Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript

Science. 2000 Feb 25;287(5457):1500-3. doi: 10.1126/science.287.5457.1500.

Abstract

Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT(-) virus but not with LAT(+) viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells. Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.

Publication types

  • Comment
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Line
  • Genes, Viral
  • Herpesvirus 1, Human / genetics
  • Herpesvirus 1, Human / physiology*
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Keratitis, Herpetic / pathology*
  • Keratitis, Herpetic / virology*
  • Mutation
  • Neurons / pathology*
  • Neurons / virology
  • Poly(ADP-ribose) Polymerases / immunology
  • Poly(ADP-ribose) Polymerases / metabolism
  • Rabbits
  • Transcription, Genetic
  • Trigeminal Ganglion / pathology
  • Trigeminal Ganglion / virology
  • Virus Activation
  • Virus Latency / genetics*

Substances

  • Poly(ADP-ribose) Polymerases