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Human herpesvirus 6 (HHV-6)-associated dysfunction of blood monocytes

E M Burd1, D R Carrigan

  • 1Department of Pathology, Medical College of Wisconsin, Milwaukee 53226.

Virus Research
|July 1, 1993
PubMed

Insights

Human herpesvirus 6 (HHV-6) infection significantly impairs monocyte function, decreasing their respiratory burst capacity. This viral effect on immune cells may contribute to persistent HHV-6 infections in immunocompromised individuals.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Human herpesvirus 6 (HHV-6) is a member of the herpesvirus family.
  • HHV-6 has been linked to marrow failure and interstitial pneumonitis in transplant patients, with macrophages as the primary infected cells.
  • Previous studies indicated HHV-6 suppresses macrophage outgrowth from human marrow.

Purpose of the Study:

  • To investigate the effects of HHV-6 on the function of peripheral blood monocytes.
  • To determine the mechanism by which HHV-6 impacts monocyte activation pathways.

Main Methods:

  • Exposure of normal human marrow and peripheral blood monocytes to HHV-6 strains (Type A and Type B).
  • Assay of monocyte respiratory burst capacity using luminol-enhanced chemiluminescence with phorbol myristate acetate and opsonized zymosan.
  • Cell sorting (fluorescence-activated cell sorter) to isolate monocyte populations.
  • Ultracentrifugation of viral stock to identify the suppressive factor.

Main Results:

  • HHV-6 exposure suppressed growth factor-induced macrophage outgrowth by over 90%.
  • Respiratory burst capacity of peripheral blood monocytes decreased by 83% +/- 13% within 15 minutes of HHV-6 exposure.
  • The suppressive effect was mediated solely by monocytes and did not affect responses to opsonized zymosan, suggesting interference with the protein kinase C pathway.
  • The suppressive factor was found in the supernatant fraction, not associated with infectious virus particles.

Conclusions:

  • HHV-6 infection can induce a defect in a major monocyte activation pathway.
  • This impairment of monocyte function may play a role in persistent HHV-6 infections, particularly in immunocompromised patients.
  • Further research is needed to elucidate the precise mechanisms and clinical implications of HHV-6-induced monocyte dysfunction.

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