Mutagenesis of the herpesvirus saimiri terminal repeat region reveals important elements for virus production.
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.
White
Robert E
RE
Department of Virology, Faculty of Medicine, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom. robert.e.white@imperial.ac.uk
Carline
Lindsay
L
Allday
Martin J
MJ
D000818:Animals; D016645:Aotidae; D001483:Base Sequence; D002460:Cell Line; D022202:Chromosomes, Artificial, Bacterial; D017353:Gene Deletion; D005816:Genetic Complementation Test; D016679:Genome, Viral; D006567:Herpesvirus 2, Saimiriine / Q000235:genetics*; D008969:Molecular Sequence Data; D016296:Mutagenesis; D010957:Plasmids / Q000378:metabolism; D011994:Recombinant Proteins / Q000737:chemistry; D020079:Terminal Repeat Sequences; D014779:Virus Replication
D011994:Recombinant Proteins