS-cluster B), and hybrid strains (MDS-cluster BH). The first two clusters matched respectively mitochondrial clades A and C, while the other two belonged to mitochondrial clade B. The 24Sα rDNA and microsatellite profiling data were combined into multilocus genotypes that were analyzed by the haplotype reconstruction program PHASE. We identified 141 haplotypes that were clearly distributed into three haplogroups (X, Y, and Z). All strains belonging to T. cruzi I (MDS-cluster A) were Z/Z, the T. cruzi II strains (MDS-cluster C) were Y/Y, and those belonging to MDS-cluster B (unclassified T. cruzi) had X/X haplogroup genotypes. The strains grouped in the MDS-cluster BH were X/Y, confirming their hybrid character. Based on these results we propose the following minimal scenario for T. cruzi evolution. In a distant past there were at a minimum three ancestral lineages that we may call, respectively, T. cruzi I, T. cruzi II, and T. cruzi III. At least two hybridization events involving T. cruzi II and T. cruzi III produced evolutionarily viable progeny. In both events, the mitochondrial recipient (as identified by the mitochondrial clade of the hybrid strains) was T. cruzi II and the mitochondrial donor was T. cruzi III.
Highlights
The parasite protozoan Trypanosoma cruzi causes Chagas disease, a malady that afflicts almost 20 million people in South America and Central America, with more than 20,000 deaths reported each year [1,2]
By partitioning the variability within and between mitochondrial clades we found that for cytochrome oxidase subunit II (COII), cytochrome b (CYb), and NADH dehydrogenase subunit 1 (ND1), respectively, 97%, 91%, and 68% of the genetic variability was found among clades
Our first strategy was to perform the phylogenetic analysis of T. cruzi populations by using microsatellite data
Summary
The parasite protozoan Trypanosoma cruzi causes Chagas disease, a malady that afflicts almost 20 million people in South America and Central America, with more than 20,000 deaths reported each year [1,2]. It is estimated that the parasite emerged as a species well over 150 million years ago, originally infecting primitive mammals dispersed throughout Laurasia and Gondwanaland, regions that originated North and South America, respectively [3]. The first contact with humans occurred much more recently, in the late Pleistocene, 15,000–20,000 years ago, when humans first peopled the Americas—Homo sapiens is a very recent new host for T. cruzi. There is convincing molecular evidence for the presence of T. cruzi DNA in mummies exhumed in Northern Chile and Southern Peru and dating as far back as 9,000 years before the present day. There is convincing molecular evidence for the presence of T. cruzi DNA in mummies exhumed in Northern Chile and Southern Peru and dating as far back as 9,000 years before the present day. [4]
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