Evidence map›Paper›PMID 31979279›Full record

ArticleMicroorganisms2020

Olanrewaju B Morenikeji, Jessica L Metelski, Megan E Hawkes, Anna L Capria, Brooke N Seamans, Catherine O Falade, Olusola Ojurongbe, Bolaji N Thomas

Open access · goldAbstract read
In one paragraph

Article in Microorganisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Article
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

8 authors at 3 institutions in 2 countries.

Olanrewaju B MorenikejiDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Jessica L MetelskiDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Megan E HawkesDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Anna L CapriaDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Brooke N SeamansDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Catherine O FaladeDepartment of Pharmacology & Therapeutics, College of Medicine, University of Ibadan, Ibadan P.M.B 3017, Nigeria.
Olusola OjurongbeDepartment of Medical Microbiology and Parasitology, Ladoke Akintola University of Technology, Osogbo P.M.B. 4000, Nigeria.
Bolaji N ThomasDepartment of Biomedical Sciences, College of Health Sciences and Technology, Rochester Institute of Technology, Rochester, NY 14623, USA.
Rochester Institute of Technology · USLadoke Akintola University of Technology · NGUniversity of Ibadan · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malaria remains a significant disease, causing epic health problems and challenges all over the world, especially in sub-Saharan Africa. CD209 and CD28 genes act as co-stimulators and regulators of the immune system, while the STAT6 gene has been reported to mediate cytokine-induced responses. Single nucleotide polymorphisms of these genes might lead to differential disease susceptibility among populations at risk for malaria, due to alterations in the immune response. We aim to identify key drivers of the immune response to malaria infection among the three SNPs: CD209 (rs4804803), CD28 (rs35593994) and STAT6 (rs3024974). After approval and informed consent, we genotyped blood samples from a total of 531 children recruited from Nigeria using the Taqman SNP genotyping assay and performed comparative analysis of clinical covariates among malaria-infected children. Our results reveal the CD209 (rs4804803) polymorphism as a susceptibility factor for malaria infection, significantly increasing the risk of disease among children, but not CD28 (rs35593994) or STAT6 (rs3024974) polymorphisms. Specifically, individuals with the homozygous mutant allele (rs4804803G/G) for the CD209 gene have a significantly greater susceptibility to malaria, and presented with higher mean parasitemia. This observation may be due to a defective antigen presentation and priming, leading to an ineffective downstream adaptive immune response needed to combat infection, as well as the resultant higher parasitemia and disease manifestation. We conclude that the

Indexed as

AfricaCD209CD28childrenhost geneticsKeywords: malariaparasitemiapolymorphismSTAT6

Identifiers

PMID31979279
PMCPMC7074881
OpenAlexW3002275373

What OpenQuestion holds

Textmetadata
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.