Evidence map›Paper›PMID 24477590›Full record

ReviewMolecular biology reports2014

TLR3 plays significant roles against hepatitis B virus.

Masoud Karimi-Googheri, Mohammad Kazemi Arababadi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-weighted citation impact, top 5% 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, 58 citations in OpenAlex.

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  12. HCFC2 is needed for IRF1- and IRF2-dependentThe Journal of experimental medicine · 2017
    Article
  13. Article
  14. Article
  15. Regulation of TLR3 Activation by S100A9.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  16. TLR3 Plays Significant Roles against HBV-Associated HCC.Gastroenterology research and practice · 2015
    Article
  17. 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

2 authors at 2 institutions in 1 country.

Masoud Karimi-GoogheriDepartment of Immunology, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Mohammad Kazemi Arababadi
Kerman University of Medical Sciences · IRRafsanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis B virus (HBV) as the main prevalent infectious agent, play important roles in inducing severe liver diseases. Previous studies demonstrated that during prolonged forms of hepatitis B infection including chronic, asymptomatic and occult forms, patients are unable to eradicate HBV from hepatocytes completely. The main mechanisms responsible for development of the forms of hepatitis B are yet to be identified. Investigators suggested that the various genetic and immunological parameters of the patients may are responsible for resulting in the prolonged infection forms. It has been evidenced that TLRs play key roles in inducing appropriate immune responses, against viral infections. Therefore, these molecules can be considered as crucial sensors for HBV detection to induce immune responses against this virus. It has also been documented that the TLR3 detects intracellular viral dsRNA and subsequently activates NF-κB via the TRIF pathway. Therefore, impaired TLR3 expression may result in inappropriate immune responses against HBV which is reported in prolonged forms of hepatitis B. This review collected the recent information regarding the important roles of TLR3 in immune responses against HBV and also the status of TLR3 expression and its genetic variations in prolonged forms of HBV infections.

Indexed as

Hepatitis B, ChronicHepatitis B virusHumansImmunotherapyInterferon Type ILigandsSignal TransductionToll-Like Receptor 3Interferon Type ILigandsToll-Like Receptor 3

Identifiers

PMID24477590
OpenAlexW1974033282

What OpenQuestion holds

Textmetadata
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.