One of the most noticeable alterations of the persistently infected endothelial cells described here is the extent of change in their cellular morphology and properties. Though we did not test the oncogenic potential of these cells, endothelial cells achieved anchorage-independent growth, a property frequently associated with oncogenic transformation. These cells also underwent significant changes in protein expression on the cell surface, with down-regulation of the cellular adhesion proteins ICAM-1 (CD54) and VCAM-1 (CD106). While there was decreased expression of ICAM-1 and VCAM-1, changes in cell surface expression were not global, since Thy1 expression remained positive on these cells (Fig. 6B) . It is worth noting that infection of endothelial cells with KSHV results in down-regulation of MHC class I, PE-CAM (CD31), and ICAM-1 (CD54), but not LFA-3 (CD58) or Fas (CD95), and the viral genes K3 and K5 have been demonstrated to regulate this outcome [61] [62] [63] [64] [65] [66] . The contribution of the mK3 gene of cHV68 to persistent endothelial cell infection remains untested. Down-regulation of certain surface markers but not others during viral infection indicates a specific phenomenon, rather than global down-regulation, and provides further evidence that an active process was responsible for the observed endothelial cell outcome of cHV68 infection.