ArticleNature2012
Genome-wide association study indicates two novel resistance loci for severe malaria.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
161 citing papers in PubMed, 4 syntheses or guidelines pooled it, 278 citations in OpenAlex.
- Trans-ethnic genome-wide association study of severe COVID-19.Communications biology · 2021Pooled it
- Genetic factors affect the susceptibility to bacterial infections in diabetes.Scientific reports · 2021Pooled it
- Common Genetic Polymorphisms Influence Blood Biomarker Measurements in COPD.PLoS genetics · 2016Pooled it
- Imputation-based meta-analysis of severe malaria in three African populations.PLoS genetics · 2013Pooled it
- Human genetic variants and age are the strongest predictors of humoral immune responses to common pathogens and vaccines.Genome medicine · 2018Trial
- Quantitative analysis of DNA-GATA1 binding alterations linked to hematopoietic disorders.The FEBS journal · 2026Article
- Comparative genomic analysis of pigs differing in survival following African swine fever virus infection.Veterinary research communications · 2026Article
- Genetic Determinants of Infectious Diseases in the Qatari Population.Epidemiologia (Basel, Switzerland) · 2026Article
- Adaptive admixture at ACKR1, the Duffy blood group locus, may have shaped Plasmodium vivax prevalence in Oman.American journal of human genetics · 2026Article
- Article
- Article
- Insights into human history and complex traits from the genomes of African populations.Molecular biology and evolution · 2026Review
- Article
- Malaria vaccines: Current developments and immunological insights.New microbes and new infections · 2025Article
- Plasma membrane calcium ATPases and cerebellar pathology: what's the role in the ataxia?Biology direct · 2025Review
- Human genetic variations conferring resistance to malaria.Journal of translational medicine · 2025Review
- Unraveling an enhancer-silencer regulatory element showing epistatic interaction with a variant that escaped genome-wide association studies.Cell genomics · 2025Article
- A metabolite-based resistance mechanism against malaria.Science (New York, N.Y.) · 2025Article
- Fetal hemoglobin enables malaria parasite growth in sickle cells but augments production of transmission stage parasites.PloS one · 2025Article
- Article
101 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 4 institutions in 2 countries.
Funding
Abstract
Malaria causes approximately one million fatalities per year, mostly among African children. Although highlighted by the strong protective effect of the sickle-cell trait, the full impact of human genetics on resistance to the disease remains largely unexplored. Genome-wide association (GWA) studies are designed to unravel relevant genetic variants comprehensively; however, in malaria, as in other infectious diseases, these studies have been only partly successful. Here we identify two previously unknown loci associated with severe falciparum malaria in patients and controls from Ghana, West Africa. We applied the GWA approach to the diverse clinical syndromes of severe falciparum malaria, thereby targeting human genetic variants influencing any step in the complex pathogenesis of the disease. One of the loci was identified on chromosome 1q32 within the ATP2B4 gene, which encodes the main calcium pump of erythrocytes, the host cells of the pathogenic stage of malaria parasites. The second was indicated by an intergenic single nucleotide polymorphism on chromosome 16q22.2, possibly linked to a neighbouring gene encoding the tight-junction protein MARVELD3. The protein is expressed on endothelial cells and might therefore have a role in microvascular damage caused by endothelial adherence of parasitized erythrocytes. We also confirmed previous reports on protective effects of the sickle-cell trait and blood group O. Our findings underline the potential of the GWA approach to provide candidates for the development of control measures against infectious diseases in humans.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.