About: Epigenetic Landscape during Coronavirus Infection

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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
title	Epigenetic Landscape during Coronavirus Infection
Creator	Baric, Ralph Schäfer, Alexandra
source	Medline; PMC
abstract	Coronaviruses (CoV) comprise a large group of emerging human and animal pathogens, including the highly pathogenic severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) strains. The molecular mechanisms regulating emerging coronavirus pathogenesis are complex and include virus–host interactions associated with entry, replication, egress and innate immune control. Epigenetics research investigates the genetic and non-genetic factors that regulate phenotypic variation, usually caused by external and environmental factors that alter host expression patterns and performance without any change in the underlying genotype. Epigenetic modifications, such as histone modifications, DNA methylation, chromatin remodeling, and non-coding RNAs, function as important regulators that remodel host chromatin, altering host expression patterns and networks in a highly flexible manner. For most of the past two and a half decades, research has focused on the molecular mechanisms by which RNA viruses antagonize the signaling and sensing components that regulate induction of the host innate immune and antiviral defense programs upon infection. More recently, a growing body of evidence supports the hypothesis that viruses, even lytic RNA viruses that replicate in the cytoplasm, have developed intricate, highly evolved, and well-coordinated processes that are designed to regulate the host epigenome, and control host innate immune antiviral defense processes, thereby promoting robust virus replication and pathogenesis. In this article, we discuss the strategies that are used to evaluate the mechanisms by which viruses regulate the host epigenome, especially focusing on highly pathogenic respiratory RNA virus infections as a model. By combining measures of epigenome reorganization with RNA and proteomic datasets, we articulate a spatial-temporal data integration approach to identify regulatory genomic clusters and regions that play a crucial role in the host’s innate immune response, thereby defining a new viral antagonism mechanism following emerging coronavirus infection.
has issue date	2017-02-15(xsd:dateTime)
bibo:doi	10.3390/pathogens6010008
bibo:pmid	28212305
has license	cc-by
sha1sum (hex)	8e631c0c0bdbb5cf13818b5b71d39c145b045955
schema:url	https://doi.org/10.3390/pathogens6010008
resource representing a document's title	Epigenetic Landscape during Coronavirus Infection
has PubMed Central identifier	PMC5371896
has PubMed identifier	28212305
schema:publication	Pathogens
resource representing a document's body	covid:8e631c0c0bdbb5cf13818b5b71d39c145b045955#body_text
is schema:about of	named entity 'control' named entity 'The' named entity 'play' named entity 'expression' named entity 'innate immune' named entity 'infections' named entity 'phenotypic variation' named entity 'altering' named entity 'epigenome' named entity 'SARS-CoV' named entity 'chromatin remodeling' named entity 'chromatin' named entity 'GENOTYPE' named entity 'FOCUSING' named entity 'SENSING' named entity 'CODING' named entity 'RNA' named entity 'DNA METHYLATION' named entity 'INNATE IMMUNE RESPONSE' named entity 'INVESTIGATES' named entity 'ANTAGONISM' named entity 'REGULATING' named entity 'REGULATORS' named entity 'PAST' named entity 'PROTEOMIC' named entity 'CLUSTERS' named entity 'CHROMATIN REMODELING' named entity 'FOLLOWING' named entity 'PROMOTING' named entity 'RECENTLY' named entity 'TEMPORAL' named entity 'PHENOTYPIC VARIATION' named entity 'NEW' named entity 'CONTROL' named entity 'ANIMAL PATHOGENS' named entity 'GROWING' named entity 'REPLICATE' named entity 'IMPORTANT' named entity 'STRATEGIES' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'CAUSED BY' named entity 'INCLUDING' named entity 'RESPIRATORY' named entity 'HOST' named entity 'ROLE' named entity 'RNAS' named entity 'EPIGENOME' named entity 'SIGNALING' named entity 'LYTIC' named entity 'REORGANIZATION' named entity 'FLEXIBLE' named entity 'MECHANISM' named entity 'ARTICLE' named entity 'EVALUATE' named entity 'CHANGE IN' named entity 'VIRUS REPLICATION' named entity 'SPATIAL' named entity 'VIRAL' named entity 'COMPONENTS' named entity 'INFECTION' named entity 'REPLICATION' named entity 'ENVIRONMENTAL FACTORS' named entity 'PATTERNS' named entity 'EVOLVED' named entity 'ALTER' named entity 'ASSOCIATED WITH' named entity '27S' named entity 'RNA VIRUS INFECTIONS' named entity 'ANTIVIRAL' named entity 'NETWORKS' named entity 'OF EVIDENCE' named entity 'IMMUNE' named entity 'GENOMIC' named entity 'LARGE' named entity 'MEASURES' named entity 'RNA VIRUSES' named entity 'PATHOGENIC' named entity 'DATA INTEGRATION' named entity 'PROGRAMS' named entity 'HALF'

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