While cHV68 may have evolved mechanisms that promote persistent infection of endothelial cells (e.g. the v-cyclin), it is also possible that endothelial cells have a cellular program that limits the cellular lysis typically observed during productive infection. This putative cellular adaptation may be particularly important in limiting destruction of blood vessel integrity during viral infection. A recent report of host cell response to cHV68 in three different cell types (fibroblasts, endothelial precursor cells and macrophages) identified 148 genes whose expression was altered in endothelial precursor cells, but not macrophages or fibroblasts [67] . Taken together with the unique endothelial cell outcome of cHV68 infection reported here, these data make a compelling argument for cell type specific responses to productive cHV68 infection.