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Recent Issues in Varicella-Zoster Virus Latency.

Peter G E Kennedy1, Trine H Mogensen2,3, Randall J Cohrs4

  • 1Institute of Neuroscience and Psychology, University of Glasgow, Glasgow G61 1QH, UK.

Viruses
|October 26, 2021
PubMed
Summary

Varicella-zoster virus (VZV) latency involves restricted gene transcription, including VZV gene 63 and a novel VLT transcript. Epigenetic regulation and host immunity influence VZV reactivation syndromes.

Keywords:
epigeneticsgene expressionimmunitylatencyneuronreactivationvaricella-zostervirus

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Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Varicella-zoster virus (VZV) causes chickenpox and shingles after latency in neurons.
  • Understanding VZV latency is crucial for managing reactivation syndromes.

Purpose of the Study:

  • To review recent advances in alphaherpesvirus latency, focusing on VZV ganglionic latency.
  • To explore viral gene transcription, epigenetic regulation, and immunological aspects of VZV latency.

Main Methods:

  • Review of recent literature on VZV latency.
  • Analysis of viral gene transcription during latency.
  • Investigation of epigenetic mechanisms regulating VZV gene expression.
  • Examination of host immunity's role in VZV reactivation.

Main Results:

  • VZV gene transcription during latency is highly restricted.
  • Key transcripts include VZV gene 63 and a novel VZV transcript (VLT).
  • Epigenetic regulation plays a significant role in VZV gene transcription.
  • Inborn errors in host immunity can predispose individuals to VZV reactivation.

Conclusions:

  • Recent research has clarified the restricted nature of VZV gene transcription during latency.
  • Epigenetic mechanisms and host immunity are critical factors in VZV latency and reactivation.
  • Further research into these areas will advance understanding and management of VZV-associated diseases.