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[Herpesvirus latency].

N Langeland1

  • 1Biokjemisk institutt/Senter for virologisk forskning, Universitetet i Bergen.

Tidsskrift for Den Norske Laegeforening : Tidsskrift for Praktisk Medicin, Ny Raekke
|September 10, 1990
PubMed
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This review explores molecular mechanisms of herpes virus latency, focusing on herpes simplex virus and varicella-zoster virus. It highlights key RNA transcripts and sensory ganglia as sites of latent infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Context:

  • Herpesviruses establish lifelong infections by entering a latent state.
  • Understanding viral latency is crucial for developing effective antiviral therapies.
  • Herpes simplex virus (HSV) latency research provides a model for general viral latency.

Purpose:

  • To review current knowledge on the molecular mechanisms underlying herpesvirus latency.
  • To consolidate findings on latency-associated transcripts and proteins across different herpesviruses.
  • To identify knowledge gaps, particularly concerning cytomegalovirus (CMV) latency.

Summary:

  • Herpes simplex virus (HSV) latency involves residence in sensory ganglia, characterized by a specific RNA transcript but no identified HSV-specific proteins.

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  • Varicella-zoster virus (VZV) latency also occurs in sensory ganglia and is associated with multiple latency-associated transcripts.
  • Epstein-Barr virus (EBV) latency is debated, with emerging evidence for latency-associated proteins; cytomegalovirus (CMV) latency remains poorly understood.
  • Impact:

    • Provides a foundational understanding of herpesvirus latency mechanisms.
    • Informs future research directions for investigating viral persistence and reactivation.
    • Highlights the need for further studies on less understood herpesviruses like CMV.