Evidence map›Paper›PMID 23913866›Full record

ArticleHepatology (Baltimore, Md.)2014

Kinetic differences in the induction of interferon stimulated genes by interferon-α and interleukin 28B are altered by infection with hepatitis C virus.

Nikolaus Jilg, Wenyu Lin, Jian Hong, Esperance A Schaefer, David Wolski, James Meixong, Kaku Goto, Cynthia Brisac, Pattranuch Chusri, Dahlene N Fusco and 7 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hepatology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

74 citing papers in PubMed, 108 citations in OpenAlex.

  1. Review
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  5. Function of Interferon Lambda Receptor 1 Variants in Stem Cell-Derived Hepatocytes with Abrogated EndogenousJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2025
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14 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 2 countries.

Nikolaus JilgGastrointestinal Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
Wenyu Lin
Jian Hong
Esperance A Schaefer
David Wolski
James Meixong
Kaku Goto
Cynthia Brisac
Pattranuch Chusri
Dahlene N Fusco
Stephane Chevaliez
Jay Luther
Kattareeya Kumthip
Thomas J Urban
Lee F Peng
Georg M Lauer
Raymond T Chung
Harvard University · USDuke University · USTokyo Medical University · JP

Funding

Virology CoreU19AI082630 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI GEORG Michael LAUER · 2009 to 2026
$48.1M
Discovery and Assessment of Genetic Determinants of HCV and HIV ControlR01DA033541 · NIDA · MASSACHUSETTS GENERAL HOSPITAL · PI CHUNG, RAYMOND T, KIM, ARTHUR Y · 2011 to 2015
$3.4M
INVESTIGATIVE ENDOCRINOLOGYT32DK007004 · NIDDK · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI SURKS, MARTIN I · 1986 to 1994
–
NIAID NIH HHS AI082630NIAID NIH HHS U19 AI082630NIDA NIH HHS R01 DA033541NIDDK NIH HHS N01-DK-7-004/HHSN26L7200700004C
6 · The paper itself

Abstract

unlabelledSeveral genome-wide association studies (GWAS) have identified a genetic polymorphism associated with the gene locus for interleukin 28B (IL28B), a type III interferon (IFN), as a major predictor of clinical outcome in hepatitis C. Antiviral effects of the type III IFN family have previously been shown against several viruses, including hepatitis C virus (HCV), and resemble the function of type I IFN including utilization of the intracellular Janus kinase signal transducer and activator of transcription (JAK-STAT) pathway. Effects unique to IL28B that would distinguish it from IFN-α are not well defined. By analyzing the transcriptomes of primary human hepatocytes (PHH) treated with IFN-α or IL28B, we sought to identify functional differences between IFN-α and IL28B to better understand the roles of these cytokines in the innate immune response. Although our data did not reveal distinct gene signatures, we detected striking kinetic differences between IFN-α and IL28B stimulation for interferon stimulated genes (ISGs). While gene induction was rapid and peaked at 8 hours of stimulation with IFN-α in PHH, IL28B produced a slower, but more sustained increase in gene expression. We confirmed these findings in the human hepatoma cell line Huh7.5.1. Interestingly, in HCV-infected cells the rapid response after stimulation with IFN-α was blunted, and the induction pattern resembled that caused by IL28B.

conclusionThe kinetics of gene induction are fundamentally different for stimulations with either IFN-α or IL28B in hepatocytes, suggesting distinct roles of these cytokines within the immune response. Furthermore, the observed differences are substantially altered by infection with HCV.

Indexed as

Carcinoma, HepatocellularCell Line, TumorComorbidityDose-Response Relationship, DrugGene Expression Regulation, NeoplasticHepatitis CHepatocytesHumansInterferon-alphaInterferon LambdaInterferonsInterleukinsLiver NeoplasmsPhosphorylationSTAT1 Transcription FactorTime FactorsInterferon-alphaInterferon Lambdainterferon-lambda, humanInterferonsInterleukinsSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID23913866
PMCPMC3909557
OpenAlexW2088793982

What OpenQuestion holds

Textmetadata
LicenceTDM
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.