About: A Systematic Analysis of Host Factors Reveals a Med23-Interferon-λ Regulatory Axis against Herpes Simplex Virus Type 1 Replication

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About: A Systematic Analysis of Host Factors Reveals a Med23-Interferon-λ Regulatory Axis against Herpes Simplex Virus Type 1 Replication Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A Systematic Analysis of Host Factors Reveals a Med23-Interferon-λ Regulatory Axis against Herpes Simplex Virus Type 1 Replication
Creator	Boutell, C Crump, C Griffiths, S Koegl, M Zenner, H
Source	Medline; PMC
abstract	Herpes simplex virus type 1 (HSV-1) is a neurotropic virus causing vesicular oral or genital skin lesions, meningitis and other diseases particularly harmful in immunocompromised individuals. To comprehensively investigate the complex interaction between HSV-1 and its host we combined two genome-scale screens for host factors (HFs) involved in virus replication. A yeast two-hybrid screen for protein interactions and a RNA interference (RNAi) screen with a druggable genome small interfering RNA (siRNA) library confirmed existing and identified novel HFs which functionally influence HSV-1 infection. Bioinformatic analyses found the 358 HFs were enriched for several pathways and multi-protein complexes. Of particular interest was the identification of Med23 as a strongly anti-viral component of the largely pro-viral Mediator complex, which links specific transcription factors to RNA polymerase II. The anti-viral effect of Med23 on HSV-1 replication was confirmed in gain-of-function gene overexpression experiments, and this inhibitory effect was specific to HSV-1, as a range of other viruses including Vaccinia virus and Semliki Forest virus were unaffected by Med23 depletion. We found Med23 significantly upregulated expression of the type III interferon family (IFN-λ) at the mRNA and protein level by directly interacting with the transcription factor IRF7. The synergistic effect of Med23 and IRF7 on IFN-λ induction suggests this is the major transcription factor for IFN-λ expression. Genotypic analysis of patients suffering recurrent orofacial HSV-1 outbreaks, previously shown to be deficient in IFN-λ secretion, found a significant correlation with a single nucleotide polymorphism in the IFN-λ3 (IL28b) promoter strongly linked to Hepatitis C disease and treatment outcome. This paper describes a link between Med23 and IFN-λ, provides evidence for the crucial role of IFN-λ in HSV-1 immune control, and highlights the power of integrative genome-scale approaches to identify HFs critical for disease progression and outcome.
has issue date	2013-08-08(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1003514
bibo:pmid	23950709
has license	cc-by
sha1sum (hex)	a7344a564121bf1e3f995911e78c17b1b2aee903
schema:url	https://doi.org/10.1371/journal.ppat.1003514
resource representing a document's title	A Systematic Analysis of Host Factors Reveals a Med23-Interferon-λ Regulatory Axis against Herpes Simplex Virus Type 1 Replication
has PubMed Central identifier	PMC3738494
has PubMed identifier	23950709
schema:publication	PLoS Pathog
resource representing a document's body	covid:a7344a564121bf1e3f995911e78c17b1b2aee903#body_text
is schema:about of	named entity 'diseases' named entity 'polymerase' named entity 'existing' named entity 'linked' named entity 'small interfering RNA' named entity 'functionally' named entity 'HERPES SIMPLEX VIRUS TYPE 1' named entity 'SUFFERING' named entity 'NEUROTROPIC VIRUS' named entity 'IDENTIFIED' named entity 'OUTBREAKS' named entity 'GAIN' named entity 'INDIVIDUALS' named entity 'TO IDENTIFY' named entity 'SCREEN' named entity 'VIRUSES' named entity 'INTERACTION' named entity 'INVOLVED' named entity 'EXPERIMENTS' named entity 'PROVIDES EVIDENCE FOR' named entity 'LINK' named entity 'OROFACIAL' named entity 'UPREGULATED EXPRESSION' named entity 'EXPRESSION' named entity 'FOUND' named entity 'RANGE' named entity 'PROTEIN LEVEL' named entity 'VIRUS REPLICATION' named entity 'SMALL INTERFERING RNA' named entity 'FUNCTION' named entity 'INHIBITORY EFFECT' named entity 'MENINGITIS' named entity 'BIOINFORMATIC' named entity 'SIGNIFICANT' named entity 'NOVEL' named entity 'RNA POLYMERASE II' named entity 'CONFIRMED' named entity 'MED23' named entity 'RNA INTERFERENCE' named entity 'IRF7' named entity 'TRANSCRIPTION FACTOR' named entity 'IMMUNOCOMPROMISED' named entity 'DIRECTLY' named entity 'REPLICATION' named entity 'INCLUDING' named entity 'YEAST TWO-HYBRID' named entity 'HSV-1' named entity 'APPROACHES' named entity 'IMMUNE CONTROL' named entity 'PREVIOUSLY' named entity 'PATIENTS' named entity 'VIRAL COMPONENT' named entity 'DISEASE PROGRESSION' named entity 'PROTEIN COMPLEXES' named entity 'CAUSING' named entity 'HARMFUL' named entity 'PATHWAYS' named entity 'GENITAL' named entity 'SPECIFIC' named entity 'RECURRENT' named entity 'SYNERGISTIC' named entity 'TRANSCRIPTION FACTORS' named entity 'DISEASE' named entity 'INDUCTION' named entity 'VESICULAR' named entity 'LINKS' named entity 'MULTI' named entity 'HFS' named entity 'IDENTIFICATION' named entity 'ENRICHED' named entity 'MAJOR' named entity 'ITS' named entity 'SINGLE NUCLEOTIDE POLYMORPHISM' named entity 'AXIS' named entity 'INTERFERON' named entity 'ANALYSIS' named entity 'GENE OVEREXPRESSION'

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