Depletion of TAX1BP1 Amplifies Innate Immune Responses during Respiratory Syncytial Virus Infection.


Journal

Journal of virology
ISSN: 1098-5514
Titre abrégé: J Virol
Pays: United States
ID NLM: 0113724

Informations de publication

Date de publication:
27 10 2021
Historique:
pubmed: 26 8 2021
medline: 25 12 2021
entrez: 25 8 2021
Statut: ppublish

Résumé

Respiratory syncytial virus (RSV) is the main cause of acute respiratory infections in young children and also has a major impact on the elderly and immunocompromised people. In the absence of a vaccine or efficient treatment, a better understanding of RSV interactions with the host antiviral response during infection is needed. Previous studies revealed that cytoplasmic inclusion bodies (IBs), where viral replication and transcription occur, could play a major role in the control of innate immunity during infection by recruiting cellular proteins involved in the host antiviral response. We recently showed that the morphogenesis of IBs relies on a liquid-liquid-phase separation mechanism depending on the interaction between viral nucleoprotein (N) and phosphoprotein (P). These scaffold proteins are expected to play a central role in the recruitment of cellular proteins to IBs. Here, we performed a yeast two-hybrid screen using RSV N protein as bait and identified the cellular protein TAX1BP1 as a potential partner of this viral protein. This interaction was validated by pulldown and immunoprecipitation assays. We showed that TAX1BP1 suppression has only a limited impact on RSV infection in cell cultures. However, RSV replication is decreased in TAX1BP1-deficient (TAX1BP1 knockout [TAX1BP1

Identifiants

pubmed: 34431698
doi: 10.1128/JVI.00912-21
pmc: PMC8549506
doi:

Substances chimiques

Intracellular Signaling Peptides and Proteins 0
Neoplasm Proteins 0
Nucleocapsid Proteins 0
TAX1BP1 protein, human 0
TAX1BP1 protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0091221

Subventions

Organisme : Agence Nationale de la Recherche (ANR)
ID : ANR-13-IVS3-0007
Organisme : Governo Brasil (Brazilian Government)
ID : RESPISYNCELL 2013/50299-2

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Auteurs

Delphyne Descamps (D)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Andressa Peres de Oliveira (A)

Departamento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.

Lorène Gonnin (L)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Sarah Madrières (S)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Jenna Fix (J)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Carole Drajac (C)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Quentin Marquant (Q)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Edwige Bouguyon (E)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Vincent Pietralunga (V)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Hidekatsu Iha (H)

Department of Infectious Diseases, Faculty of Medicine, Oita University Idaiga-oka, Hasama Yufu, Japan.

Armando Morais Ventura (A)

Departamento de Microbiologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, Brazil.

Frédéric Tangy (F)

Unité de Génomique Virale et Vaccination, Institut Pasteurgrid.428999.7, CNRS UMR-3569, Paris, France.

Pierre-Olivier Vidalain (PO)

Unité de Génomique Virale et Vaccination, Institut Pasteurgrid.428999.7, CNRS UMR-3569, Paris, France.
CIRI, Centre International de Recherche en Infectiologie, Université Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS de Lyon, Lyon, France.

Jean-François Eléouët (JF)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

Marie Galloux (M)

Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France.

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