Cellular transcriptional profiling in human lung epithelial cells infected by different subtypes of influenza A viruses reveals an overall down-regulation of the host p53 pathway

Olivier Terrier, Laurence Josset, Julien Textoris, Virginie Marcel, Gaelle Cartet, Olivier Ferraris, Catherine N'Guyen, Bruno Lina, Jean-Jacques Diaz, Jean-Christophe Bourdon, Manuel Rosa-Calatrava

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    31 Citations (Scopus)

    Abstract

    Background: Influenza viruses can modulate and hijack several cellular signalling pathways to efficiently support their replication. We recently investigated and compared the cellular gene expression profiles of human lung A549 cells infected by five different subtypes of human and avian influenza viruses (Josset et al. Plos One 2010). Using these transcriptomic data, we have focused our analysis on the modulation of the p53 pathway in response to influenza infection.

    Results: Our results were supported by both RT-qPCR and western blot analyses and reveal multiple alterations of the p53 pathway during infection. A down-regulation of mRNA expression was observed for the main regulators of p53 protein stability during infection by the complete set of viruses tested, and a significant decrease in p53 mRNA expression was also observed in H5N1 infected cells. In addition, several p53 target genes were also down-regulated by these influenza viruses and the expression of their product reduced.

    Conclusions: Our data reveal that influenza viruses cause an overall down-regulation of the host p53 pathway and highlight this pathway and p53 protein itself as important viral targets in the altering of apoptotic processes and in cell-cycle regulation.

    Original languageEnglish
    Article number285
    Number of pages11
    JournalVirology Journal
    Volume8
    DOIs
    Publication statusPublished - 8 Jun 2011

    Keywords

    • SIGNALING PATHWAY
    • VIRAL REPLICATION
    • IMMUNE-RESPONSE
    • CYCLE ARREST
    • APOPTOSIS
    • DEATH
    • GENE
    • ACCUMULATION
    • MECHANISMS
    • INDUCTION

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