About: Manipulation or capitulation: virus interactions with autophagy

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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
has title	Manipulation or capitulation: virus interactions with autophagy
Creator	Randall, Glenn Jordan, Tristan
Source	Elsevier; Medline; PMC
abstract	Autophagy is a homeostatic process that functions to balance cellular metabolism and promote cell survival during stressful conditions by delivering cytoplasmic components for lysosomal degradation and subsequent recycling. During viral infection, autophagy can act as a surveillance mechanism that delivers viral antigens to the endosomal/lysosomal compartments that are enriched in immune sensors. Additionally, activated immune sensors can signal to activate autophagy. To evade this antiviral activity, many viruses elaborate functions to block the autophagy pathway at a variety of steps. Alternatively, some viruses actively subvert autophagy for their own benefit. Manipulated autophagy has been proposed to facilitate nearly every stage of the viral lifecycle in direct and indirect ways. In this review, we synthesize the extensive literature on virus-autophagy interactions, emphasizing the role of autophagy in antiviral immunity and the mechanisms by which viruses subvert autophagy for their own benefit.
has issue date	2012-02-01(xsd:dateTime)
bibo:doi	10.1016/j.micinf.2011.09.007
bibo:pmid	22051604
has license	green-oa
sha1sum (hex)	ef425d406ff3747c64de40c9147815959523bf23
schema:url	https://doi.org/10.1016/j.micinf.2011.09.007
resource representing a document's title	Manipulation or capitulation: virus interactions with autophagy
has PubMed Central identifier	PMC3264745
has PubMed identifier	22051604
schema:publication	Microbes and Infection
resource representing a document's body	covid:ef425d406ff3747c64de40c9147815959523bf23#body_text
is schema:about of	named entity 'VIRUS' named entity 'autophagy' named entity 'mechanisms' named entity 'ACT' named entity 'BLOCK' named entity 'CONDITIONS' named entity 'STRESSFUL' named entity 'SENSORS' named entity 'ACTIVATED' named entity 'MECHANISM' named entity 'DIRECT' named entity 'PROPOSED' named entity 'CYTOPLASMIC' named entity 'COMPARTMENTS' named entity 'THEIR' named entity 'INDIRECT' named entity 'ELABORATE' named entity 'IS A' named entity 'HOMEOSTATIC PROCESS' named entity 'VIRAL ANTIGENS' named entity 'INTERACTIONS' named entity 'VARIETY' named entity 'MECHANISMS' named entity 'BALANCE' named entity 'ANTIVIRAL ACTIVITY' named entity 'NEARLY' named entity 'AUTOPHAGY PATHWAY' named entity 'SURVEILLANCE' named entity 'ANTIVIRAL' named entity 'SYNTHESIZE' named entity 'IMMUNITY' named entity 'ACTIVATE' named entity 'INTERACTIONS' named entity 'CELL SURVIVAL' named entity 'CELLULAR METABOLISM' named entity 'LYSOSOMAL DEGRADATION' named entity 'IMMUNE' named entity 'EXTENSIVE' named entity 'AUTOPHAGY' named entity 'VIRUSES' named entity 'VIRAL INFECTION' named entity 'SUBSEQUENT' named entity 'ROLE' named entity 'ENRICHED' named entity 'AUTOPHAGY' named entity 'STEPS' named entity 'RECYCLING' named entity 'SIGNAL' named entity 'PROMOTE' named entity 'BENEFIT' named entity 'VIRAL' named entity 'COMPONENTS' named entity 'STAGE' named entity 'REVIEW' named entity 'FUNCTIONS' named entity 'MANIPULATION' named entity 'LITERATURE' named entity 'viruses' named entity 'viral' named entity 'promote' named entity 'steps' named entity 'interactions' named entity 'autophagy' named entity 'viruses' named entity 'antiviral' named entity 'homeostatic' named entity 'Autophagy' named entity 'autophagy' named entity 'viral infection' named entity 'autophagy' named entity 'endosomal' named entity 'Lamp2' named entity 'LC3' named entity 'PI3P' named entity 'autophagy' named entity 'PAMPs' named entity 'virions' named entity 'poliovirus' named entity 'viral replication' named entity 'HIV-1'

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