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Autophagy-Virus Interplay: From Cell Biology to Human Disease

Autophagy is a highly conserved intracellular degradation process that targets protein aggregates and damaged organelles. Autophagy is also implicated in numerous viral infections, including human immunodeficiency virus-1 (HIV-1), influenza A (IAV) and herpes simplex virus-1 (HSV-1). Depending on th...

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Autores principales: Ahmad, Liyana, Mostowy, Serge, Sancho-Shimizu, Vanessa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6252315/
https://www.ncbi.nlm.nih.gov/pubmed/30510929
http://dx.doi.org/10.3389/fcell.2018.00155
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author Ahmad, Liyana
Mostowy, Serge
Sancho-Shimizu, Vanessa
author_facet Ahmad, Liyana
Mostowy, Serge
Sancho-Shimizu, Vanessa
author_sort Ahmad, Liyana
collection PubMed
description Autophagy is a highly conserved intracellular degradation process that targets protein aggregates and damaged organelles. Autophagy is also implicated in numerous viral infections, including human immunodeficiency virus-1 (HIV-1), influenza A (IAV) and herpes simplex virus-1 (HSV-1). Depending on the virus, autophagy can restrict or promote viral replication, and play key roles in modulating inflammation and cell survival. In this review, we consider examples of autophagy-virus interplay, highlighting the protective role of autophagy in human infections. We summarize recent discoveries and emerging themes illuminating autophagy’s role in immunity and inflammation upon viral infection. Finally, we discuss future prospects and therapeutic implications, and potential caveats associated with using autophagy to control viral infections in humans.
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spelling pubmed-62523152018-12-03 Autophagy-Virus Interplay: From Cell Biology to Human Disease Ahmad, Liyana Mostowy, Serge Sancho-Shimizu, Vanessa Front Cell Dev Biol Cell and Developmental Biology Autophagy is a highly conserved intracellular degradation process that targets protein aggregates and damaged organelles. Autophagy is also implicated in numerous viral infections, including human immunodeficiency virus-1 (HIV-1), influenza A (IAV) and herpes simplex virus-1 (HSV-1). Depending on the virus, autophagy can restrict or promote viral replication, and play key roles in modulating inflammation and cell survival. In this review, we consider examples of autophagy-virus interplay, highlighting the protective role of autophagy in human infections. We summarize recent discoveries and emerging themes illuminating autophagy’s role in immunity and inflammation upon viral infection. Finally, we discuss future prospects and therapeutic implications, and potential caveats associated with using autophagy to control viral infections in humans. Frontiers Media S.A. 2018-11-19 /pmc/articles/PMC6252315/ /pubmed/30510929 http://dx.doi.org/10.3389/fcell.2018.00155 Text en Copyright © 2018 Ahmad, Mostowy and Sancho-Shimizu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Ahmad, Liyana
Mostowy, Serge
Sancho-Shimizu, Vanessa
Autophagy-Virus Interplay: From Cell Biology to Human Disease
title Autophagy-Virus Interplay: From Cell Biology to Human Disease
title_full Autophagy-Virus Interplay: From Cell Biology to Human Disease
title_fullStr Autophagy-Virus Interplay: From Cell Biology to Human Disease
title_full_unstemmed Autophagy-Virus Interplay: From Cell Biology to Human Disease
title_short Autophagy-Virus Interplay: From Cell Biology to Human Disease
title_sort autophagy-virus interplay: from cell biology to human disease
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6252315/
https://www.ncbi.nlm.nih.gov/pubmed/30510929
http://dx.doi.org/10.3389/fcell.2018.00155
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