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Herpes simplex virus interferes with monocyte accessory cell function

A R Hayward1, G S Read, M Cosyns

  • 1Department of Pediatrics, University of Colorado School of Medicine, Denver 80262.

Journal of Immunology (Baltimore, Md. : 1950)
|January 1, 1993
PubMed
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Herpes Simplex Virus (HSV) can impair immune cells. HSV infection reduces monocytes' ability to stimulate T cells, crucial for immune responses in newborns and immunocompromised adults.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Herpes Simplex Virus (HSV) is a significant human pathogen, particularly dangerous for immunocompromised adults and neonates.
  • Understanding how HSV evades host immune responses is critical for developing effective treatments.

Purpose of the Study:

  • To investigate the in vitro effect of HSV on the function of human monocytes, specifically their ability to stimulate T cells.
  • To determine the mechanisms by which HSV interferes with immune cell accessory functions.

Main Methods:

  • Human neonatal monocytes were cultured with HSV.
  • Monocyte-derived accessory cell function was assessed by measuring T cell proliferation in response to staphylococcal enterotoxin B.
  • Production of cytokines IL-1 alpha and TNF-beta was measured after stimulation.

Related Experiment Videos

  • HSV mutants and inactivation methods were used to identify viral components involved.

    • Main Results:

    • Overnight culture with HSV rendered monocytes unable to present staphylococcal enterotoxin B and stimulate T cell proliferation.
    • This interference required live HSV and was restored by Interleukin-2 (IL-2).
    • HSV-infected monocytes showed reduced production of IL-1 alpha and TNF-beta.
    • Both wild-type HSV and a mutant lacking the virion host shutoff protein impaired IL-1 synthesis and T cell stimulation.

    Conclusions:

    • HSV interferes with the ability of human monocytes to provide essential costimulatory factors for T cell activation.
    • This immune evasion mechanism may involve secondary shutoff pathways that reduce host protein synthesis or secretion following HSV infection.