Transcriptional activation is not responsible for increased levels of autonomously expressed simian virus 40 T-antigen in herpes simplex virus-infected cells.

Herpes simplex virus type 1 (HSV-1) superinfection of CV-1 cells weakly transactivated a plasmid-borne metallothionein 1 (MT-1) promoter, but activated the expression of a marker gene controlled by an authentic HSV-1 promoter to a high level. In contrast, CMT-3 cells, which are CV-1 cells stably transformed with the simian virus 40 (SV40) large T-antigen (T-Ag) gene controlled by the MT-1 promoter, contained high levels of T-Ag following HSV-1 superinfection, but only if cells were preincubated in the presence of heavy-metal ions. This T-Ag was functional in that it could mediate the increase in copy number of a marker plasmid containing the SV40 origin of DNA replication. Pulse and continuous labeling of preinduced CMT-3 cells showed that T-Ag expression was not induced by HSV-1; but rather, HSV-1 superinfection resulted in the stabilization of pre-existing protein.