Abstract
Background: Trypanosoma cruzi has a high rate of biological and genetic variability, and its population structure is divided into seven distinct genetic groups (TcI-TcVI and Tcbat). Due to immigration, Chagas disease (ChD), caused by T. cruzi, has become a serious global health problem including in Europe. Therefore, the aim of this study was to evaluate the existence of genetic variability within discrete typing unit (DTU) TcV of T. cruzi in Bolivian patients with chronic ChD residing in Barcelona, Spain.Methods: The DNA was extracted from the peripheral blood of 27 patients infected with T. cruzi DTU TcV and the fragments of the genetic material were amplificated through the low stringency single primer-polymerase chain reaction (LSSP-PCR). The data generated after amplification were submitted to bioinformatics analysis.Results: Of the 27 patients evaluated in the study, 8/27 (29.6%) were male and 19/27 (70.4%) female, 17/27 (62.9%) were previously classified with the indeterminate clinical form of Chagas disease and 10/27 (37.1%) with Chagas cardiomyopathy. The LSSP-PCR detected 432 band fragments from 80 to 1,500 bp. The unweighted pair-group method analysis and principal coordinated analysis data demonstrated the existence of three distinct genetic groups with moderate-high rates of intraspecific genetic variability/diversity that had shared parasite's alleles in patients with the indeterminate and cardiomyopathy forms of ChD.Conclusions: This study demonstrated the existence of a moderate to high rate of intra-DTU TcV variability in T. cruzi. Certain alleles of the parasite were associated with the absence of clinical manifestations in patients harboring the indeterminate form of ChD. These results support the need to search for increasingly specific targets in the genome of T. cruzi to be correlated with its main biological properties and clinical features in patients with chronic ChD.
Highlights
Chagas disease (ChD) is caused by the hemoflagellate protozoan Trypanosoma cruzi and chronic Chagas cardiomyopathy is the most severe manifestation [1]
There is evidence for Latin American immigration to northern countries in Europe as well [10, 26]. These population movements have increased the occurrence of ChD in these countries [9], since a considerable proportion of Latin American immigrants are chronically infected with T. cruzi, added to the occurrence of autochthone cases transmitted by mechanisms independent to triatomine vectors
Through unweighted pair-group method analysis (UPGMA) and principal coordinated analysis (PCoA) of random amplification of polymorphic DNA, the existence of a high rate of genetic variability within discrete typing units (DTUs) TcII and TcVI of T. cruzi in samples from patients with chronic ChD residing in an important endemic region of Minas Gerais state, Brazil
Summary
Chagas disease (ChD) is caused by the hemoflagellate protozoan Trypanosoma cruzi and chronic Chagas cardiomyopathy is the most severe manifestation [1]. The genetic structure of T. cruzi is currently divided into seven distinct genetic groups, known as discrete typing units (DTUs), TcI–TcVI, and TcBat [3, 4]. Population movement over recent years has led to an increased prevalence of ChD in these countries, primarily due to high numbers of Latin American immigrants chronically infected with T. cruzi [10]. Trypanosoma cruzi has a high rate of biological and genetic variability, and its population structure is divided into seven distinct genetic groups (TcI-TcVI and Tcbat). The aim of this study was to evaluate the existence of genetic variability within discrete typing unit (DTU) TcV of T. cruzi in Bolivian patients with chronic ChD residing in Barcelona, Spain
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