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Augmentation of interferon production after cell-differentiation of U937 cells by TPA

T Indoh1, S Shirakawa, T Kubota

  • 1Department of Microbiology, Sapporo Medical University School of Medicine, Hokkaido, Japan.

Insights

Mumps virus establishes persistent infections in human lymphoid and monocyte cells. Interferon (IFN) and TPA treatments minimally induced 2

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Persistent mumps virus infections were established in human T-cell lymphoid (Molt-4, TALL-1, CCRF-CEM) and monocyte (U937, THP-1) cell lines.
  • 2',5'-Oligoadenylate synthetase (2-5AS) activity, a key component of the interferon-stimulated antiviral response, showed limited induction by interferon (IFN) or TPA in these persistently infected cells.

Purpose of the Study:

  • To investigate the impact of persistent mumps virus infection on the induction of 2',5'-Oligoadenylate synthetase (2-5AS) activity and interferon (IFN) production.
  • To explore the role of cell differentiation in modulating the IFN response in mumps virus-infected monocyte cells.

Main Methods:

  • Establishing persistent mumps virus infections in human lymphoid and monocyte cell lines.
  • Treating infected cells with interferon (IFN) and TPA (12-O-tetradecanoyl-phorbol-13-acetate).
  • Measuring 2-5AS activity, synthetase mRNA levels, and IFN production.

Main Results:

  • Persistent mumps virus infection in lymphoid and monocyte cells resulted in only slight induction of 2-5AS activity by IFN or TPA.
  • IFN or TPA treatment did not increase synthetase mRNA levels in persistently infected cells.
  • TPA induced cell differentiation and augmented IFN production in U937 cells persistently infected with mumps virus (U937-MP), with similar IFN production observed in differentiated U937 cells.

Conclusions:

  • Persistent mumps virus infection may impair the induction of the 2-5AS pathway by IFN and TPA.
  • Cell differentiation in U937 cells appears to be associated with the restoration or development of IFN inducibility, suggesting a potential mechanism for antiviral defense.
  • These findings highlight complex interactions between persistent viral infections, cellular differentiation, and innate immune responses.

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