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J Gen Virol. 2018 Apr;99(4):489-500. doi: 10.1099/jgv.0.001040. Epub 2018 Mar 5.

Role of p53/NF-κB functional balance in respiratory syncytial virus-induced inflammation response.

Author information

1
1​Laboratoire des Pathogènes Emergents, Fondation Mérieux, Centre International de Recherche en Infectiologie (CIRI), INSERM U1111, CNRS UMR5308, ENS Lyon, Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France.
2
2​Virologie et Pathologie Humaine - VirPath team, Centre International de Recherche en Infectiologie (CIRI), INSERM U1111, CNRS UMR5308, ENS Lyon, Université Claude Bernard Lyon 1, Université de Lyon, Lyon, France.
3
3​Hospices Civils de Lyon, Centre National de Référence des Virus Influenza France Sud, Laboratoire de Virologie, Groupement Hospitalier Nord, Lyon, France.
4
†​Present address: Center of Excellence for Tropical Infectious Diseases, Medical Diagnostic Discovery Department (MD3) bioMérieux, Brazil.

Abstract

The interplay between respiratory syncytial virus (RSV) and the p53 pathway has only been reported in a limited number of studies, yet the underlying abrogation mechanisms of p53 activity during the time course of infection, possibly involving viral proteins, remained unclear. Here, we demonstrate that RSV infection impairs global p53 transcriptional activity, notably via its proteasome-dependent degradation at late stages of infection. We also demonstrate that NS1 and NS2 contribute to the abrogation of p53 activity, and used different experimental strategies (e.g. siRNA, small molecules) to underline the antiviral contribution of p53 in the context of RSV infection. Notably, our study highlights a strong RSV-induced disequilibrium of the p53/NF-κB functional balance, which appears to contribute to the up-regulation of the expression of several proinflammatory cytokines and chemokines.

KEYWORDS:

NF-kB; RSV; inflammation and immune response; p53; virus/host interactions

PMID:
29504924
DOI:
10.1099/jgv.0.001040
[Indexed for MEDLINE]

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