Evidence map›Paper›PMID 25844529›Full record

ArticlePloS one2015

TLR9 2848 GA heterozygotic status possibly predisposes fetuses and newborns to congenital infection with human cytomegalovirus.

Wioletta Wujcicka, Edyta Paradowska, Mirosława Studzińska, Zuzanna Gaj, Jan Wilczyński, Zbigniew Leśnikowski, Dorota Nowakowska

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  4. TheCells · 2021
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  16. Possible role of TLR4 and TLR9 SNPs in protection against congenital toxoplasmosis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2015
    Article
  17. Review
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

7 authors at 3 institutions in 1 country.

Wioletta WujcickaScientific Laboratory of Center of Medical Laboratory Diagnostics, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Edyta ParadowskaLaboratory of Molecular Virology and Biological Chemistry, Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland.
Mirosława StudzińskaLaboratory of Molecular Virology and Biological Chemistry, Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland.
Zuzanna GajScientific Laboratory of Center of Medical Laboratory Diagnostics, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Jan WilczyńskiDepartment of Perinatology and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Zbigniew LeśnikowskiLaboratory of Molecular Virology and Biological Chemistry, Institute of Medical Biology, Polish Academy of Sciences, Lodz, Poland.
Dorota NowakowskaDepartment of Perinatology and Gynecology, Polish Mother's Memorial Hospital-Research Institute, Lodz, Poland.
Polish Mother’s Memorial Hospital Research Institute · PLInstitute for Medical Biology · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSome single nucleotide polymorphisms (SNP), located in Toll-like receptor (TLR) genes, were reported to be associated with human cytomegalovirus (HCMV) infections. The study was aimed to assess the correlation of SNPs at TLR4 and TLR9 genes with the occurrence of congenital cytomegaly, based on available samples.

methodsReported case-control study included both HCMV infected and non-infected fetuses and newborns. The specimens were classified to the molecular analyses, based on serological features of the recent infection and HCMV DNAemia in body fluids. TLR SNPs were studied, using multiplex nested PCR-RFLP assay, and determined genotypes were confirmed by sequencing. Hardy-Weinberg equilibrium was assessed for the identified genotypes. The linkage disequilibrium was also estimated for TLR4 SNPs. A relationship between the status of TLR genotypes and congenital cytomegaly development was estimated, using a logistic regression model.

resultsHardy Weinberg equilibrium was observed for almost all SNPs, both infected and non-infected patients, with exception of TLR4 896 A>G polymorphism in the control group (P≤0.050). TLR4 896 A>G and 1196 C>T SNPs were found in linkage disequilibrium in both study groups (P≤0.050). The CC genotype at TLR4 1196 SNP and the GA variant at TLR9 2848 G>A SNP were significantly associated with HCMV infection (P≤0.050). The risk of congenital cytomegaly was higher in heterozygotes at TLR9 SNP than in the carriers of other genotypic variants at the reported locus (OR 4.81; P≤0.050). The GC haplotype at TLR4 SNPs and GCA variants at TLR4 and TLR9 SNPs were significantly associated with HCMV infection (P≤0.0001). The ACA variants were more frequent among fetuses and neonates with symptomatic, rather than asymptomatic cytomegaly (P≤0.0001).

conclusionsTLR4 and TLR9 polymorphisms may contribute to the development of congenital infection with HCMV in fetuses and neonates. The TLR9 2848 GA heterozygotic status possibly predisposes to HCMV infection, increasing the risk of congenital cytomegaly development.

Indexed as

Polymorphism, Single NucleotideCase-Control StudiesCytomegalovirus InfectionsFetusGenetic Predisposition to DiseaseHumansInfant, NewbornLinkage DisequilibriumRetrospective StudiesToll-Like Receptor 4Toll-Like Receptor 9TLR4 protein, humanTLR9 protein, humanToll-Like Receptor 4Toll-Like Receptor 9

Identifiers

PMID25844529
PMCPMC4386761
OpenAlexW2067859468

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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.