Endothelial cells serve as a natural site of infection and possible viral reservoir of HCMV [36] [37] [38] [39] [40] , suggesting a role for HCMVinfected endothelial cells in viral spread and persistence. Additionally, recent reports implicate circulating endothelial progenitor cells as potential reservoirs of KSHV and possible precursors of KS spindle cells [41, 42] . However, the specific mechanisms by which infected endothelial cells contribute to the pathogenesis of these human viruses remains unclear. Murine cHV68 pathogenesis involves dissemination from the lung to lymph nodes, spleen, and peritoneum [12, 15] . In light of this systemic spread, cHV68 likely encounters an endothelial cell barrier.