Journal of NeuroVirology

, Volume 9, Issue 2, pp 194–204

Herpes simplex virus-1 and varicella-zoster virus latency in ganglia


  • Bradley M. Mitchell
    • Cullen Eye Institute, Department of Ophthalmology and Department of Molecular Virology and MicrobiologyBaylor College of Medicine
  • David C. Bloom
    • Molecular Genetics and Microbiology, College of MedicineUniversity of Florida
    • Department of NeurologyUniversity of Colorado Health Sciences Center
  • Donald H. Gilden
    • Department of NeurologyUniversity of Colorado Health Sciences Center
    • Department of MicrobiologyUniversity of Colorado Health Sciences Center
  • Peter G. E. Kennedy
    • Department of NeurologyUniversity of Glasgow, Institute of Neurological Sciences, Southern General Hospital NHS Trust

DOI: 10.1080/13550280390194000

Cite this article as:
Mitchell, B.M., Bloom, D.C., Cohrs, R.J. et al. Journal of NeuroVirology (2003) 9: 194. doi:10.1080/13550280390194000


Two human alpha-herpesviruses, herpes simplex virus (HSV)-1 and varicella zoster virus (VZV), account for the most frequent and serious neurologic disease caused by any of the eight human herpesviruses. Both HSV-1 and VZV become latent in ganglia. In this review, the authors describe features of latency for these viruses, such as distribution, prevalence, abundance, and configuration of viral DNA in latently infected human ganglia, as well as transcription, translation, and cell type infected. Studies of viral latency in animal models are also discussed. For each virus, remaining questions and future studies to understand the mechanism of latency are discussed with respect to prevention of serious cutaneous, ocular, and neurologic disease produced by virus reactivation.


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© Journal of NeuroVirology, Inc. 2003