Depletion of CoREST does not improve the replication of ICP0 null mutant herpes simplex virus type 1.
It has been proposed that the cellular corepressor protein CoREST is involved in repressing herpes simplex virus type 1 (HSV-1) infection in the absence of the viral regulatory protein ICP0. This proposal predicts that depletion of CoREST should improve the plaque-forming efficiency and replication of ICP0 null mutant virus. To test this hypothesis, human HepaRG cells that were highly depleted of CoREST were isolated using RNA interference technology. Depletion of CoREST had no effect on the replication of ICP0 null mutant HSV-1, demonstrating that CoREST does not play an influential role in regulating HSV-1 infection in this cell type.
Everett
Roger D
RD
MRC Virology Unit, Institute of Virology, Church Street, Glasgow G11 5JR, Scotland, United Kingdom. r.everett@mrcvu.gla.ac.uk
D000818:Animals; D056970:Co-Repressor Proteins; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000502:physiology*; D006801:Humans; D017874:Immediate-Early Proteins / Q000502:physiology*; D009154:Mutation; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D034622:RNA Interference; D012097:Repressor Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D044767:Ubiquitin-Protein Ligases / Q000502:physiology*; D014779:Virus Replication
D056970:Co-Repressor Proteins; D017874:Immediate-Early Proteins; D009419:Nerve Tissue Proteins; C121019:RCOR1 protein, human; D012097:Repressor Proteins; D044767:Ubiquitin-Protein Ligases; C051804:Vmw110 protein, Human herpesvirus 1