Investigation of IFN Type-I Receptor and IFN Regulatory Factor Expression Relating to Induction of 2', 5'-Oligoadenylate Synthetase in Cells Persistently Infected with the Mumps Virus

  • FUJII Nobuhiro
    Department of Microbiology, Sapporo Medical University School of Medicine
  • YOKOSAWA Noriko
    Department of Microbiology, Sapporo Medical University School of Medicine
  • ISHIDA Setsuko
    Cancer Research Institute, Sapporo Medical University School of Medicine
  • SHIRAKAWA Sachiko
    Department of Microbiology, Sapporo Medical University School of Medicine
  • KUBOTA Toru
    Department of Microbiology, Sapporo Medical University School of Medicine
  • INDOH Tomokazu
    Department of Microbiology, Sapporo Medical University School of Medicine
  • FUJINAGA Kei
    Cancer Research Institute, Sapporo Medical University School of Medicine
  • YASHIKI Teruo
    Laboratory of Technology, College of Medical Technology, Hokkaido University

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Abstract

Poor induction of interferon-induced 2', 5'-oligoadenylate synthetase (2-5AS) activity has been demonstrated in cells persistently infected with the mumps virus or human T-lymphotropic virus type-I (HTLV-I). The suppression of 2-5AS induction is the result of the repression of 2-5AS gene expression at the transcription level. In a general way, after the binding of interferon-α (IFN-α) to cell surface-specific receptors, expression of 2-5AS gene is thought to be regulated by some transacting factors, IFN-regulatory factors (IRF-1 and IRF-2) and the IFN-stimulated gene factor (ISGF-3, a complex consisting of STAT 1α, STAT-2 and p48). To clarify the cause of the suppression mechanism(s), fluctuation in the number of IFN receptors and the levels of mRNAs in both IRF-1 and IRF-2 were examined in cells persistently infected with the mumps virus (FLMT and KBMT). There were few defferences in the number of IFN receptors and the level of IRF-2 mRNA between persistently infected cells and uninfected control cells. After the treatment of cells with INF, a slight reduction of IRF-1 mRNA was found in persistently infected cells as compared with that of the uninfected control cells.

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