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Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation
Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral protein...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988245/ https://www.ncbi.nlm.nih.gov/pubmed/24736649 http://dx.doi.org/10.1371/journal.pone.0095197 |
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author | Arnoldi, Francesca De Lorenzo, Giuditta Mano, Miguel Schraner, Elisabeth M. Wild, Peter Eichwald, Catherine Burrone, Oscar R. |
author_facet | Arnoldi, Francesca De Lorenzo, Giuditta Mano, Miguel Schraner, Elisabeth M. Wild, Peter Eichwald, Catherine Burrone, Oscar R. |
author_sort | Arnoldi, Francesca |
collection | PubMed |
description | Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle. |
format | Online Article Text |
id | pubmed-3988245 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-39882452014-04-21 Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation Arnoldi, Francesca De Lorenzo, Giuditta Mano, Miguel Schraner, Elisabeth M. Wild, Peter Eichwald, Catherine Burrone, Oscar R. PLoS One Research Article Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle. Public Library of Science 2014-04-15 /pmc/articles/PMC3988245/ /pubmed/24736649 http://dx.doi.org/10.1371/journal.pone.0095197 Text en © 2014 Arnoldi et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Arnoldi, Francesca De Lorenzo, Giuditta Mano, Miguel Schraner, Elisabeth M. Wild, Peter Eichwald, Catherine Burrone, Oscar R. Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title | Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title_full | Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title_fullStr | Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title_full_unstemmed | Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title_short | Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation |
title_sort | rotavirus increases levels of lipidated lc3 supporting accumulation of infectious progeny virus without inducing autophagosome formation |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988245/ https://www.ncbi.nlm.nih.gov/pubmed/24736649 http://dx.doi.org/10.1371/journal.pone.0095197 |
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