About: Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response

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About: Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response
Creator	Falcón, Ana Nieto, Amelia Marcos-Villar, Laura Landeras-Bueno, Sara Zamarreño, Noelia Díaz-Colunga, Juan Esteller, Manel Sandoval, Juan
Source	PMC
abstract	Influenza virus stablishes a network of virus-host functional interactions, which depends on chromatin dynamic and therefore on epigenetic modifications. Using an unbiased search, we analyzed the epigenetic changes at DNA methylation and post-translational histone modification levels induced by the infection. DNA methylation was unaltered, while we found a general decrease on histone acetylation, which correlates with transcriptional inactivation and may cooperate with the impairment of cellular transcription that causes influenza virus infection. A particular increase in H3K79 methylation was observed and the use of an inhibitor of the specific H3K79 methylase, Dot1L enzyme, or its silencing, increased influenza virus replication. The antiviral response was reduced in conditions of Dot1L downregulation, since decreased nuclear translocation of NF-kB complex, and IFN-β, Mx1 and ISG56 expression was detected. The data suggested a control of antiviral signaling by methylation of H3K79 and consequently, influenza virus replication was unaffected in IFN pathway-compromised, Dot1L-inhibited cells. H3K79 methylation also controlled replication of another potent interferon-inducing virus such as vesicular stomatitis virus, but did not modify amplification of respiratory syncytial virus that poorly induces interferon signaling. Epigenetic methylation of H3K79 might have an important role in controlling interferon-induced signaling against viral pathogens.
has issue date	2018-01-19(xsd:dateTime)
bibo:doi	10.1038/s41598-018-19370-6
bibo:pmid	29352168
has license	cc-by
sha1sum (hex)	35f89b8e3ddf5b85ff55314dd423adf1019ac410
schema:url	https://doi.org/10.1038/s41598-018-19370-6
resource representing a document's title	Epigenetic control of influenza virus: role of H3K79 methylation in interferon-induced antiviral response
has PubMed Central identifier	PMC5775356
has PubMed identifier	29352168
schema:publication	Sci Rep
resource representing a document's body	covid:35f89b8e3ddf5b85ff55314dd423adf1019ac410#body_text
is schema:about of	named entity 'data' named entity 'antiviral' named entity 'antiviral' named entity 'DOT1L' named entity 'VIRAL PATHOGENS' named entity 'HISTONE ACETYLATION' named entity 'SILENCING' named entity 'IMPORTANT' named entity 'ANALYZED' named entity 'DNA METHYLATION' named entity 'IMPAIRMENT' named entity 'SEARCH' named entity 'CAUSES' named entity 'ANTIVIRAL' named entity 'INTERFERON SIGNALING' named entity 'INTERFERON' named entity 'INFLUENZA VIRUS' named entity 'conditions' named entity 'inhibitor' named entity 'epigenetic' named entity 'IFN-β' named entity 'nuclear' named entity 'respiratory syncytial virus' named entity 'transcriptional' named entity 'cooperate' named entity 'virus' named entity 'Epigenetic' named entity 'control' named entity 'enzyme' named entity 'NF-kB' named entity 'interferon' named entity 'post-translational' named entity 'DNA methylation' named entity 'histone acetylation' named entity 'methylation' named entity 'IFN' named entity 'methylation' named entity 'ISG56' named entity 'antiviral' named entity 'interferon' named entity 'Influenza virus' named entity 'NF-κB' named entity 'IFN' named entity 'monoclonal antibody' named entity 'Confocal' named entity 'NF-κB' named entity 'H3K4me3' named entity '7.5' named entity 'WSN' named entity 'MDCK' named entity 'California' named entity 'TNF-α' named entity 'methylation' named entity 'HCV' named entity '0.45' named entity 'Dot1L' named entity 'epigenetic modification' named entity 'demethylation' named entity 'NF-κB' named entity 'influenza virus' named entity 'Dot1L' named entity 'Assay' named entity 'Histone acetylation' named entity 'HCMV' named entity 'Pearson correlation coefficient' named entity 'silencers' named entity 'obligate intracellular parasites' named entity 'Dot1L' named entity 'silencers' named entity 'colorimetric assays' named entity 'shRNAs' named entity 'Dot1L' named entity 'gene transcription' named entity 'promoter methylation'

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