Evidence map›Paper›PMID 24211829›Full record

ArticleExperimental and molecular pathology2014

Interferon alpha induced intrahepatic pSTAT1 inversely correlate with serum HCV RNA levels in chronic HCV infection.

Feyza Gunduz, Chaithanya Mallikarjun, Luis A Balart, Srikanta Dash

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

Article in Experimental and molecular pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
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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

4 authors at 1 institution in 1 country.

Feyza GunduzGastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, LA 70112, USA; Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Chaithanya MallikarjunGastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Luis A BalartGastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Srikanta DashGastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, LA 70112, USA; Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112, USA. Electronic address: sdash@tulane.edu.
Tulane University · US

Funding

Hepatitis C Virus and Hepatocellular CarcinomaR01CA089121 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DASH, SRIKANTA · 2001 to 2016
$2.7M
IL-28B genotype and HCV treatment clearanceR01AI103106 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI DASH, SRIKANTA · 2013 to 2016
$1.5M
Hepatocarcinogenesis Secondary to Hepatitis CR01CA127481 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DASH, SRIKANTA · 2008 to 2012
$1.4M
RELATION OF HEPATITIS C VIRUS--HEPATOCELLULAR CARCINOMAR01CA054576 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DASH, SRIKANTA · 1992 to 2000
$245k
NCI NIH HHS CA089121NCI NIH HHS CA127481NCI NIH HHS R01 CA054576NCI NIH HHS R01 CA089121NCI NIH HHS R01 CA127481NIAID NIH HHS AI103106NIAID NIH HHS R01 AI103106
6 · The paper itself

Abstract

backgroundThe Jak-STAT signaling of hepatitis C virus (HCV) infected hepatocyte is critical for the antiviral action of endogenously produced interferon (IFN) as well as exogenously administered interferon alpha (IFN-α). The activation of cellular Jak-STAT signaling by IFN-α results in the phosphorylation and nuclear translocation of pSTAT1 and pSTAT2 proteins to induce antiviral gene transcription. Clinical studies show that chronic HCV patients with high viral load show poor response to interferon alpha and ribavirin combination therapy.

aimWe seek to determine whether the IFN-α induced activation of pSTAT1 and pSTAT2 in hepatocytes isolated from liver biopsy of patients chronically infected with hepatitis C virus could be related to the viral load.

methodHepatocytes were isolated from liver biopsies of 18 chronic HCV patients using the collagen digestion method. Induction of pSTAT1 protein in the isolated hepatocyte was measured after IFN-α treatment. The fold change in the levels of pStat1 in the cell lysates due to IFN-treatment was measured by Western blot analysis followed by densitometry analysis.

resultsResults of our study indicate that IFN-α induced pSTAT1 levels vary in chronically infected hepatocytes from chronic HCV patients. Semi-quantitative analysis of the pSTAT1 bands revealed a median induction of 7.4-fold in non-infected primary hepatocytes and 2.3-fold in chronic hepatitis C patients (p < 0.001). Total STAT1 levels were not significantly different between treated and untreated primary hepatocytes. We also found a significantly inverse correlation between the intrahepatic pSTAT1 inductions with the serum HCV RNA levels.

conclusionWe have developed an antibody based Western blot detection method to measure intrahepatic pStat1 and pStat2 levels to assess the cellular response to exogenous IFN-alpha. Our results indicate that pStat1 activation is a good indicator to assess the level of HCV replication in chronic HCV patients.

Indexed as

Antiviral AgentsBlotting, WesternDNA, ViralHepacivirusHepatitis C, ChronicHepatocytesHumansImmunoenzyme TechniquesInterferon-alphaPhosphorylationPolymerase Chain ReactionSTAT1 Transcription FactorSTAT2 Transcription FactorViral LoadAntiviral AgentsDNA, ViralInterferon-alphaSTAT1 protein, humanSTAT1 Transcription FactorSTAT2 protein, humanSTAT2 Transcription FactorChronic HCV infectionInterferon-alphaJak-Stat signalingLiver biopsypStat1pStat2

Identifiers

PMID24211829
PMCPMC4365860
OpenAlexW2023430076

What OpenQuestion holds

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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.