To determine the role of the v-cyclin in endothelial cell infection, we infected MB114 cells with either wildtype cHV68 or a v-cyclin deficient cHV68 (v-cyclin.STOP cHV68) [18] . Cells were harvested at six days post-infection and cultured as described previously. As per previously published reports in fibroblasts, we determined that the v-cyclin was dispensable for cHV68 growth in endothelial cell lines by multi-step growth assays (data not shown Because viability of MB114 cells after infection was impaired in the absence of the v-cyclin, we next determined the effect of this viral gene on persistent viral replication in viable endothelial cells. Cell free supernatants from infected MB114 cells were titered by plaque assay (Fig. 7C) . Infections with both wildtype and vcyclin.STOP virus resulted in persistent viral production up to 30 days post-infection. Total viral titers from v-cyclin.STOP infections were significantly less than wildtype infections at 12 and 24 days, however, an equivalent amount of virus was produced per cell as in wildtype cHV68 infections. Cell surface protein expression of ICAM-1, VCAM-1, and Thy1 was the same following infection with either wildtype or v-cyclin.STOP virus ( Fig. 6B and Fig. S3B ), thus the v-cyclin was not required for the surface phenotype of infected endothelial cells and the surface phenotype of infected endothelial cells did not predict survival. Therefore, upon infection, the primary function of the v-cyclin was to promote the viability of endothelial cells.