| Literature DB >> 34225842 |
James A Watson1,2, Carolyne M Ndila1,2, Thomas N Williams3,4, Chris C Holmes5,6, Nicholas J White1,2, Sophie Uyoga3, Alexander Macharia3, Gideon Nyutu3, Shebe Mohammed3, Caroline Ngetsa3, Neema Mturi3, Norbert Peshu3, Benjamin Tsofa3, Kirk Rockett7,8, Stije Leopold1,2, Hugh Kingston1,2, Elizabeth C George9, Kathryn Maitland3,4, Nicholas Pj Day1,2, Arjen M Dondorp1,2, Philip Bejon2,3.
Abstract
Severe falciparum malaria has substantially affected human evolution. Genetic association studies of patients with clinically defined severe malaria and matched population controls have helped characterise human genetic susceptibility to severe malaria, but phenotypic imprecision compromises discovered associations. In areas of high malaria transmission, the diagnosis of severe malaria in young children and, in particular, the distinction from bacterial sepsis are imprecise. We developed a probabilistic diagnostic model of severe malaria using platelet and white count data. Under this model, we re-analysed clinical and genetic data from 2220 Kenyan children with clinically defined severe malaria and 3940 population controls, adjusting for phenotype mis-labelling. Our model, validated by the distribution of sickle trait, estimated that approximately one-third of cases did not have severe malaria. We propose a data-tilting approach for case-control studies with phenotype mis-labelling and show that this reduces false discovery rates and improves statistical power in genome-wide association studies.Entities:
Keywords: GWAS; complete blood count; diagnosis; epidemiology; genetics; genomics; global health; human; severe malaria
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Year: 2021 PMID: 34225842 PMCID: PMC8315799 DOI: 10.7554/eLife.69698
Source DB: PubMed Journal: Elife ISSN: 2050-084X Impact factor: 8.140