Evidence map›Paper›PMID 21516087›Full record

ArticleNature medicine2011

EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy.

Joachim Lupberger, Mirjam B Zeisel, Fei Xiao, Christine Thumann, Isabel Fofana, Laetitia Zona, Christopher Davis, Christopher J Mee, Marine Turek, Sebastian Gorke and 16 more

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 406 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
406citing papers in PubMed, 2 pooled it
27.9field-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

406 citing papers in PubMed, 2 syntheses or guidelines pooled it, 688 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

26 authors at 9 institutions in 4 countries.

Joachim LupbergerInstitut National de la Santé et de la Recherche Médicale, U748, Strasbourg, France.
Mirjam B Zeisel
Fei Xiao
Christine Thumann
Isabel Fofana
Laetitia Zona
Christopher Davis
Christopher J Mee
Marine Turek
Sebastian Gorke
Cathy Royer
Benoit Fischer
Muhammad N Zahid
Dimitri Lavillette
Judith Fresquet
François-Loïc Cosset
S Michael Rothenberg
Thomas Pietschmann
Arvind H Patel
Patrick Pessaux
Michel Doffoël
Wolfgang Raffelsberger
Olivier Poch
Jane A McKeating
Laurent Brino
Thomas F Baumert
Inserm · FRUniversité de Strasbourg · FRUniversity of Birmingham · GBÉcole Normale Supérieure de Lyon · FRHôpitaux Universitaires de Strasbourg · FRCenter for Experimental and Clinical Infection Research · DEMassachusetts General Hospital · USMRC University of Glasgow Centre for Virus Research · GBUniversity of Freiburg · DE

Funding

PARD3 Alterations, Circulating Tumors Cells and Metastasis in Head and Neck CanceK08DE020139 · NIDCR · MASSACHUSETTS GENERAL HOSPITAL · PI ROTHENBERG, STEPHEN MICHAEL · 2010 to 2014
$684k
Howard Hughes Medical InstituteMedical Research Council G0400802Medical Research Council G0801976Medical Research Council MC_U130184144NIDCR NIH HHS 1K08DE020139-01A1Wellcome Trust
6 · The paper itself

Abstract

Hepatitis C virus (HCV) is a major cause of liver disease, but therapeutic options are limited and there are no prevention strategies. Viral entry is the first step of infection and requires the cooperative interaction of several host cell factors. Using a functional RNAi kinase screen, we identified epidermal growth factor receptor and ephrin receptor A2 as host cofactors for HCV entry. Blocking receptor kinase activity by approved inhibitors broadly impaired infection by all major HCV genotypes and viral escape variants in cell culture and in a human liver chimeric mouse model in vivo. The identified receptor tyrosine kinases (RTKs) mediate HCV entry by regulating CD81-claudin-1 co-receptor associations and viral glycoprotein-dependent membrane fusion. These results identify RTKs as previously unknown HCV entry cofactors and show that tyrosine kinase inhibitors have substantial antiviral activity. Inhibition of RTK function may constitute a new approach for prevention and treatment of HCV infection.

Indexed as

Virus InternalizationAnimalsAntigens, CDAntiviral AgentsBase SequenceCell LineClaudin-1ErbB ReceptorsErlotinib HydrochlorideHepacivirusHepatitis CHost-Pathogen InteractionsHumansLigandsMembrane ProteinsMiceAntigens, CDAntiviral AgentsCD81 protein, humanCd81 protein, mouseClaudin-1CLDN1 protein, humanCldn1 protein, mouseErbB ReceptorsErlotinib HydrochlorideLigandsMembrane ProteinsProtein Kinase InhibitorsQuinazolinesReceptor, EphA2RNA, Small InterferingTetraspanin 28

Identifiers

PMID21516087
PMCPMC3938446
OpenAlexW2064526034

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.