Evidence map›Paper›PMID 28541483›Full record

ArticleThe Journal of infectious diseases2017

Malaria Host Candidate Genes Validated by Association With Current, Recent, and Historical Measures of Transmission Intensity.

Nuno Sepúlveda, Alphaxard Manjurano, Susana G Campino, Martha Lemnge, John Lusingu, Raimos Olomi, Kirk A Rockett, Christina Hubbart, Anna Jeffreys, Kate Rowlands and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 3 countries.

Nuno SepúlvedaLondon School of Hygiene and Tropical Medicine.
Alphaxard ManjuranoLondon School of Hygiene and Tropical Medicine.
Susana G CampinoLondon School of Hygiene and Tropical Medicine.
Martha LemngeNational Institute for Medical Research, Dar es Salaam, Tanzania.
John LusinguNational Institute for Medical Research, Dar es Salaam, Tanzania.
Raimos OlomiJoint Malaria Programme, Kilimanjaro Christian Medical Centre, Moshi.
Kirk A RockettWellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom.
Christina HubbartWellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom.
Anna JeffreysWellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom.
Kate RowlandsWellcome Trust Centre for Human Genetics, University of Oxford, United Kingdom.
Taane G ClarkLondon School of Hygiene and Tropical Medicine.
Eleanor M RileyLondon School of Hygiene and Tropical Medicine.
Chris J DrakeleyLondon School of Hygiene and Tropical Medicine.
MalariaGEN Consortium
Centre for Human Genetics · GBLondon School of Hygiene & Tropical Medicine · GBNational Institute for Medical Research · TZKilimanjaro Christian Medical Centre · TZUniversity of Lisbon · PTWellcome Sanger Institute · GB

Funding

Medical Research Council G0600718Medical Research Council MR/K000551/1Medical Research Council MR/M01360X/1Wellcome TrustWellcome Trust 090770/Z/09/ZWellcome Trust WT077383/Z/05/Z
6 · The paper itself

Abstract

Background: Human malaria susceptibility is determined by multiple genetic factors. It is unclear, however, which genetic variants remain important over time. Methods: Genetic associations of 175 high-quality polymorphisms within several malaria candidate genes were examined in a sample of 8096 individuals from northeast Tanzania using altitude, seroconversion rates, and parasite rates as proxies of historical, recent, and current malaria transmission intensity. A principal component analysis was used to derive 2 alternative measures of overall malaria propensity of a location across different time scales. Results: Common red blood cell polymorphisms (ie, hemoglobin S, glucose-6-phosphate dehydrogenase, and α-thalassemia) were the only ones to be associated with all 3 measures of transmission intensity and the first principal component. Moderate associations were found between some immune response genes (ie, IL3 and IL13) and parasite rates, but these could not be reproduced using the alternative measures of malaria propensity. Conclusions: We have demonstrated the potential of using altitude and seroconversion rate as measures of malaria transmission capturing medium- to long-term time scales to detect genetic associations that are likely to persist over time. These measures also have the advantage of minimizing the deleterious effects of random factors affecting parasite rates on the respective association signals.

Indexed as

Genetic Association StudiesAdolescentAdultalpha-ThalassemiaChildChild, PreschoolCross-Sectional StudiesErythrocytesFemaleGlucosephosphate DehydrogenaseHemoglobin, SickleHost-Parasite InteractionsHumansInfantInterleukin-3Linear ModelsGlucosephosphate DehydrogenaseHemoglobin, SickleIL3 protein, humanInterleukin-3genetic associationMalariaSNPtransmission intensity

Identifiers

PMID28541483
PMCPMC5853769
OpenAlexW2630491195

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.