Population genetics of trypanosoma brucei rhodesiense: clonality and diversity within and between foci

Duffy, C.W., MacLean, L., Sweeney, L., Cooper, A., Turner, C.M.R., Tait, A., Sternberg, J., Morrison, L.J. and MacLeod, A. (2013) Population genetics of trypanosoma brucei rhodesiense: clonality and diversity within and between foci. PLoS Neglected Tropical Diseases, 7(11), e2526. (doi:10.1371/journal.pntd.0002526)

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Abstract

African trypanosomes are unusual among pathogenic protozoa in that they can undergo their complete morphological life cycle in the tsetse fly vector with mating as a non-obligatory part of this development. Trypanosoma brucei rhodesiense, which infects humans and livestock in East and Southern Africa, has classically been described as a host-range variant of the non-human infective Trypanosoma brucei that occurs as stable clonal lineages. We have examined T. b. rhodesiense populations from East (Uganda) and Southern (Malawi) Africa using a panel of microsatellite markers, incorporating both spatial and temporal analyses. Our data demonstrate that Ugandan T. b. rhodesiense existed as clonal populations, with a small number of highly related genotypes and substantial linkage disequilibrium between pairs of loci. However, these populations were not stable as the dominant genotypes changed and the genetic diversity also reduced over time. Thus these populations do not conform to one of the criteria for strict clonality, namely stability of predominant genotypes over time, and our results show that, in a period in the mid 1990s, the previously predominant genotypes were not detected but were replaced by a novel clonal population with limited genetic relationship to the original population present between 1970 and 1990. In contrast, the Malawi T. b. rhodesiense population demonstrated significantly greater diversity and evidence for frequent genetic exchange. Therefore, the population genetics of T. b. rhodesiense is more complex than previously described. This has important implications for the spread of the single copy T. b. rhodesiense gene that allows human infectivity, and therefore the epidemiology of the human disease, as well as suggesting that these parasites represent an important organism to study the influence of optional recombination upon population genetic dynamics.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:MacLeod, Professor Annette and Tait, Professor Andy and Sweeney, Mrs Lindsay and Turner, Professor Charles and Cooper, Dr Anneli
Authors: Duffy, C.W., MacLean, L., Sweeney, L., Cooper, A., Turner, C.M.R., Tait, A., Sternberg, J., Morrison, L.J., and MacLeod, A.
College/School:College of Medical Veterinary and Life Sciences > Institute of Biodiversity Animal Health and Comparative Medicine
College of Medical Veterinary and Life Sciences > School of Veterinary Medicine
College of Medical Veterinary and Life Sciences > Institute of Infection Immunity and Inflammation
Journal Name:PLoS Neglected Tropical Diseases
Publisher:Public Library of Science
ISSN:1935-2727
ISSN (Online):1935-2727
Copyright Holders:Copyright © 2013 The Authors
First Published:First published in PLoS Neglected Tropical Diseases 7(11):e2526
Publisher Policy:Reproduced under a Creative Commons License
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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
558211The origins and mechanisms of human infectivity in African trypanosomes.Annette MacleodWellcome Trust (WELLCOME)095201/Z/10/ZRI BIODIVERSITY ANIMAL HEALTH & COMPMED