This conserved outcome of endothelial cell infection is particularly striking given that endothelial cells display phenotypic heterogeneity in structure and function depending on anatomic location [33] [34] [35] . Based on the persistent infection observed in diverse endothelial cell lines, and heightened viability of primary endothelial cells following infection, we propose that cHV68 may have evolved machinery to specifically promote persistent infection in endothelial cells.