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Autophagy during viral infection — a double-edged sword

Autophagy is a powerful tool that host cells use to defend against viral infection. Double-membrane vesicles, termed autophagosomes, deliver trapped viral cargo to the lysosome for degradation. Specifically, autophagy initiates an innate immune response by cooperating with pattern recognition recept...

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Detalles Bibliográficos
Autores principales: Choi, Younho, Bowman, James W., Jung, Jae U.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6907743/
https://www.ncbi.nlm.nih.gov/pubmed/29556036
http://dx.doi.org/10.1038/s41579-018-0003-6
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author Choi, Younho
Bowman, James W.
Jung, Jae U.
author_facet Choi, Younho
Bowman, James W.
Jung, Jae U.
author_sort Choi, Younho
collection PubMed
description Autophagy is a powerful tool that host cells use to defend against viral infection. Double-membrane vesicles, termed autophagosomes, deliver trapped viral cargo to the lysosome for degradation. Specifically, autophagy initiates an innate immune response by cooperating with pattern recognition receptor signalling to induce interferon production. It also selectively degrades immune components associated with viral particles. Following degradation, autophagy coordinates adaptive immunity by delivering virus-derived antigens for presentation to T lymphocytes. However, in an ongoing evolutionary arms race, viruses have acquired the potent ability to hijack and subvert autophagy for their benefit. In this Review, we focus on the key regulatory steps during viral infection in which autophagy is involved and discuss the specific molecular mechanisms that diverse viruses use to repurpose autophagy for their life cycle and pathogenesis.
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spelling pubmed-69077432019-12-12 Autophagy during viral infection — a double-edged sword Choi, Younho Bowman, James W. Jung, Jae U. Nat Rev Microbiol Review Article Autophagy is a powerful tool that host cells use to defend against viral infection. Double-membrane vesicles, termed autophagosomes, deliver trapped viral cargo to the lysosome for degradation. Specifically, autophagy initiates an innate immune response by cooperating with pattern recognition receptor signalling to induce interferon production. It also selectively degrades immune components associated with viral particles. Following degradation, autophagy coordinates adaptive immunity by delivering virus-derived antigens for presentation to T lymphocytes. However, in an ongoing evolutionary arms race, viruses have acquired the potent ability to hijack and subvert autophagy for their benefit. In this Review, we focus on the key regulatory steps during viral infection in which autophagy is involved and discuss the specific molecular mechanisms that diverse viruses use to repurpose autophagy for their life cycle and pathogenesis. Nature Publishing Group UK 2018-03-19 2018 /pmc/articles/PMC6907743/ /pubmed/29556036 http://dx.doi.org/10.1038/s41579-018-0003-6 Text en © Macmillan Publishers Ltd., part of Springer Nature 2018 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
spellingShingle Review Article
Choi, Younho
Bowman, James W.
Jung, Jae U.
Autophagy during viral infection — a double-edged sword
title Autophagy during viral infection — a double-edged sword
title_full Autophagy during viral infection — a double-edged sword
title_fullStr Autophagy during viral infection — a double-edged sword
title_full_unstemmed Autophagy during viral infection — a double-edged sword
title_short Autophagy during viral infection — a double-edged sword
title_sort autophagy during viral infection — a double-edged sword
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6907743/
https://www.ncbi.nlm.nih.gov/pubmed/29556036
http://dx.doi.org/10.1038/s41579-018-0003-6
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