Evidence map›Paper›PMID 31278068›Full record

ArticleEBioMedicine2019

Integrated OMICS platforms identify LAIR1 genetic variants as novel predictors of cross-sectional and longitudinal susceptibility to severe malaria and all-cause mortality in Kenyan children.

Angela O Achieng, Nicolas W Hengartner, Evans Raballah, Qiuying Cheng, Samuel B Anyona, Nick Lauve, Bernard Guyah, Ivy Foo-Hurwitz, John M Ong'echa, Benjamin H McMahon and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 19 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

13 authors at 6 institutions in 2 countries.

Angela O AchiengUniversity of New Mexico-Kenya Global Health Programs, Kisumu and Siaya, Kenya; Department of Biomedical Sciences and Technology, School of Public Health and Community Development, Maseno University, Maseno, Kenya.
Nicolas W HengartnerTheoretical Biology and Biophysics Group, Theoretical Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Evans RaballahUniversity of New Mexico-Kenya Global Health Programs, Kisumu and Siaya, Kenya; Department of Medical Laboratory Sciences, School of Public Health Biomedical Sciences and Technology, Masinde Muliro University of Science and Technology, Kakamega, Kenya.
Qiuying ChengUniversity of New Mexico, Center for Global Health, Department of Internal Medicine, NM, USA.
Samuel B AnyonaUniversity of New Mexico-Kenya Global Health Programs, Kisumu and Siaya, Kenya; Department of Medical Biochemistry, School of Medicine, Maseno University, Maseno, Kenya.
Nick LauveUniversity of New Mexico, Center for Global Health, Department of Internal Medicine, NM, USA.
Bernard GuyahDepartment of Biomedical Sciences and Technology, School of Public Health and Community Development, Maseno University, Maseno, Kenya.
Ivy Foo-HurwitzUniversity of New Mexico, Center for Global Health, Department of Internal Medicine, NM, USA.
John M Ong'echaKenya Medical Research Institute, Centre for Global Health Research, Kisumu, Kenya.
Benjamin H McMahonTheoretical Biology and Biophysics Group, Theoretical Division, Los Alamos National Laboratory, Los Alamos, NM, USA.
Collins OumaUniversity of New Mexico-Kenya Global Health Programs, Kisumu and Siaya, Kenya; Department of Biomedical Sciences and Technology, School of Public Health and Community Development, Maseno University, Maseno, Kenya.
Christophe G LambertUniversity of New Mexico, Center for Global Health, Department of Internal Medicine, NM, USA.
Douglas J PerkinsUniversity of New Mexico-Kenya Global Health Programs, Kisumu and Siaya, Kenya; University of New Mexico, Center for Global Health, Department of Internal Medicine, NM, USA. Electronic address: Dperkins@salud.unm.edu.
Center for Global Health · USMaseno University · KEUniversity of New Mexico · USLos Alamos National Laboratory · USKenya Medical Research Institute · KEMasinde Muliro University of Science and Technology · KE

Funding

Harnessing the Malarial Immunity Omics Landscape in Vaccinated and Unvaccinated Children for Improved Therapeutic StrategiesR01AI130473 · NIAID · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Samuel Bonuke Anyona, Douglas Jay Perkins · 2018 to 2026
$5.6M
TRAINING AND RESEARCH ON SEVERE MALARIAL ANEMIAD43TW005884 · FIC · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Collins Ouma, Douglas Jay Perkins · 2002 to 2026
$5.2M
FIC NIH HHS D43 TW005884NIAID NIH HHS R01 AI130473
6 · The paper itself

Abstract

backgroundSevere malarial anaemia (SMA) is a leading cause of childhood mortality in holoendemic Plasmodium falciparum regions.

methodsTo gain an improved understanding of SMA pathogenesis, whole genome and transcriptome profiling was performed in Kenyan children (n=144, 3-36months) with discrete non-SMA and SMA phenotypes. Leukocyte associated immunoglobulin like receptor 1 (LAIR1) emerged as a predictor of susceptibility to SMA (P<1×10

findingsInheritance of the 16,231 recessive genotype (AA) increased susceptibility to SMA at enrolment (OR=1.903, 95%CI: 1.252-2.891, P=0.003), and longitudinally (RR=1.527, 95%CI: 1.119-2.083, P=0.008). Carriage of the 18,835 GA genotype protected against SMA cross-sectionally (OR=0.672, 95%CI: 0.480-0.9439, P=0.020). Haplotype carriage (C16231A/G18835A) also altered cross-sectional susceptibility to SMA: CG (OR=0.717, 95%CI: 0.527-0.9675, P=0.034), CA (OR=0.745, 95%CI: 0.536-1.036, P=0.080), and AG (OR=1.641, 95%CI: 1.160-2.321, P=0.005). Longitudinally, CA carriage was protective against SMA (RR=0.715, 95%CI: 0.554-0.923, P=0.010), while AG carriage had an additive effect on enhanced SMA risk (RR=1.283, 95%CI: 1.057-1.557, P=0.011). Variants that protected against SMA had elevated LAIR1 transcripts, while those with enhanced risk had lower expression (P<0.05). Inheritance of 18,835 GA reduced all-cause mortality by 44.8% (HR=0.552, 95%CI: 0.329-0.925, P=0.024), while AG haplotype carriage increased susceptibility by 68% (HR=1.680, 95%CI: 1.020-2.770, P=0.040).

interpretationThese findings suggest LAIR1 is important for modulating susceptibility to SMA and all-cause childhood mortality.

Indexed as

AnemiaChild, PreschoolFemaleGene Expression RegulationGenotypeHaplotypesHumansInfantKenyaLeukocytes, MononuclearMalaria, FalciparumMalePhagocytosisReceptors, ImmunologicSignal Transductionleukocyte-associated immunoglobulin-like receptor 1Receptors, ImmunologicAll-cause mortalityLeukocyte associated immunoglobulin like receptor 1Plasmodium falciparum malariaSevere malarial anaemia

Identifiers

PMID31278068
PMCPMC6642287
OpenAlexW2955758793

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.