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...

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Autores principales:	Francesca Arnoldi, Giuditta De Lorenzo, Miguel Mano, Elisabeth M Schraner, Peter Wild, Catherine Eichwald, Oscar R Burrone
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/91f5ca427fab47bca2101ed0b9d2cdb2
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spelling	oai:doaj.org-article:91f5ca427fab47bca2101ed0b9d2cdb22021-11-18T08:23:07ZRotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.1932-620310.1371/journal.pone.0095197https://doaj.org/article/91f5ca427fab47bca2101ed0b9d2cdb22014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24736649/?tool=EBIhttps://doaj.org/toc/1932-6203Replication 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.Francesca ArnoldiGiuditta De LorenzoMiguel ManoElisabeth M SchranerPeter WildCatherine EichwaldOscar R BurronePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 4, p e95197 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.
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	article
author	Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone
author_facet	Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone
author_sort	Francesca Arnoldi
title	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_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_sort	rotavirus increases levels of lipidated lc3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/91f5ca427fab47bca2101ed0b9d2cdb2
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Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.

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