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Interplay between Intrinsic and Innate Immunity during HIV Infection
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...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721663/ https://www.ncbi.nlm.nih.gov/pubmed/31426525 http://dx.doi.org/10.3390/cells8080922 |
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author | Bergantz, Louis Subra, Frédéric Deprez, Eric Delelis, Olivier Richetta, Clémence |
author_facet | Bergantz, Louis Subra, Frédéric Deprez, Eric Delelis, Olivier Richetta, Clémence |
author_sort | Bergantz, Louis |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-6721663 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-67216632019-09-10 Interplay between Intrinsic and Innate Immunity during HIV Infection Bergantz, Louis Subra, Frédéric Deprez, Eric Delelis, Olivier Richetta, Clémence Cells Review 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. MDPI 2019-08-17 /pmc/articles/PMC6721663/ /pubmed/31426525 http://dx.doi.org/10.3390/cells8080922 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Bergantz, Louis Subra, Frédéric Deprez, Eric Delelis, Olivier Richetta, Clémence Interplay between Intrinsic and Innate Immunity during HIV Infection |
title | Interplay between Intrinsic and Innate Immunity during HIV Infection |
title_full | Interplay between Intrinsic and Innate Immunity during HIV Infection |
title_fullStr | Interplay between Intrinsic and Innate Immunity during HIV Infection |
title_full_unstemmed | Interplay between Intrinsic and Innate Immunity during HIV Infection |
title_short | Interplay between Intrinsic and Innate Immunity during HIV Infection |
title_sort | interplay between intrinsic and innate immunity during hiv infection |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721663/ https://www.ncbi.nlm.nih.gov/pubmed/31426525 http://dx.doi.org/10.3390/cells8080922 |
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