Herpes simplex virus and varicella zoster virus, the house guests who never leave

Paul R Kinchington1, Anthony J St Leger, Jean-Marc G Guedon

  • 1Department of Ophthalmology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Hendricksrr@upmc.edu.

Herpesviridae
|June 14, 2012
PubMed

Insights

Human alphaherpesviruses like herpes simplex virus (HSV-1, HSV-2) and varicella zoster virus (VZV) cause lifelong latent infections. This review contrasts HSV-1 and VZV infection patterns, immune responses, and pathogenesis.

Area of Science:

  • Virology
  • Immunology
  • Neuroscience

Background:

  • Human alphaherpesviruses, including herpes simplex viruses (HSV-1, HSV-2) and varicella zoster virus (VZV), establish persistent latent infections in sensory neurons.
  • These viruses can reactivate, leading to recurrent diseases with distinct pathologies despite genetic similarities.
  • Understanding these differences is crucial for managing viral infections and developing targeted therapies.

Purpose of the Study:

  • To review and highlight the key differences in infection patterns between HSV-1 and VZV.
  • To compare the host immune responses elicited by HSV-1 and VZV infections.
  • To elucidate the distinct pathogenetic mechanisms underlying HSV-1 and VZV diseases.

Main Methods:

  • Literature review of existing studies on HSV-1 and VZV.
  • Comparative analysis of viral infection dynamics, latency establishment, and reactivation.
  • Synthesis of data on cellular and humoral immune responses to each virus.
  • Examination of pathobiological mechanisms leading to clinical manifestations.

Main Results:

  • HSV-1 and VZV exhibit differential tropism and latency sites within the nervous system.
  • Distinct immune evasion strategies and inflammatory responses are associated with HSV-1 and VZV.
  • Pathologies arising from HSV-1 and VZV infections vary significantly in clinical presentation and severity.

Conclusions:

  • HSV-1 and VZV, while related, display unique characteristics in their interaction with the host.
  • Differences in infection patterns, immune responses, and pathogenesis necessitate distinct clinical management approaches.
  • Further research into these specific viral attributes can inform the development of novel antiviral strategies.

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