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    Population genomics of virulence genes of Plasmodium falciparum in clinical isolates from Uganda

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    Author
    Ruybal-Pesantez, S; Tiedje, KE; Tonkin-Hill, G; Rask, TS; Kamya, MR; Greenhouse, B; Dorsey, G; Duffy, MF; Day, KP
    Date
    2017-09-18
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Day, Karen; Tiedje, Kathryn; Duffy, Michael
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Ruybal-Pesantez, S., Tiedje, K. E., Tonkin-Hill, G., Rask, T. S., Kamya, M. R., Greenhouse, B., Dorsey, G., Duffy, M. F. & Day, K. P. (2017). Population genomics of virulence genes of Plasmodium falciparum in clinical isolates from Uganda. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/s41598-017-11814-9.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255094
    DOI
    10.1038/s41598-017-11814-9
    Abstract
    Plasmodium falciparum causes a spectrum of malarial disease from asymptomatic to uncomplicated through to severe. Investigations of parasite virulence have associated the expression of distinct variants of the major surface antigen of the blood stages known as Pf EMP1 encoded by up to 60 var genes per genome. Looking at the population genomics of var genes in cases of uncomplicated malaria, we set out to determine if there was any evidence of a selective sweep of specific var genes or clonal epidemic structure related to the incidence of uncomplicated disease in children. By sequencing the conserved DBLα domain of var genes from six sentinel sites in Uganda we found that the parasites causing uncomplicated P. falciparum disease in children were highly diverse and that every child had a unique var DBLα repertoire. Despite extensive var DBLα diversity and minimal overlap between repertoires, specific DBLα types and groups were conserved at the population level across Uganda. This pattern was the same regardless of the geographic distance or malaria transmission intensity. These data lead us to propose that any parasite can cause uncomplicated malarial disease and that these diverse parasite repertoires are composed of both upsA and non-upsA var gene groups.

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