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    Signalome-wide assessment of host cell response to hepatitis C virus

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    Author
    Haqshenas, G; Wu, J; Simpson, KJ; Daly, RJ; Netter, HJ; Baumert, TF; Doerig, C
    Date
    2017-05-08
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Simpson, Kaylene
    Affiliation
    Clinical Pathology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Haqshenas, G., Wu, J., Simpson, K. J., Daly, R. J., Netter, H. J., Baumert, T. F. & Doerig, C. (2017). Signalome-wide assessment of host cell response to hepatitis C virus. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/ncomms15158.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259344
    DOI
    10.1038/ncomms15158
    Abstract
    Host cell signalling during infection with intracellular pathogens remains poorly understood. Here we report on the use of antibody microarray technology to detect variations in the expression levels and phosphorylation status of host cell signalling proteins during hepatitis C virus (HCV) replication. Following transfection with HCV RNA, the JNK and NF-κB pathways are suppressed, while the JAK/STAT5 pathway is activated; furthermore, components of the apoptosis and cell cycle control machineries are affected in the expression and/or phosphorylation status. RNAi-based hit validation identifies components of the JAK/STAT, NF-κB, MAPK and calcium-induced pathways as modulators of HCV replication. Selective chemical inhibition of one of the identified targets, the JNK activator kinase MAP4K2, does impair HCV replication. Thus this study provides a comprehensive picture of host cell pathway mobilization by HCV and uncovers potential therapeutic targets. The strategy of identifying targets for anti-infective intervention within the host cell signalome can be applied to any intracellular pathogen.

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