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Effect of cytokines on Japanese encephalitis virus production by human monocytes

H Hasegawa1, Y Satake, Y Kobayashi

  • 1First Department of Internal Medicine, School of Medicine, Ehime University.

Insights

Japanese encephalitis (JE) virus replicates in human monocytes. Interferon-alpha and Interferon-gamma inhibited virus production, while antibodies enhanced it, with complex cytokine interactions observed.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human monocytes are susceptible to Japanese encephalitis (JE) virus infection.
  • Cytokines play a crucial role in modulating host immune responses to viral infections.
  • The interaction between JE virus, monocytes, and cytokines is not fully understood.

Purpose of the Study:

  • To investigate the effect of various cytokines on JE virus replication in human monocytes.
  • To determine the role of anti-JE virus antibodies in modulating JE virus production by monocytes.
  • To elucidate the combined effects of cytokines and antibodies on JE virus production.

Main Methods:

  • In vitro culture of human monocytes infected with JE virus.
  • Treatment of infected monocytes with specific cytokines (IFN-alpha, IFN-gamma, IL-1 alpha, IL-2, IL-3, GM-CSF, G-CSF, TNF-alpha) and anti-JE virus antibody.
  • Quantification of JE virus production in treated and untreated monocyte cultures.

Main Results:

  • Interferon-alpha and Interferon-gamma inhibited JE virus production in monocytes without antibody.
  • Anti-JE virus antibody increased JE virus production, likely via Fc receptor-mediated uptake.
  • Interferon-gamma and GM-CSF enhanced virus production in the presence of antibody, while Interferon-alpha inhibited it.

Conclusions:

  • Human monocytes support JE virus replication.
  • Interferons exhibit antiviral activity against JE virus in monocytes, while antibodies can enhance viral production.
  • Specific cytokines differentially modulate JE virus production in monocytes, depending on the presence or absence of antibodies, highlighting complex immune regulatory mechanisms.

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