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    Proteomics informed by transcriptomics for characterising differential cellular susceptibility to Nelson Bay orthoreovirus infection

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    Author
    Mok, L; Wynne, JW; Tachedjian, M; Shiell, B; Ford, K; Matthews, DA; Bacic, A; Michalski, WP
    Date
    2017-08-14
    Source Title
    BMC Genomics
    Publisher
    BMC
    University of Melbourne Author/s
    Bacic, Anthony
    Affiliation
    School of BioSciences
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Mok, L., Wynne, J. W., Tachedjian, M., Shiell, B., Ford, K., Matthews, D. A., Bacic, A. & Michalski, W. P. (2017). Proteomics informed by transcriptomics for characterising differential cellular susceptibility to Nelson Bay orthoreovirus infection. BMC GENOMICS, 18 (1), https://doi.org/10.1186/s12864-017-3994-x.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256711
    DOI
    10.1186/s12864-017-3994-x
    Abstract
    BACKGROUND: Nelson Bay orthoreovirus (NBV) is a fusogenic bat borne virus with an unknown zoonotic potential. Previous studies have shown that NBV can infect and replicate in a wide variety of cell types derived from their natural host (bat), as well as from human, mouse and monkey. Within permissive cells, NBV induced significant cytopathic effects characterised by cell-cell fusion and syncytia formation. To understand the molecular events that underpin NBV infection we examined the host transcriptome and proteome response of two cell types, derived from bat (PaKiT03) and mouse (L929), to characterise differential cellular susceptibility to NBV. RESULTS: Despite significant differences in NBV replication and cytopathic effects in the L929 and PaKiT03 cells, the host response was remarkably similar in these cells. At both the transcriptome and proteome level, the host response was dominated by IFN production and signalling pathways. The majority of proteins up-regulated in L929 and PaKiT03 cells were also up-regulated at the mRNA (gene) level, and included many important IFN stimulated genes. Further functional experimentation demonstrated that stimulating IFN signalling prior to infection, significantly reduced NBV replication in PaKiT03 cells. Moreover, inhibiting IFN signalling (through specific siRNAs) increased NBV replication in L929 cells. In line with the significant cytopathic effects seen in PaKiT03 cells, we also observed a down-regulation of genes involved in cell-cell junctions, which may be related to the fusogenic effects of NBV. CONCLUSIONS: This study provides new multi-dimensional insights into the host response of mammalian cells to NBV infection. We show that IFN activity is capable of reducing NBV replication, although it is unlikely that this is solely responsible for the reduced replication of NBV in L929 cells. The molecular events that underpin the fusogenic cytopathic effects described here will prove valuable for identifying potential therapeutic targets against fusogenic orthoreovirus.

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