Insights into malaria susceptibility using genome-wide data on 17,000 individuals from Africa, Asia and Oceania
Nature Communications, ISSN: 2041-1723, Vol: 10, Issue: 1, Page: 5732
2019
- 108Citations
- 196Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations108
- Citation Indexes105
- CrossRef105
- 94
- Policy Citations3
- Policy Citation3
- Captures196
- Readers196
- 196
- Mentions1
- News Mentions1
- News1
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New insights into our multi-millenia battle with malaria
Humans have long been thwarted by 'the fever'. References to malaria's infamous febricity are found across antiquity, from writings by the four thousand-year-old Vedic sages of ancient India to the Greek physician Hippocrates. But the disease, caused by a group of parasites belonging to the Plasmodium genus, has troubled our ancestors and close relatives for much longer. A range of malaria species
Article Description
The human genetic factors that affect resistance to infectious disease are poorly understood. Here we report a genome-wide association study in 17,000 severe malaria cases and population controls from 11 countries, informed by sequencing of family trios and by direct typing of candidate loci in an additional 15,000 samples. We identify five replicable associations with genome-wide levels of evidence including a newly implicated variant on chromosome 6. Jointly, these variants account for around one-tenth of the heritability of severe malaria, which we estimate as ~23% using genome-wide genotypes. We interrogate available functional data and discover an erythroid-specific transcription start site underlying the known association in ATP2B4, but are unable to identify a likely causal mechanism at the chromosome 6 locus. Previously reported HLA associations do not replicate in these samples. This large dataset will provide a foundation for further research on thegenetic determinants of malaria resistance in diverse populations.
Bibliographic Details
Springer Science and Business Media LLC
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