Evidence map›Paper›PMID 18467494›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2008

Interferon signaling and treatment outcome in chronic hepatitis C.

Magdalena Sarasin-Filipowicz, Edward J Oakeley, Francois H T Duong, Verena Christen, Luigi Terracciano, Witold Filipowicz, Markus H Heim

Open access · greenAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 313 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
313citing papers in PubMed, 1 pooled it
32.4field-weighted citation impact, top 1% 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

313 citing papers in PubMed, 1 synthesis or guideline pooled it, 638 citations in OpenAlex.

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  11. Systemic cytokine and interferon responsiveness Patterns in HIV and HCV mono and co-infections.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
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253 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Magdalena Sarasin-FilipowiczDepartment of Biomedicine, University of Basel, CH-4031 Basel, Switzerland.
Edward J Oakeley
Francois H T Duong
Verena Christen
Luigi Terracciano
Witold Filipowicz
Markus H Heim
University of Basel · CHFriedrich Miescher Institute · CHUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. The current standard therapy for chronic hepatitis C (CHC) consists of a combination of pegylated IFN alpha (pegIFNalpha) and ribavirin. It achieves a sustained viral clearance in only 50-60% of patients. To learn more about molecular mechanisms underlying treatment failure, we investigated IFN-induced signaling in paired liver biopsies collected from CHC patients before and after administration of pegIFNalpha. In patients with a rapid virological response to treatment, pegIFNalpha induced a strong up-regulation of IFN-stimulated genes (ISGs). As shown previously, nonresponders had high expression levels of ISGs before therapy. Analysis of posttreatment biopsies of these patients revealed that pegIFNalpha did not induce expression of ISGs above the pretreatment levels. In accordance with ISG expression data, phosphorylation, DNA binding, and nuclear localization of STAT1 indicated that the IFN signaling pathway in nonresponsive patients is preactivated and refractory to further stimulation. Some features characteristic of nonresponders were more accentuated in patients infected with HCV genotypes 1 and 4 compared with genotypes 2 and 3, providing a possible explanation for the poor response of the former group to therapy. Taken together with previous findings, our data support the concept that activation of the endogenous IFN system in CHC not only is ineffective in clearing the infection but also may impede the response to therapy, most likely by inducing a refractory state of the IFN signaling pathway.

Indexed as

Signal TransductionAdultBiopsyFemaleGene Expression RegulationGenotypeHepacivirusHepatitis C, ChronicHumansInterferon-alphaInterferon alpha-2Interferon Regulatory FactorsJanus KinasesLeukocytes, MononuclearLiverMaleInterferon-alphaInterferon alpha-2Interferon Regulatory FactorsJanus KinasesRecombinant ProteinsSTAT Transcription Factors

Identifiers

PMID18467494
PMCPMC2383932
OpenAlexW2038576929

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.