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Related Experiment Videos

Varicella virus-mononuclear cell interaction.

Tiffany M White1, Donald H Gilden

  • 1Departments of Neurology and Microbiology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.

Advances in Virus Research
|January 15, 2004
PubMed
Summary

Varicella zoster virus (VZV) infects mononuclear cells (MNCs) during various disease stages. This review examines VZV and simian varicella virus (SVV) interactions with MNCs in human and primate infections.

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Area of Science:

  • Virology
  • Immunology
  • Neurology

Background:

  • Varicella zoster virus (VZV) causes chickenpox, establishes latency, and can reactivate, leading to shingles (zoster) and postherpetic neuralgia (PHN).
  • VZV can also cause chronic pain without a rash (zoster sine herpete), and viremia (virus in blood) is observed across these conditions.
  • Simian varicella virus (SVV) in primates serves as a model, exhibiting similar virologic and pathogenic features to VZV in humans.

Purpose of the Study:

  • To review the literature on Varicella zoster virus (VZV) infection of peripheral blood mononuclear cells (MNCs) in humans during varicella, PHN, and zoster sine herpete.
  • To explore the role of VZV DNA, RNA, and protein detection in diagnosing VZV-associated neurological diseases.
  • To review the interaction of SVV with MNCs in primates, comparing it to VZV in humans.

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Main Methods:

  • Literature review of studies on VZV infection of human MNCs.
  • Analysis of studies involving experimental VZV infection of human MNCs in vitro.
  • Review of literature on SVV-MNC interactions in naturally occurring and experimentally induced simian varicella.

Main Results:

  • VZV DNA is detected in MNCs during varicella, zoster, PHN, and zoster sine herpete, indicating viremia's role.
  • VZV infection of MNCs can be productive in vitro, with specific subpopulations identified as targets.
  • SVV infection of primate MNCs mirrors VZV findings, with viral DNA detectable during acute infection and persisting post-infection.

Conclusions:

  • VZV infection of MNCs is a significant aspect of VZV pathogenesis and diagnosis across various clinical presentations.
  • PHN may be linked to chronic VZV ganglionitis, supported by VZV detection in MNCs.
  • SVV serves as a valuable model for understanding VZV-MNC interactions and the role of viremia in pathogenesis.