Browsing by Author "Elilan Somaskantharajah"

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    Admixture into and within sub-Saharan Africa
    (2016-06-21) George B.J. Busby; Gavin Band; Quang Si Le; Muminatou Jallow; Edith Bougama; Valentina D. Mangano; Lucas N. Amenga-Etego; Anthony Enimil; Tobias Apinjoh; Carolyne M. Ndila; Alphaxard Manjurano; Vysaul Nyirongo; Ogobara Doumba; Kirk A. Rockett; Dominic P. Kwiatkowski; Chris C.A. Spencer; Aaron Vanderwal; Abier Elzein; Aceme Nyika; Alieu Mendy; Alistair Miles; Andrea Diss; Angeliki Kerasidou; Angie Green; Anna E. Jeffreys; Bronwyn MacInnis; Catherine Hughes; Catherine Moyes; Christina Hubbart; Cinzia Malangone; Claire Potter; Daniel Mead; David Barnwell; Dushyanth Jyothi; Eleanor Drury; Elilan Somaskantharajah; Eliza Hilton; Ellen Leffler; Gareth Maslen; George Busby; Geraldine M. Clarke; Ioannis Ragoussis; Jacob Almagro Garcia; Jane Rogers; Jantina deVries; Jennifer Shelton; Jiannis Ragoussis; Jim Stalker; Joanne Rodford; John O'Brien; Wellcome Trust Centre for Human Genetics; Wellcome Trust Sanger Institute; Medical Research Council Unit; Royal Victoria Teaching Hospital Gambia; Centre National de Recherche et de Formation sur le Paludisme; Università degli Studi di Roma La Sapienza; Navrongo Health Research Center; Komfo Anokye Teaching Hospital; University of Buea; Wellcome Trust Research Laboratories Nairobi; Kilimanjaro Christian Medical College; London School of Hygiene & Tropical Medicine; University of Malawi College of Medicine; University of Bamako; National Institute for Biological Standards and Control; Wellcome Trust; Bernhard Nocht Institut fur Tropenmedizin Hamburg; University of Maryland, Baltimore; National Institute of Allergy and Infectious Diseases; Foundation for the National Institutes of Health; Institut Pasteur de Dakar; Institut Pasteur, Paris; Medical Research Council Laboratories Gambia; University of Ghana; Kwame Nkrumah University of Science and Technology
    © Busby et al. Similarity between two individuals in the combination of genetic markers along their chromosomes indicates shared ancestry and can be used to identify historical connections between different population groups due to admixture. We use a genome-wide, haplotype-based, analysis to characterise the structure of genetic diversity and gene-flow in a collection of 48 sub-Saharan African groups. We show that coastal populations experienced an influx of Eurasian haplotypes over the last 7000 years, and that Eastern and Southern Niger-Congo speaking groups share ancestry with Central West Africans as a result of recent population expansions. In fact, most sub-Saharan populations share ancestry with groups from outside of their current geographic region as a result of gene-flow within the last 4000 years. Our in-depth analysis provides insight into haplotype sharing across different ethno-linguistic groups and the recent movement of alleles into new environments, both of which are relevant to studies of genetic epidemiology.
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    Genome-wide and fine-resolution association analysis of malaria in West Africa
    (2009-06-01) Muminatou Jallow; Yik Ying Teo; Kerrin S. Small; Kirk A. Rockett; Panos Deloukas; Taane G. Clark; Katja Kivinen; Kalifa A. Bojang; David J. Conway; Margaret Pinder; Giorgio Sirugo; Fatou Sisay-Joof; Stanley Usen; Sarah Auburn; Suzannah J. Bumpstead; Susana Campino; Alison Coffey; Andrew Dunham; Andrew E. Fry; Angela Green; Rhian Gwilliam; Sarah E. Hunt; Michael Inouye; Anna E. Jeffreys; Alieu Mendy; Aarno Palotie; Simon Potter; Jiannis Ragoussis; Jane Rogers; Kate Rowlands; Elilan Somaskantharajah; Pamela Whittaker; Claire Widden; Peter Donnelly; Bryan Howie; Jonathan Marchini; Andrew Morris; Miguel Sanjoaquin; Eric Akum Achidi; Tsiri Agbenyega; Angela Allen; Olukemi Amodu; Patrick Corran; Abdoulaye Djimde; Amagana Dolo; Ogobara K. Doumbo; Chris Drakeley; Sarah Dunstan; Jennifer Evans; Jeremy Farrar; Deepika Fernando; Tran Tinh Hien; Rolf D. Horstmann; Muntaser Ibrahim; Nadira Karunaweera; Gilbert Kokwaro; Kwadwo A. Koram; Martha Lemnge; Julie Makani; Kevin Marsh; Pascal Michon; David Modiano; Malcolm E. Molyneux; Ivo Mueller; Michael Parker; Norbert Peshu; Christopher V. Plowe; Odile Puijalon; John Reeder; Hugh Reyburn; Eleanor M. Riley; Anavaj Sakuntabhai; Pratap Singhasivanon; Sodiomon Sirima; Adama Tall; Terrie E. Taylor; Mahamadou Thera; Marita Troye-Blomberg; Thomas N. Williams; Michael Wilson; Dominic P. Kwiatkowski; Medical Research Council Laboratories Gambia; Wellcome Trust Centre for Human Genetics; Wellcome Trust Sanger Institute; University of Oxford; University of Malawi College of Medicine; University of Buea; Kwame Nkrumah University of Science and Technology; Papua New Guinea Institute of Medical Research; Weatherall Institute of Molecular Medicine; University of Ibadan; National Institute for Biological Standards and Control; University of Bamako; London School of Hygiene & Tropical Medicine; Kilimanjaro Christian Medical Centre; UCL; Bernhard Nocht Institut fur Tropenmedizin Hamburg; University of Colombo Faculty of Medicine; Khartoum University; Wellcome Trust Research Laboratories Nairobi; University of Ghana; National Institute for Medical Research Tanga; Muhimbili University of Health and Allied Sciences; Universita degli Studi di Roma La Sapienza; Blantyre Malaria Project; University of Maryland, Baltimore; Institut Pasteur, Paris; Mahidol University; Centre National de Recherche et de Formation sur le Paludisme; Lnstitut Pasteur de Dakar; Michigan State University; Department of Molecular Biosciences, The Wenner-Gren Institute
    We report a genome-wide association (GWA) study of severe malaria in The Gambia. The initial GWA scan included 2,500 children genotyped on the Affymetrix 500K GeneChip, and a replication study included 3,400 children. We used this to examine the performance of GWA methods in Africa. We found considerable population stratification, and also that signals of association at known malaria resistance loci were greatly attenuated owing to weak linkage disequilibrium (LD). To investigate possible solutions to the problem of low LD, we focused on the HbS locus, sequencing this region of the genome in 62 Gambian individuals and then using these data to conduct multipoint imputation in the GWA samples. This increased the signal of association, from P = 4 × 10 7 to P = 4 × 10 14, with the peak of the signal located precisely at the HbS causal variant. Our findings provide proof of principle that fine-resolution multipoint imputation, based on population-specific sequencing data, can substantially boost authentic GWA signals and enable fine mapping of causal variants in African populations.