Evidence map›Paper›PMID 22996292›Full record

ArticleHepatology (Baltimore, Md.)2013

IFITM1 is a tight junction protein that inhibits hepatitis C virus entry.

Courtney Wilkins, Jessica Woodward, Daryl T-Y Lau, Amy Barnes, Michael Joyce, Nicola McFarlane, Jane A McKeating, D Lorne Tyrrell, Michael Gale

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.

0numbers the graph read from it
0cells of the map it votes in
120citing papers in PubMed
7.0field-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.

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

120 citing papers in PubMed, 154 citations in OpenAlex.

  1. Trial
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  9. IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes.bioRxiv : the preprint server for biology · 2025
    Article
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  20. [Interferon-related gene array in predicting the efficacy of interferon therapy in chronic hepatitis B].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023
    Article

60 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

9 authors at 4 institutions in 3 countries.

Courtney WilkinsDepartment of Immunology, University of Washington, Seattle, WA 98195, USA.
Jessica Woodward
Daryl T-Y Lau
Amy Barnes
Michael Joyce
Nicola McFarlane
Jane A McKeating
D Lorne Tyrrell
Michael Gale
University of Alberta · CAUniversity of Washington · USUniversity of Birmingham · GBBeth Israel Deaconess Medical Center · US

Funding

Virus-Host Interactions in Hepatitis C Virus (HCV) InfectionsU19AI040035 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI THOMAS, DAVID L · 1996 to 2009
$12.0M
Mechanisms Of Pathogen Recognition And Innate Immune Control Of Hepatitis C VirusU19AI088778 · NIAID · UNIVERSITY OF WASHINGTON · PI LAU, DARYL T · 2010 to 2014
$4.2M
The Host Response to Hepatitis C VirusR01AI060389 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI GALE, MICHAEL · 2003 to 2012
$3.4M
Racial Differences in IFN Transcriptional ResponseR01DK068598 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI LAU, DARYL T · 2005 to 2009
$1.8M
INNATE IMMUNE DEFENSE AGAINST HCV and HIV: THE CHIMERIC MOUSE MODELR01DA024563 · NIDA · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2007 to 2011
$1.7M
The Host Response to Hepatitis C VirusR56AI060389 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2014 to 2014
$494k
Medical Research Council G1100247Medical Research Council G9818340NIAID NIH HHS AI060389NIAID NIH HHS R01 AI060389NIAID NIH HHS U19 AI040035NIAID NIH HHS U19 AI088778NIDA NIH HHS DA024563NIDA NIH HHS R01 DA024563NIDDK NIH HHS DK068598-01NIDDK NIH HHS R01 DK068598
6 · The paper itself

Abstract

unlabelledType 1 interferon (IFN) continues to be the foundation for the current standard of care combination therapy for chronic hepatitis C virus (HCV) infection, yet the component interferon-stimulated genes (ISGs) that mediate the antiviral actions of IFN are not fully defined. Interferon-induced transmembrane protein 1 (IFITM1) is an ISG product that suppresses early stage infection by a number of viruses through an unknown mechanism of action. Moreover, the actions of IFITM1 on HCV infection are not fully elucidated. Here we identify IFITM1 as a hepatocyte tight junction protein and a potent anti-HCV effector molecule. IFITM1 expression is induced early during IFN treatment of hepatocytes and accumulates at hepatic tight junctions in HCV-infected human patient liver during IFN therapy. Additionally, we found that IFITM1 interacts with HCV coreceptors, including CD81 and occludin, to disrupt the process of viral entry. Thus, IFITM1 is an anti-HCV ISG whose actions impart control of HCV infection through interruption of viral coreceptor function.

conclusionThis study defines IFITM1 as an ISG effector with action against HCV entry. Design of therapy regimens to enhance IFITM1 expression should improve the virologic response among HCV patients undergoing treatment with type I IFN.

Indexed as

Antigens, DifferentiationAntiviral AgentsCells, CulturedHepacivirusHepatitis CHumansInterferon Type IReceptors, VirusTetraspanin 28Tight Junction ProteinsVirus ReplicationAntigens, DifferentiationAntiviral AgentsInterferon Type Ileu-13 antigenReceptors, VirusTetraspanin 28Tight Junction Proteins

Identifiers

PMID22996292
PMCPMC3566288
OpenAlexW1984466323

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.