About: Interferon-beta treatment increases human papillomavirus early gene transcription and viral plasmid genome replication by activating interferon regulatory factor (IRF)-1

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About: Interferon-beta treatment increases human papillomavirus early gene transcription and viral plasmid genome replication by activating interferon regulatory factor (IRF)-1 Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Interferon-beta treatment increases human papillomavirus early gene transcription and viral plasmid genome replication by activating interferon regulatory factor (IRF)-1
Creator	Anson, James Bossler, Aaron Harada, Hisashi Haugen, Thomas Klingelhutz, Aloysius Lace, Michael Taniguchi, Tadatsugu Turek, Lubomir
Source	PMC
abstract	Interferons (IFNs) have been used to treat mucosal lesions caused by human papillomavirus (HPV) infection, such as intraepithelial precursor lesions to cancer of the uterine cervix, genital warts or recurrent respiratory papillomatosis, to potentially reduce or eliminate replicating HPV plasmid genomes. Mucosal HPVs have evolved mechanisms that impede IFN-β synthesis and downregulate genes induced by IFN. Here we show that these HPV types directly subvert a cellular transcriptional response to IFN-β as a potential boost in infection. Treatment with low levels of human IFN-β induced initial amplification of HPV-16 and HPV-11 plasmid genomes and increased HPV-16 or HPV-31 DNA copy numbers up to 6-fold in HPV-immortalized keratinocytes. IFN treatment also increased early gene transcription from the major early gene promoters in HPV-16, HPV-31 and HPV-11. Furthermore, mutagenesis of the viral genomes and ectopic interferon regulatory factor (IRF) expression in transfection experiments using IRF-1 (−/−) , IRF-2 (−/−) and dual knockout cell lines determined that these responses are due to the activation of IRF-1 interaction with a conserved interferon response element demonstrated in several mucosal HPV early gene promoters. Our results provide a molecular explanation for the varying clinical outcomes of IFN therapy of papillomatoses and define an assay for the modulation of the HPV gene program by IFNs as well as other cytokines and signaling molecules in infection and therapy.
has issue date	2009-06-18(xsd:dateTime)
bibo:doi	10.1093/carcin/bgp150
bibo:pmid	19541854
has license	no-cc
sha1sum (hex)	60705896848dadf424a0a985ca63d7d4a2dce23e
schema:url	https://doi.org/10.1093/carcin/bgp150
resource representing a document's title	Interferon-beta treatment increases human papillomavirus early gene transcription and viral plasmid genome replication by activating interferon regulatory factor (IRF)-1
has PubMed Central identifier	PMC7110192
has PubMed identifier	19541854
schema:publication	Carcinogenesis
resource representing a document's body	covid:60705896848dadf424a0a985ca63d7d4a2dce23e#body_text
is schema:about of	named entity 'PLASMID GENOME' named entity 'gene' named entity 'amplification' named entity 'IRF-1' named entity 'Interferons' named entity 'response' named entity 'human papillomavirus' named entity 'INCREASES' named entity 'GENE TRANSCRIPTION' named entity 'LEVELS' named entity 'HPV' named entity 'DUAL' named entity 'GENE TRANSCRIPTION' named entity 'PROVIDE' named entity 'COPY' named entity 'PROGRAM' named entity 'RESPONSE TO' named entity 'INTRAEPITHELIAL' named entity 'TRANSCRIPTIONAL' named entity 'MUCOSAL' named entity 'SIGNALING MOLECULES' named entity 'GENES' named entity 'NUMBERS' named entity 'HERE' named entity 'IFN' named entity 'GENE' named entity 'ACTIVATING' named entity 'USED' named entity 'EVOLVED' named entity 'HUMAN PAPILLOMAVIRUS ' named entity 'MECHANISMS' named entity 'GENE PROMOTERS' named entity 'TREAT' named entity 'ASSAY' named entity 'UP TO' named entity 'TRANSFECTION' named entity 'INTERFERON REGULATORY FACTOR' named entity 'EARLY GENE' named entity 'REPLICATION' named entity 'TREATMENT' named entity 'INTERFERON-BETA' named entity 'IRF-1' named entity 'VARYING' named entity 'ECTOPIC' named entity 'EXPERIMENTS' named entity 'PLASMID' named entity 'DNA' named entity 'DETERMINED' named entity 'DUE TO' named entity 'HPV-16' named entity 'REDUCE' named entity 'VIRAL' named entity 'LESIONS' named entity 'CLINICAL OUTCOMES' named entity 'IMMORTALIZED' named entity 'OUR' named entity 'INTERFERON REGULATORY FACTOR' named entity 'KERATINOCYTES' named entity 'CYTOKINES' named entity 'VIRAL PLASMID' named entity 'ACTIVATION' named entity 'RESPONSE ELEMENT' named entity 'RESPONSES' named entity 'PAPILLOMATOSES' named entity 'DEMONSTRATED' named entity 'CELLULAR' named entity 'IRF-2' named entity 'HAVE' named entity 'GENOMES' named entity 'POTENTIAL' named entity 'MOLECULAR' named entity 'BOOST' named entity 'CAUSED BY' named entity 'HPV-11'

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