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.
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.
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.
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