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The Interaction between Nidovirales and Autophagy Components
Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruse...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537674/ https://www.ncbi.nlm.nih.gov/pubmed/28696396 http://dx.doi.org/10.3390/v9070182 |
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author | Cong, Yingying Verlhac, Pauline Reggiori, Fulvio |
author_facet | Cong, Yingying Verlhac, Pauline Reggiori, Fulvio |
author_sort | Cong, Yingying |
collection | PubMed |
description | Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruses, usurp autophagy in order to promote their propagation. Nidovirales are an order of enveloped viruses with large single-stranded positive RNA genomes. Four virus families (Arterividae, Coronaviridae, Mesoniviridae, and Roniviridae) are part of this order, which comprises several human and animal pathogens of medical and veterinary importance. In host cells, Nidovirales induce membrane rearrangements including autophagosome formation. The relevance and putative mechanism of autophagy usurpation, however, remain largely elusive. Here, we review the current knowledge about the possible interplay between Nidovirales and autophagy. |
format | Online Article Text |
id | pubmed-5537674 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-55376742017-08-04 The Interaction between Nidovirales and Autophagy Components Cong, Yingying Verlhac, Pauline Reggiori, Fulvio Viruses Review Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruses, usurp autophagy in order to promote their propagation. Nidovirales are an order of enveloped viruses with large single-stranded positive RNA genomes. Four virus families (Arterividae, Coronaviridae, Mesoniviridae, and Roniviridae) are part of this order, which comprises several human and animal pathogens of medical and veterinary importance. In host cells, Nidovirales induce membrane rearrangements including autophagosome formation. The relevance and putative mechanism of autophagy usurpation, however, remain largely elusive. Here, we review the current knowledge about the possible interplay between Nidovirales and autophagy. MDPI 2017-07-11 /pmc/articles/PMC5537674/ /pubmed/28696396 http://dx.doi.org/10.3390/v9070182 Text en © 2017 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 Cong, Yingying Verlhac, Pauline Reggiori, Fulvio The Interaction between Nidovirales and Autophagy Components |
title | The Interaction between Nidovirales and Autophagy Components |
title_full | The Interaction between Nidovirales and Autophagy Components |
title_fullStr | The Interaction between Nidovirales and Autophagy Components |
title_full_unstemmed | The Interaction between Nidovirales and Autophagy Components |
title_short | The Interaction between Nidovirales and Autophagy Components |
title_sort | interaction between nidovirales and autophagy components |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537674/ https://www.ncbi.nlm.nih.gov/pubmed/28696396 http://dx.doi.org/10.3390/v9070182 |
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