2. Academic Validation
  3. Autophagy Promotes Infectious Particle Production of Mopeia and Lassa Viruses

Autophagy Promotes Infectious Particle Production of Mopeia and Lassa Viruses

  • Viruses. 2019 Mar 23;11(3):293. doi: 10.3390/v11030293.
Nicolas Baillet 1 2,  Sophie Krieger 3 4,  Alexandra Journeaux 5 6,  Valérie Caro 7,  Frédéric Tangy 8,  Pierre-Olivier Vidalain 9,  Sylvain Baize 10 11
Affiliations

Affiliations

  • 1 Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, 69007 Lyon, France. nicolas.baillet@hotmail.fr.
  • 2 Centre International de Recherche en Infectiologie (INSERM U1111, CNRS UMR5308, ENS Lyon, Université Lyon I), 69007 Lyon, France. nicolas.baillet@hotmail.fr.
  • 3 Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, 69007 Lyon, France. sophieeve@live.fr.
  • 4 Centre International de Recherche en Infectiologie (INSERM U1111, CNRS UMR5308, ENS Lyon, Université Lyon I), 69007 Lyon, France. sophieeve@live.fr.
  • 5 Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, 69007 Lyon, France. alexandra.journeaux@pasteur.fr.
  • 6 Centre International de Recherche en Infectiologie (INSERM U1111, CNRS UMR5308, ENS Lyon, Université Lyon I), 69007 Lyon, France. alexandra.journeaux@pasteur.fr.
  • 7 Unité Environnement et Risques Infectieux, CIBU, Infection et Epidémiologie, Institut Pasteur, 75015 Paris, France. valerie.caro@pasteur.fr.
  • 8 Unité de Génomique Virale et Vaccination, Institut Pasteur, CNRS UMR-3569, 75015 Paris, France. frederic.tangy@pasteur.fr.
  • 9 Unité de Génomique Virale et Vaccination, Institut Pasteur, CNRS UMR-3569, 75015 Paris, France. pierre-olivier.vidalain@parisdescartes.fr.
  • 10 Unité de Biologie des Infections Virales Emergentes, Institut Pasteur, 69007 Lyon, France. sylvain.baize@pasteur.fr.
  • 11 Centre International de Recherche en Infectiologie (INSERM U1111, CNRS UMR5308, ENS Lyon, Université Lyon I), 69007 Lyon, France. sylvain.baize@pasteur.fr.
PMID: 30909570 DOI: 10.3390/v11030293
Abstract

Lassa virus (LASV) and Mopeia virus (MOPV) are two closely related Old-World mammarenaviruses. LASV causes severe hemorrhagic fever with high mortality in humans, whereas no case of MOPV Infection has been reported. Comparing MOPV and LASV is a powerful strategy to unravel pathogenic mechanisms that occur during the course of pathogenic Arenavirus infection. We used a yeast two-hybrid approach to identify cell partners of MOPV and LASV Z matrix protein in which two Autophagy adaptors were identified, NDP52 and TAX1BP1. Autophagy has emerged as an important cellular defense mechanism against viral infections but its role during Arenavirus infection has not been shown. Here, we demonstrate that Autophagy is transiently induced by MOPV, but not LASV, in infected cells two days after Infection. Impairment of the early steps of Autophagy significantly decreased the production of MOPV and LASV infectious particles, whereas a blockade of the degradative steps impaired only MOPV infectious particle production. Our study provides insights into the role played by Autophagy during MOPV and LASV Infection and suggests that this process could partially explain their different pathogenicity.

Keywords

LASV; MOPV; NDP52; TAX1BP1; Z matrix protein; autophagy; replication; yeast two-hybrid screening.

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