Evidence map›Paper›PMID 24555572›Full record

ReviewJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2014

Genetic variants at the IFNL3 locus and their association with hepatitis C virus infections reveal novel insights into host-virus interactions.

Sreedhar Chinnaswamy

Open access · greenAbstract readReview
In one paragraph

Review in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Epigenetic scars of CD8Nature immunology · 2021
    Trial
  2. Review
  3. IFN-λ3 is induced byInfection and immunity · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. 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

1 author at 1 institution in 1 country.

Sreedhar ChinnaswamyNational Institute of Biomedical Genomics , Kalyani, West Bengal, India .
National Institute of Biomedical Genomics · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human genetic variation plays a critical role in both spontaneous clearance of and response to interferon (IFN)-based therapies against hepatitis C virus (HCV) as shown by the success of recent genome-wide association studies (GWAS). Several GWAS and later validation studies have shown that single nucleotide polymorphisms (SNPs) at the IFNL3 (formerly IL28B) locus on chromosome 19 are involved in eliminating HCV in human patients. No doubt that this information is helping clinicians worldwide in making better clinical decisions in anti-HCV therapy, but the biological mechanisms involving the SNPs leading to differential responses to therapy and spontaneous clearance of HCV remain elusive. Recent reports including the discovery of a novel IFN (IFN-λ4) gene at the IFNL3 locus and in vitro functional studies implicating 2 SNPs as causal variants lead to novel conclusions and perhaps to new directions in research. An attempt is made in this review to summarize the major findings of the GWAS, the efforts involved in the discovery of causal SNPs; and to explain the biological basis for spontaneous clearance and response to treatment in HCV infections.

Indexed as

Genetic VariationPolymorphism, Single NucleotideHepacivirusHepatitis C, ChronicHost-Pathogen InteractionsHumansInterferon LambdaInterferonsInterleukinsTreatment OutcomeInterferon Lambdainterferon-lambda, humanInterferonsInterleukins

Identifiers

PMID24555572
PMCPMC4080901
OpenAlexW1564740638

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.