Distinct Contributions of Autophagy Receptors in Measles Virus Replication
by
Denitsa S. Petkova 1,2,3,4,5, Pauline Verlhac 1,2,3,4,5,†, Aurore Rozières 1,2,3,4,5,†, Joël Baguet 1,2,3,4,5, Mathieu Claviere 1,2,3,4,5, Carole Kretz-Remy 6
, Renaud Mahieux 1,2,3,4,5,7, Christophe Viret 1,2,3,4,5 and Mathias Faure 1,2,3,4,5,8,9,*
, Renaud Mahieux 1,2,3,4,5,7, Christophe Viret 1,2,3,4,5 and Mathias Faure 1,2,3,4,5,8,9,*
1
CIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France
2
INSERM, U1111, 69007 Lyon, France
3
CNRS, UMR5308, 69007 Lyon, France
4
Ecole Normale Supérieure de Lyon, 69007 Lyon, France
5
Université Lyon 1, Centre International de Recherche en Infectiologie, Avenue Tony Garnier 69365 Lyon CEDEX 07, France
6
Institut NeuroMyoGène, CNRS UMR5310, INSERM U1217, Université Lyon 1, F-69622 Villeurbanne, France; Université de Lyon, Lyon France
7
Equipe labellisée Ligue nationale contre le cancer, France
8
Equipe labellisée Fondation pour la Recherche Médicale FRM, France
9
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; https://doi.org/10.3390/v9050123
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.
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Keywords:
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.
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