Mutagenesis of the herpesvirus saimiri terminal repeat region reveals important elements for virus production

J Virol. 2007 Jun;81(12):6765-70. doi: 10.1128/JVI.02579-06. Epub 2007 Apr 11.

Abstract

Deletion of the terminal repeats (TR) from herpesvirus saimiri (HVS) renders it unable to produce infectious virus or generate plaques. However, a TR-deleted HVS bacterial artificial chromosome can form replication compartments. Complementation of this mutant shows that one copy of the TR, plus the right junction of the genome with the TR, is sufficient for efficient plaque formation and generation of infectious virus. Within the TR unit, the region around the cleavage site of the genome appears both necessary and sufficient for virus production. Analysis of episomes from productive cells indicates a propensity to amplify TR numbers during the lytic cycle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aotidae
  • Base Sequence
  • Cell Line
  • Chromosomes, Artificial, Bacterial
  • Gene Deletion
  • Genetic Complementation Test
  • Genome, Viral
  • Herpesvirus 2, Saimiriine / genetics*
  • Molecular Sequence Data
  • Mutagenesis*
  • Plasmids / metabolism
  • Recombinant Proteins / chemistry
  • Terminal Repeat Sequences*
  • Virus Replication*

Substances

  • Recombinant Proteins