Evidence map›Paper›PMID 30143709›Full record

ArticleScientific reports2018

Polymorphisms in the Toll-like receptor 3 (TLR3) gene are associated with the natural course of hepatitis B virus infection in Caucasian population.

Janett Fischer, Eleni Koukoulioti, Eckart Schott, Balazs Fülöp, Renate Heyne, Thomas Berg, Florian van Bömmel

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  4. Frontiers in cellular and infection microbiology · 2025
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  7. TLR3 Gene Polymorphism in HCV Infection in the Kazakh Population of Western Kazakhstan.Asian Pacific journal of cancer prevention : APJCP · 2023
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  8. Analysis of associations between theFrontiers in cellular and infection microbiology · 2023
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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

7 authors.

Janett FischerDepartment of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany. janett.fischer@medizin.uni-leipzig.de.
Eleni KoukouliotiDepartment of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany.ORCID 0000-0002-8791-9954
Eckart SchottDepartment of Gastroenterology, Hepatology and Diabetology, Internal Medicine II, HELIOS Hospital Emil von Behring, Berlin, Germany.
Balazs FülöpDepartment of Internal Medicine and Gastroenterology, HELIOS Hospital Berlin-Buch, Berlin, Germany.
Renate HeyneLiver and Study Center Checkpoint, Berlin, Germany.
Thomas BergDepartment of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany.
Florian van BömmelDepartment of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immunity can induce spontaneous hepatitis B surface antigen (HBsAg) seroclearance (SC) of hepatitis B virus (HBV) infection or transition towards an inactive carrier state. Toll-like receptor (TLR) 3 signalling has been linked to these processes. Alterations in the TLR3 gene might impair immune responses against HBV. In our study, we analysed the impact of the TLR3 polymorphisms rs3775291 and rs5743305 on the natural course of HBV infection. In this retrospective study, a Caucasian cohort of 621 patients with chronic HBV infection (CHB), 239 individuals with spontaneous HBsAg SC, and 254 healthy controls were enrolled. In the CHB group, 49% of patients were inactive carriers, and 17% were HBeAg-positive. The TLR3 rs3775291 A allele was associated with a reduced likelihood of spontaneous HBsAg SC and HBeAg SC, and an increased risk of developing chronic hepatitis B. In haplotype analysis, the haplotype including both risk variants rs3775291A and rs5743305A had the lowest likelihood of HBsAg SC. Further research in larger cohorts and functional analyses are needed to shed light on the impact of TLR3 signalling.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseCase-Control StudiesCohort StudiesFemaleHaplotypesHepatitis B, ChronicHepatitis B Surface AntigensHepatitis B virusHumansLogistic ModelsMaleMiddle AgedPolymorphism, Single NucleotideToll-Like Receptor 3White PeopleHepatitis B Surface AntigensTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID30143709
PMCPMC6109130

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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.