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Distinct Contributions of Autophagy Receptors in Measles Virus Replication

by 1,2,3,4,5, 1,2,3,4,5,†, 1,2,3,4,5,†, 1,2,3,4,5, 1,2,3,4,5, 6, 1,2,3,4,5,7, 1,2,3,4,5 and 1,2,3,4,5,8,9,*
CIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France
INSERM, U1111, 69007 Lyon, France
CNRS, UMR5308, 69007 Lyon, France
Ecole Normale Supérieure de Lyon, 69007 Lyon, France
Université Lyon 1, Centre International de Recherche en Infectiologie, Avenue Tony Garnier 69365 Lyon CEDEX 07, France
Institut NeuroMyoGène, CNRS UMR5310, INSERM U1217, Université Lyon 1, F-69622 Villeurbanne, France; Université de Lyon, Lyon France
Equipe labellisée Ligue nationale contre le cancer, France
Equipe labellisée Fondation pour la Recherche Médicale FRM, France
Institut Universitaire de France, France
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Christian Münz
Viruses 2017, 9(5), 123;
Received: 31 January 2017 / Revised: 13 May 2017 / Accepted: 18 May 2017 / Published: 22 May 2017
(This article belongs to the Special Issue Viruses and Autophagy)
Autophagy is a potent cell autonomous defense mechanism that engages the lysosomal pathway to fight intracellular pathogens. Several autophagy receptors can recognize invading pathogens in order to target them towards autophagy for their degradation after the fusion of pathogen-containing autophagosomes with lysosomes. However, numerous intracellular pathogens can avoid or exploit autophagy, among which is measles virus (MeV). This virus induces a complete autophagy flux, which is required to improve viral replication. We therefore asked how measles virus interferes with autophagy receptors during the course of infection. We report that in addition to NDP52/CALCOCO2 and OPTINEURIN/OPTN, another autophagy receptor, namely T6BP/TAXIBP1, also regulates the maturation of autophagosomes by promoting their fusion with lysosomes, independently of any infection. Surprisingly, only two of these receptors, NDP52 and T6BP, impacted measles virus replication, although independently, and possibly through physical interaction with MeV proteins. Thus, our results suggest that a restricted set of autophagosomes is selectively exploited by measles virus to replicate in the course of infection. View Full-Text
Keywords: autophagosome; maturation; measles virus; autophagy receptor autophagosome; maturation; measles virus; autophagy receptor
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MDPI and ACS Style

Petkova, D.S.; Verlhac, P.; Rozières, A.; Baguet, J.; Claviere, M.; Kretz-Remy, C.; Mahieux, R.; Viret, C.; Faure, M. Distinct Contributions of Autophagy Receptors in Measles Virus Replication. Viruses 2017, 9, 123.

AMA Style

Petkova DS, Verlhac P, Rozières A, Baguet J, Claviere M, Kretz-Remy C, Mahieux R, Viret C, Faure M. Distinct Contributions of Autophagy Receptors in Measles Virus Replication. Viruses. 2017; 9(5):123.

Chicago/Turabian Style

Petkova, Denitsa S., Pauline Verlhac, Aurore Rozières, Joël Baguet, Mathieu Claviere, Carole Kretz-Remy, Renaud Mahieux, Christophe Viret, and Mathias Faure. 2017. "Distinct Contributions of Autophagy Receptors in Measles Virus Replication" Viruses 9, no. 5: 123.

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