First, we determined if primary lung endothelial cells could support growth of wildtype cHV68 by multi-step growth assay (Fig. 8A) . Because of the apparent role for the v-cyclin in infection of endothelial cell lines, we also analyzed growth of v-cyclin.STOP virus in primary endothelial cells. Infection proceeded with kinetics comparable to previously published infection of NIH 3T12 fibroblasts [18] . Growth curves did not differ between wildtype and v-cyclin.STOP virus. These data revealed that primary endothelial cells supported growth of cHV68, irrespective of the vcyclin.