Evidence map›Paper›PMID 25800823›Full record

ArticleLiver international : official journal of the International Association for the Study of the Liver2015

Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection.

Mark W Robinson, Elihu Aranday-Cortes, Derek Gatherer, Rachael Swann, Jolanda M P Liefhebber, Ana Da Silva Filipe, Alex Sigruener, Stephen T Barclay, Peter R Mills, Arvind H Patel and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Liver international : official journal of the International Association for the Study of the Liver, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Viral genotype correlates with distinct liver gene transcription signatures in chronic hepatitis C virus infection.Liver international : official journal of the International Association for the Study of the Liver · 2015
    Article
  10. 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

11 authors at 4 institutions in 3 countries.

Mark W RobinsonMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Elihu Aranday-CortesMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Derek GathererMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Rachael SwannMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Jolanda M P LiefhebberMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Ana Da Silva FilipeMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
Alex SigruenerInstitute of Clinical Chemistry and Laboratory Medicine, Regensburg University Medical Center, Regensburg, Germany.
Stephen T BarclayGlasgow Royal Infirmary, NHS Greater Glasgow and Clyde, Glasgow, UK.
Peter R MillsGartnavel General Hospital, NHS Greater Glasgow and Clyde, Glasgow, UK.
Arvind H PatelMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
John McLauchlanMRC - University of Glasgow Centre for Virus Research, Glasgow, UK.
MRC University of Glasgow Centre for Virus Research · GBGlasgow Royal Infirmary · GBNHS Greater Glasgow and Clyde · GBUniversity of Regensburg · DE

Funding

Medical Research Council G0801822Medical Research Council MC_U130184144Medical Research Council MC_UU_12014/1Medical Research Council MC_UU_12014/2
6 · The paper itself

Abstract

backgroundChronic hepatitis C virus (HCV) infection of the liver with either genotype 1 or genotype 3 gives rise to distinct pathologies, and the two viral genotypes respond differently to antiviral therapy.

methodsTo understand these clinical differences, we compared gene transcription profiles in liver biopsies from patients infected with either gt1 or gt3, and uninfected controls.

resultsGt1-infected biopsies displayed elevated levels of transcripts regulated by type I and type III interferons (IFN), including genes that predict response to IFN-α therapy. In contrast, genes controlled by IFN-γ were induced in gt3-infected biopsies. Moreover, IFN-γ levels were higher in gt3-infected biopsies. Analysis of hepatocyte-derived cell lines confirmed that the genes upregulated in gt3 infection were preferentially induced by IFN-γ. The transcriptional profile of gt3 infection was unaffected by IFNL4 polymorphisms, providing a rationale for the reduced predictive power of IFNL genotyping in gt3-infected patients.

conclusionsThe interactions between HCV genotypes 1 and 3 and hepatocytes are distinct. These unique interactions provide avenues to explore the biological mechanisms that drive viral genotype-specific differences in disease progression and treatment response. A greater understanding of the distinct host-pathogen interactions of the different HCV genotypes is required to facilitate optimal management of HCV infection.

Indexed as

AdultCell LineFemaleGenotypeHepatitis CHepatitis C, ChronicHost-Pathogen InteractionsHumansInterferon-gammaInterferon LambdaInterleukinsLiverMaleMiddle AgedPolymorphism, GeneticTranscription, GeneticIFNG protein, humanIFNL4 protein, humanInterferon-gammaInterferon LambdaInterleukinsgenotypeHCVinterferonISGstranscriptomics

Identifiers

PMID25800823
PMCPMC4949513
OpenAlexW2012099880

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.