Abstract

BackgroundChagas disease is a systemic pathology caused by Trypanosoma cruzi. This parasite reveals remarkable genetic variability, evinced in six Discrete Typing Units (DTUs) named from T. cruzi I to T. cruzi VI (TcI to TcVI). Recently newly identified genotypes have emerged such as TcBat in Brazil, Colombia and Panama associated to anthropogenic bats. The genotype with the broadest geographical distribution is TcI, which has recently been associated to severe cardiomyopathies in Argentina and Colombia. Therefore, new studies unraveling the genetic structure and natural history of this DTU must be pursued.ResultsWe conducted a spatial and temporal analysis on 50 biological clones of T. cruzi I (TcI) isolated from humans with different clinical phenotypes, triatomine bugs and mammal reservoirs across three endemic regions for Chagas disease in Colombia. These clones were submitted to a nuclear Multilocus Sequence Typing (nMLST) analysis in order to elucidate its genetic diversity and clustering. After analyzing 13 nuclear housekeeping genes and obtaining a 5821 bp length alignment, we detected two robust genotypes within TcI henceforth named TcIDOM (associated to human infections) and a second cluster associated to peridomestic and sylvatic populations. Additionaly, we detected putative events of recombination and an intriguing lack of linkage disequilibrium.ConclusionsThese findings reinforce the emergence of an enigmatic domestic T. cruzi genotype (TcIDOM), and demonstrates the high frequency of recombination at nuclear level across natural populations of T. cruzi. Therefore, the need to pursue studies focused on the diferential virulence profiles of TcI strains. The biological and epidemiological implications of these findings are herein discussed.

Highlights

  • Chagas disease is a systemic pathology caused by Trypanosoma cruzi

  • We calculated the typing efficiency according to the nuclear Multilocus Sequence Typing (nMLST) scheme observing the highest number of different genotypes per polymorphic sites for Hydroxy-3-methylglutaryl-CoA reductase (HMCOAR), Pyruvate dehydrogenase component E1 subunit alpha (PDH), RHO1, Leucine aminopeptidase (LAP), GPI, LYT1, STPP2, RNA bindingprotein 19 (RB19) and Trypanothion reductase (TR); and the lowest values for Glutathione peroxidase (GPX), GTP-binding protein Rab7 (GTP), Superoxide dismutase A (SODA) and Superoxide dismutase B (SODB)

  • Our results demonstrate that T. cruzi I (TcI) exhibits a pattern of unstable genotype among the six Discrete Typing Units of T. cruzi; a pattern that may be explained by the diverse number of insect vector and mammals that can be found naturally infected with this DTU

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Summary

Introduction

Chagas disease is a systemic pathology caused by Trypanosoma cruzi. This parasite reveals remarkable genetic variability, evinced in six Discrete Typing Units (DTUs) named from T. cruzi I to T. cruzi VI (TcI to TcVI). The studies focused on determining the genetic diversity of parasites is mandatory, as well as the study of the propagation mechanisms displayed by these microorganisms. These mechanisms have been partially elucidated in Toxoplasma gondii, Trypanosoma brucei, Trypanosoma cruzi, Leishmania, Giardia and other parasitic protozoa [1,2,3,4,5]. Understanding the propagation method employed by the parasitic protozoa may have important implications in the disease prevalence, which suggest a potential topic for the synergy between population genetics and public health systems

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