We demonstrated that cHV68 infection of endothelial cells resulted in a population of intact cells which persisted in culture as non-adherent cells and continued to produce new virus. Our analysis of endothelial cell infection in the presence of PAA indicated that this outcome is influenced by viral DNA replication and/or late gene synthesis ( Fig. 2B and Fig. 4A ). To begin dissecting the mechanism of persistent cHV68 in endothelial cells infected in vitro, we tested the role of the cHV68 viral cyclin (v-cyclin) in this system. We measured expression of the cHV68 vcyclin in infected MB114 endothelial cells and infected fibroblasts by RT-PCR and western analysis. Notably, the cHV68 v-cyclin gene transcript and protein were detectable in infected endothelial cells and fibroblasts ( Fig. 7A and Fig. S3A) .