ArticleParasites & vectors2016
Population genetic structure and temporal stability among Trypanosoma brucei rhodesiense isolates in Uganda.
Article in Parasites & vectors, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- In vitro culture of freshly isolated Trypanosoma brucei brucei bloodstream forms results in gene copy-number changes.PLoS neglected tropical diseases · 2021Article
- Relationship between Trypanosoma brucei rhodesiense genetic diversity and clinical spectrum among sleeping sickness patients in Uganda.BMC research notes · 2017Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundThe population structure and role of genetic exchange in African trypanosomes have been previously analyzed albeit with contradictory findings. To further investigate the role of genetic polymorphism on the population genetic structure of Trypanosoma b. rhodesiense, we hypothesized that parasite genotypes are clonal and stable over time.
methodsWe have undertaken a microsatellite marker analysis of T. b. rhodesiense isolates in a relatively new active HAT focus in Uganda (Kaberamaido-Dokolo-Amolatar) over a six-year period (2006-2012). We amplified six microsatellite markers by PCR directly from blood spotted FTA cards following whole genome amplification.
resultsThe majority of loci demonstrated an excess of heterozygosity (Ho > He, F(IS) < 0). We identified 26 unique genotypes among the 57 isolates, accounting for 45.6% genotypic polymorphism. The presence of a high proportion of samples with repeated genotypes (54.4%, 31/57), disagreement with Hardy-Weinberg equilibrium, and significant linkage disequilibrium between loci pairs, provide evidence that T. b. rhodesiense isolates from this focus are clonal. Our results show low values of F(ST)' (0-0.115) indicating negligible genetic differentiation across temporal isolates. Furthermore, predominant genotypes isolated in 2006 were still detectable in 2012.
conclusionsOur findings confirm the notion that endemicity is maintained by stable genotypes rather than an influx of new genotypes. Our results have considerable importance in understanding and tracking the spread of sleeping sickness with significant implication to disease control.
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