ArticleThe Journal of infectious diseases2015
USP38, FREM3, SDC1, DDC, and LOC727982 Gene Polymorphisms and Differential Susceptibility to Severe Malaria in Tanzania.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Significantly altered peripheral blood cell DNA methylation profile as a result of immediate effect of metformin use in healthy individuals.Clinical epigenetics · 2018Trial
- Human genetic variations conferring resistance to malaria.Journal of translational medicine · 2025Review
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- High throughput human genotyping for variants associated with malarial disease outcomes using custom targeted amplicon sequencing.Scientific reports · 2023Article
- A world free of malaria: It is time for Africa to actively champion and take leadership of elimination and eradication strategies.African health sciences · 2022Article
- Risk score prediction model based on single nucleotide polymorphism for predicting malaria: a machine learning approach.BMC bioinformatics · 2022Article
- Leveraging Mann-Whitney U test on large-scale genetic variation data for analysing malaria genetic markers.Malaria journal · 2022Article
- Analysis of spleen histopathology, splenocyte composition and haematological parameters in four strains of mice infected with Plasmodium berghei K173.Malaria journal · 2021Article
- Loss-of-function of Endothelin receptor type A results in Oro-Oto-Cardiac syndrome.American journal of medical genetics. Part A · 2020Article
- Glycocalyx breakdown is increased in African children with cerebral and uncomplicated falciparum malaria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Glycocalyx Breakdown Is Associated With Severe Disease and Fatal Outcome in Plasmodium falciparum Malaria.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2019Observational
- Genome-wide association studies of severe P. falciparum malaria susceptibility: progress, pitfalls and prospects.BMC medical genomics · 2019Review
- The deubiquitinase USP38 affects cellular functions through interacting with LSD1.Biological research · 2018Article
- Article
- Human candidate gene polymorphisms and risk of severe malaria in children in Kilifi, Kenya: a case-control association study.The Lancet. Haematology · 2018Article
- Novel genetic polymorphisms associated with severe malaria and under selective pressure in North-eastern Tanzania.PLoS genetics · 2018Article
- The role of the red blood cell in host defence against falciparum malaria: an expanding repertoire of evolutionary alterations.British journal of haematology · 2017Review
- Malaria Host Candidate Genes Validated by Association With Current, Recent, and Historical Measures of Transmission Intensity.The Journal of infectious diseases · 2017Article
- Genetic and epigenetic changes in host ABCB1 influences malaria susceptibility to Plasmodium falciparum.PloS one · 2017Article
Corrections and comments
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Authors and funding
12 authors at 7 institutions in 5 countries.
Funding
Abstract
Populations exposed to Plasmodium falciparum infection develop genetic mechanisms of protection against severe malarial disease. Despite decades of genetic epidemiological research, the sickle cell trait (HbAS) sickle cell polymorphism, ABO blood group, and other hemoglobinopathies remain the few major determinants in severe malaria to be replicated across different African populations and study designs. Within a case-control study in a region of high transmission in Tanzania (n = 983), we investigated the role of 40 new loci identified in recent genome-wide studies. In 32 loci passing quality control procedures, we found polymorphisms in USP38, FREM3, SDC1, DDC, and LOC727982 genes to be putatively associated with differential susceptibility to severe malaria. Established candidates explained 7.4% of variation in severe malaria risk (HbAS polymorphism, 6.3%; α-thalassemia, 0.3%; ABO group, 0.3%; and glucose-6-phosphate dehydrogenase deficiency, 0.5%) and the new polymorphisms, another 4.3%. The regions encompassing the loci identified are promising targets for the design of future treatment and control interventions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.