AI Article Synopsis

  • DI particle RNA replication in HEK293 cells that express VSV proteins triggers a strong activation of the interferon signaling pathways.
  • The upregulation of IFN-beta promoter, ISRE promoter, and NF-kappaB promoter activities is essential for this activation.
  • These stably modified cells provide a valuable model for studying viral replication and the immune response in host cells.

Article Abstract

We show here that replication of defective interfering (DI) particle RNA in HEK293 cells stably expressing vesicular stomatitis virus (VSV) replication proteins potently activates interferon (IFN) and IFN signaling pathways through upregulation of IFN-beta promoter, IFN-stimulated response element (ISRE) promoter, and NF-kappaB promoter activities. Replication of DI particle RNA, not mere expression of the viral replication proteins, was found to be critical for induction of IFN and IFN signaling. The stable cells supporting replication of DI RNA described in this report will be useful in further examining the innate immune signaling pathways and the host cell functions in viral genome replication.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2863789PMC
http://dx.doi.org/10.1128/JVI.02701-09DOI Listing

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