About: Interplay between Intrinsic and Innate Immunity during HIV 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
has title	Interplay between Intrinsic and Innate Immunity during HIV Infection
Creator	Richetta, Clémence Bergantz, Louis Delelis, Olivier Deprez, Eric Subra, Frédéric
Source	Medline; PMC
abstract	Restriction factors are antiviral components of intrinsic immunity which constitute a first line of defense by blocking different steps of the human immunodeficiency virus (HIV) replication cycle. In immune cells, HIV infection is also sensed by several pattern recognition receptors (PRRs), leading to type I interferon (IFN-I) and inflammatory cytokines production that upregulate antiviral interferon-stimulated genes (ISGs). Several studies suggest a link between these two types of immunity. Indeed, restriction factors, that are generally interferon-inducible, are able to modulate immune responses. This review highlights recent knowledge of the interplay between restriction factors and immunity inducing antiviral defenses. Counteraction of this intrinsic and innate immunity by HIV viral proteins will also be discussed.
has issue date	2019-08-17(xsd:dateTime)
bibo:doi	10.3390/cells8080922
bibo:pmid	31426525
has license	cc-by
sha1sum (hex)	6f402164832578c18fec0cc33d29c944acf81a26
schema:url	https://doi.org/10.3390/cells8080922
resource representing a document's title	Interplay between Intrinsic and Innate Immunity during HIV Infection
has PubMed Central identifier	PMC6721663
has PubMed identifier	31426525
schema:publication	Cells
resource representing a document's body	covid:6f402164832578c18fec0cc33d29c944acf81a26#body_text
is schema:about of	named entity 'CELLS' named entity 'INNATE IMMUNITY' named entity 'GENES' named entity 'GENERALLY' named entity 'STUDIES' named entity 'REPLICATION CYCLE' named entity 'INTERFERON' named entity 'STEPS' named entity 'DIFFERENT' named entity 'INTERFERON ' named entity 'HIV INFECTION' named entity 'INDUCIBLE' named entity 'VIRAL PROTEINS' named entity 'HUMAN IMMUNODEFICIENCY VIRUS' named entity 'RECENT' named entity 'COMPONENTS' named entity 'INFLAMMATORY' named entity 'LINE' named entity 'KNOWLEDGE' named entity 'REVIEW' named entity 'INTRINSIC' named entity 'INNATE IMMUNITY' named entity 'STIMULATED' named entity 'CYTOKINES' named entity 'INTRINSIC' named entity 'HIV INFECTION' named entity 'TYPES' named entity 'LEADING' named entity 'RESTRICTION' named entity 'BLOCKING' named entity 'INDUCING' named entity 'THESE' named entity 'PRODUCTION' named entity 'ANTIVIRAL' named entity 'IMMUNE CELLS' named entity 'IMMUNE RESPONSES' named entity 'TYPE I INTERFERON' named entity 'SUGGEST' named entity 'HIV' named entity 'MODULATE' named entity 'DEFENSE' named entity 'PATTERN RECOGNITION RECEPTORS' named entity 'LINK' named entity 'IMMUNITY' named entity 'HeLa' named entity 'HIV-2' named entity 'IFN' named entity 'Vpu' named entity 'NK cells' named entity 'virus' named entity 'innate immunity' named entity 'FADD' named entity 'immune responses' named entity 'GTPases' named entity 'dsDNA' named entity 'equine infectious anemia' named entity 'rhesus monkey' named entity 'infectivity' named entity 'HIV-2' named entity 'DEAD-box' named entity 'antiviral' named entity 'Hantaan virus' named entity 'mice' named entity 'virions' named entity 'HIV-1' named entity 'capsids' named entity 'protein' named entity 'TAK1' named entity 'IFN' named entity 'MAVS' named entity 'autophagic' named entity 'antiviral' named entity 'plasma membranes' named entity 'TRIM5α' named entity 'negative feedback loops' named entity 'virus' named entity 'cytidine deaminase'

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