Molecular Neurobiology

, Volume 7, Issue 2, pp 137–159

Molecular biology of herpes simplex virus type 1 latency in the nervous system

Authors

  • Israel Steiner
    • The Laboratory of Neurovirology, Department of Neurology, Hadassah University HospitalHebrew University-Hadassah Medical School
  • Peter G. E. Kennedy
    • The Department of Neurology, Institute of Neurological SciencesSouthern General Hospital
Article

DOI: 10.1007/BF02935640

Cite this article as:
Steiner, I. & Kennedy, P.G.E. Mol Neurobiol (1993) 7: 137. doi:10.1007/BF02935640

Abstract

Herpes simplex virus (HSV) is one of the best studied examples of viral ability to remain latent in the human nervous system and to cause recurrent disease by reactivation. Intensive effort was directed in recent years to unveil the molecular viral mechanisms and the virus-host interactions associated with latent HSV infection. The discovery of the state of the latent viral DNA in nervous tissues and of the presence of latency-associated gene expression during latent infection, both differing from the situation during viral replication, provided important clues relevant to the pathogenesis of latent HSV infection. This review summarizes the current state of knowledge on the site of latent infection, the molecular phenomena of latency, and the mechanisms of the various stages of latency: acute infection, establishment and maintenance of latency, and reactivation. This information paved the way to recent trials aiming to use herpes viruses as vectors to deliver genes into the nervous system, an issue that is also addressed in this review.

Index Entries

Herpes simplex virusviral pathogenesislatent viral infectionviral reactivationviral pathogenesisnervous systemgene therapyviral vectors
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Copyright information

© Humana Press Inc 1993