About: A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases

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About: A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases 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	A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases
Creator	Frolov, Ilya Colombo, María Delgui, Laura De, Juan Torre, La
Source	Medline; PMC
abstract	Viruses are lifeless particles designed for setting virus-host interactome assuring a new generation of virions for dissemination. This interactome generates a pressure on host organisms evolving mechanisms to neutralize viral infection, which places the pressure back onto virus, a process known as virus-host cell co-evolution. Positive-single stranded RNA (+sRNA) viruses are an important group of viral agents illustrating this interesting phenomenon. During replication, their genomic +sRNA is employed as template for translation of viral proteins; among them the RNA-dependent RNA polymerase (RdRp) is responsible of viral genome replication originating double-strand RNA molecules (dsRNA) as intermediates, which accumulate representing a potent threat for cellular dsRNA receptors to initiate an antiviral response. A common feature shared by these viruses is their ability to rearrange cellular membranes to serve as platforms for genome replication and assembly of new virions, supporting replication efficiency increase by concentrating critical factors and protecting the viral genome from host anti-viral systems. This review summarizes current knowledge regarding cellular dsRNA receptors and describes prototype viruses developing replication niches inside rearranged membranes. However, for several viral agents it's been observed both, a complex rearrangement of cellular membranes and a strong innate immune antiviral response induction. So, we have included recent data explaining the mechanism by, even though viruses have evolved elegant hideouts, host cells are still able to develop dsRNA receptors-dependent antiviral response.
has issue date	2017-01-20(xsd:dateTime)
bibo:doi	10.3389/fcimb.2017.00005
bibo:pmid	28164038
has license	cc-by
sha1sum (hex)	dc320a349f137013cc728b319144588e3854cb20
schema:url	https://doi.org/10.3389/fcimb.2017.00005
resource representing a document's title	A Novel Mechanism Underlying the Innate Immune Response Induction upon Viral-Dependent Replication of Host Cell mRNA: A Mistake of +sRNA Viruses' Replicases
has PubMed Central identifier	PMC5247633
has PubMed identifier	28164038
schema:publication	Front Cell Infect Microbiol
resource representing a document's body	covid:dc320a349f137013cc728b319144588e3854cb20#body_text
is schema:about of	named entity 'rearrange' named entity 'process' named entity 'response' named entity 'evolving' named entity 'induction' named entity 'RNA-dependent RNA polymerase' named entity 'genomic' named entity 'This' named entity 'representing' named entity 'cellular membranes' named entity 'Immune' named entity 'mRNA' named entity 'INNATE IMMUNE RESPONSE' named entity 'DSRNA' named entity 'COMPLEX' named entity 'VIRAL GENOME REPLICATION ' named entity 'VIRAL INFECTION' named entity 'A COMMON' named entity 'NEW' named entity 'CELLULAR' named entity 'INCREASE' named entity 'RNA-DEPENDENT RNA POLYMERASE' named entity 'PLACES' named entity 'CONCENTRATING' named entity 'AS VIRUS' named entity 'PARTICLES' named entity 'FEATURE' named entity 'ASSEMBLY' named entity 'VIRAL PROTEINS' named entity 'PRESSURE' named entity 'REARRANGED' named entity 'IMPORTANT' named entity 'MECHANISM' named entity 'PROTECTING' named entity 'RNA' named entity 'SETTING' named entity 'IMMUNE' named entity '27S' named entity 'DEVELOPING' named entity 'INTERMEDIATES' named entity 'ANTIVIRAL RESPONSE' named entity 'THESE' named entity 'PROTOTYPE' named entity 'OBSERVED' named entity 'DEPENDENT' named entity 'VIRIONS' named entity 'GENERATION' named entity 'EMPLOYED' named entity 'STRONG' named entity 'TO SERVE AS' named entity 'INSIDE' named entity 'MECHANISM' named entity 'GENOME' named entity 'RECENT' named entity 'HOST' named entity 'REVIEW' named entity 'MECHANISMS' named entity 'VIRAL GENOME' named entity 'CRITICAL' named entity 'GENOMIC' named entity 'VIRAL' named entity 'SYSTEMS' named entity 'NOVEL' named entity 'INDUCTION' named entity 'INCLUDED' named entity 'INDUCTION' named entity 'VIRUSES' named entity 'DATA' named entity 'TEMPLATE' named entity 'PROCESS' named entity 'SUPPORTING' named entity 'SHARED' named entity 'RECEPTORS' named entity 'DOUBLE' named entity 'HAVE' named entity 'INTERESTING' named entity 'STRAND'

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