Evidence map›Paper›PMID 10482599›Full record

ArticleJournal of virology1999

Expression of hepatitis C virus proteins inhibits signal transduction through the Jak-STAT pathway.

M H Heim, D Moradpour, H E Blum

Registry-linked trialAbstract read
In one paragraph

Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00310336 (Chronic Hepatitis C), which is not on this map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
7.8field-weighted citation impact, top 2% 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.

NCT00310336 phase2 / phase3completednot on this mapstarted 2006, after this paper: background citation

Chronic Hepatitis C: Treatment of (Peg)Interferon Alpha - Ribavirin Non-Responders With Pegylated Interferon alpha2b, Ribavirin, AdoMet and Betaine

TypeinterventionalSponsorUniversity Hospital, Basel, SwitzerlandRan2006 to 2009Enrolled30ConditionsHepatitis CArmsS-adenosyl-L-methionine, betaine, pegylated interferon alpha2b, ribavirin
3 · Its place in the literature

Who cites it

83 citing papers in PubMed, 287 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Interferon signaling and treatment outcome in chronic hepatitis C.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. A Review of Hepatitis B Virus and Hepatitis C Virus Immunopathogenesis.Journal of clinical and translational hepatology · 2021
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article

23 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 2 countries.

M H HeimDepartment of Research, University Hospital Basel, CH-4031 Basel, Switzerland.
D Moradpour
H E Blum
University Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection is a leading cause of liver disease worldwide. Alpha interferon (IFN-alpha) therapy of chronic hepatitis C leads to a sustained response in 10 to 20% of patients only. The mechanisms of viral persistence and the pathogenesis of hepatitis C are poorly understood. We established continuous human cell lines, allowing the tightly regulated expression of the entire HCV open reading frame under the control of a tetracycline-responsive promoter. Using this in vitro system, we analyzed the effect of HCV proteins on IFN-induced intracellular signaling. Expression of HCV proteins in these cells strongly inhibited IFN-alpha-induced signal transduction through the Jak-STAT pathway. Inhibition occurred downstream of STAT tyrosine phosphorylation. Inhibition of the Jak-STAT pathway was not restricted to IFN-alpha-induced signaling but was observed in leukemia inhibitory factor-induced signaling through Stat3 as well. By contrast, tumor necrosis factor alpha-induced activation of the transcription factor NF-kappaB was not affected. Interference of HCV with IFN-alpha-induced signaling through the Jak-STAT pathway could contribute to the resistance to IFN-alpha therapy observed in the majority of patients and may represent a general escape strategy of HCV contributing to viral persistence and pathogenesis of chronic liver disease.

Indexed as

Signal TransductionAntiviral AgentsCell LineDNA-Binding ProteinsHepacivirusHepatitis CHumansInterferon-alphaNF-kappa BProtein-Tyrosine KinasesSTAT1 Transcription FactorTrans-ActivatorsViral ProteinsVirus ReplicationAntiviral AgentsDNA-Binding ProteinsInterferon-alphaNF-kappa BProtein-Tyrosine KinasesSTAT1 protein, humanSTAT1 Transcription FactorTrans-ActivatorsViral Proteins

Identifiers

PMID10482599
PMCPMC112866
OpenAlexW2133929317

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.