While our initial analysis focused on the role of the v-cyclin, it is very likely that additional viral genes facilitate persistent endothelial cell infection. Lead candidates include the anti-apoptotic viral bcl-2 gene M11 and the viral GPCR (ORF 74), whose homologs in KSHV have been implicated in endothelial cell survival and transformation [56] [57] [58] [59] . Additional candidates for optimal endothelial cell infection are the ribonucleotide reductase homologs, ORF 60 and 61 of cHV68. Although the role of these genes in cHV68 infection of endothelial cells is currently untested, the MCMV ribonucleotide reductase homolog is required for in vivo replication and pathogenesis of this endothelial cell-tropic virus [60] .