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Development of nine microsatellite loci for Trypanosoma lewisi, a potential human pathogen in Western Africa and South-East Asia, and preliminary population genetics analysesuse asterix (*) to get italics
Adeline Ségard, Audrey Romero, Sophie Ravel, Philippe Truc, Gauthier Dobigny, Philippe Gauthier, Jonas Etougbetche, Henri-Joel Dossou, Sylvestre Badou, Gualbert Houéménou, Serge Morand, Kittipong Chaisiri, Camille Noûs, Thierry deMeeûsPlease use the format "First name initials family name" as in "Marie S. Curie, Niels H. D. Bohr, Albert Einstein, John R. R. Tolkien, Donna T. Strickland"
2022
<p><em>Trypanosoma lewisi</em> belongs to the so-called atypical trypanosomes that occasionally affect humans. It shares the same hosts and flea vector of other medically relevant pathogenic agents as Yersinia pestis, the agent of plague. Increasing knowledge on the population structure (reproductive mode, population size, dispersal) of this parasite thus represents a challenging but important issue. The use of polymorphic genetic markers, together with suitable population genetics tools, is a convenient way to achieve such objectives. To date, the population biology of <em>T. lewisi </em>is poorly known and, to our knowledge, no population genetics studies have ever been conducted. Here, we present the development of nine microsatellite markers of this species. We investigated their polymorphism in different countries from Africa and South-East Asia from DNAs extracted from the spleen of their rodent reservoirs (essentially rat species). Several amplification problems arose, especially with South-East Asian individuals. This led to retain only those individuals with complete genotypes (most of them originating from West Africa, notably Cotonou, Benin) to ensure an optimal estimate of heterozygosity. Our results pointed towards a mainly (at least 95-99%) clonal mode of propagation, a strong subdivision at the smallest scale available (i.e., urban neighborhoods, i.e. 0.250 km²), and a generation time most probably shorter than 4 months. In future studies, more extensive sampling at smaller geographic scales (i.e., households), within a one- or two-months window and with improved amplification conditions, should lead to a more precise picture of the fine population structure of this parasite.</p>
https://doi.org/10.5281/zenodo.7234790, https://doi.org/10.15454/WWNUPOYou should fill this box only if you chose 'All or part of the results presented in this preprint are based on data'. URL must start with http:// or https://
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Rodent-borne zoonoses; Atypical trypanosomes; Amplification issues; Clonal propagation; Wahlund effects; Heterozygosity
NonePlease indicate the methods that may require specialised expertise during the peer review process (use a comma to separate various required expertises).
Animal diseases, Disease Ecology/Evolution, Ecology of hosts, infectious agents, or vectors, Eukaryotic pathogens/symbionts, Evolution of hosts, infectious agents, or vectors, Microbiology of infections, Parasites, Population genetics of hosts, infectious agents, or vectors, Zoonoses
De-Hua Lai, [laidehua@mail.sysu.edu.cn], Zhao-Rong Lun, [lsslzr@mail.sysu.edu.cn], Martin S. Llewellyn, [martin.llewellyn@lshtm.ac.uk] or [martin.llewellyn@glasgow.ac.uk], Sérgio D. J. Pena, [spena@dcc.ufmg.br], Deborah F. Smith, [deborah.smith@york.ac.uk], James A. Cotton, [james.cotton@sanger.ac.uk] No need for them to be recommenders of PCIInfections. Please do not suggest reviewers for whom there might be a conflict of interest. Reviewers are not allowed to review preprints written by close colleagues (with whom they have published in the last four years, with whom they have received joint funding in the last four years, or with whom they are currently writing a manuscript, or submitting a grant proposal), or by family members, friends, or anyone for whom bias might affect the nature of the review - see the code of conduct
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2022-04-21 17:04:37
Annette MacLeod