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Role of the Endosomal ESCRT Machinery in HIV-1 Vpu-Induced Down-Regulation of BST2/Tetherin.
Janvier K., Pelchen-matthews A., Jean-Baptiste R., Caillet M., Marsh M., Berlioz-Torrent C.
PLoS Pathogens (2012) epub ahead of print - http://www.hal.inserm.fr/inserm-00693708
(22524180)
Role of the Endosomal ESCRT Machinery in HIV-1 Vpu-Induced Down-Regulation of BST2/Tetherin.
Katy Janvier () 1, Annegret Pelchen-matthews2, Renaud Jean-Baptiste1, Marina Caillet1, Mark Marsh2, Clarisse Berlioz-Torrent () 1, Mark Marsh Collaboration(s)
1 :  Institut Cochin
INSERM : U1016 – CNRS : UMR8104 – Université Paris V - Paris Descartes
22 rue Méchain, 75014 Paris
France
2 :  Cell Biology Unit
MRC Laboratory for Molecular Cell Biology – University College London
London
Royaume-Uni
1-Institut Cochin, Universite' Paris Descartes, CNRS (UMR 8104), Paris, France, 2-INSERM, U1016, Paris, France,
U1016
3 - Cell Biology Unit, MRC Laboratory for Molecular Cell Biology, University College London, London, United Kingdom
HRS and BST-2/Tetherin Down-Regulation
The cellular protein "Bone marrow stromal antigen 2" (BST2 also called Tetherin, CD317, HM1.24) was identified as a major mediator of the innate immune defense against the dissemination of enveloped viruses. BST2 was shown to physically trap the de novo formed viral particles at the surface of infected cells, thereby reducing viral release. Lentiviruses have evolved specific strategies to down-regulate the expression level of BST2 from the surface of the cells and as such promote viral egress. In Human Immunodeficiency Virus-1 (HIV-1), the accessory protein Vpu counters BST2 antiviral activity. However, the cellular and molecular mechanisms involved are not fully understood. Vpu-mediated antagonism of BST2 antiviral activity seems to involve complex interplay between the viral protein and host components regulating protein turnover and vesicular trafficking. This review focuses on the interplay between Vpu and the ubiquitin/endosomal pathway in countermeasures of HIV-1 to BST2 restriction.
Sciences du Vivant/Médecine humaine et pathologie/Maladies infectieuses
Anglais
1873-4251

Articles dans des revues avec comité de lecture
PLoS Pathogens
Publisher Public Library of Science
ISSN 1553-7366 (eISSN : 1553-7374)
internationale
18/04/2012
18/04/2012
epub ahead of print

This work is funded by SIDACTION, ANRS, the ANR-07-JCJC-0102 program, and is part of the activities of the HIV-ACE research network (HEALTH-F3-2008-201095) supported by a grant of the European Commission, within the Priority 1 Health work programme of the 7th Framework Programme of the EU.
Référence du projet ANR-07-JCJC-0102
Année 2007
Acronyme du projet JCJC
Titre du projet Cellular cofactors of the HIV-1 Gag and Env proteins involved in the late steps of the HIV-1 replicative cycle.
Intitulé Jeunes chercheuses & jeunes chercheurs
Acronyme de l'appel JC - CBT
Numéro Cordis 201095
Acronyme HIV ACE
Titre Targeting assembly of infectious HIV particles
Financé par HEALTH
Début 2008-03-01
Date de fin 2011-08-31
Identifiant de l'appel FP7-HEALTH-2007-A
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journal.ppat.1001265.pdf(4 MB)

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