The DNA genomes of EBV and KSHV encode an estimated 80 and 86 proteins, respectively. The degree to which these proteins are expressed differs depending on the stage of the viral life cycle. In vivo, the reservoir of EBV latent infection is resting memory B cells that have either no EBV protein expression or transient expression of the EBNA1 protein. Expression of the other latency proteins, EBNA2, EBNA3A, EBNA3B, EBNA3C, EBNA-LP, LMP-1, and LMP2A and LMP2B, has been detected in peripheral blood B cells shortly after primary infection and in B cells in tonsillar tissues [10, 11] . Lytic replication and expression of the EBV lytic proteins takes place in plasma cells and in epithelial cells [12] [13] [14] . Less is known about in vivo persistence of KSHV. B cells form a reservoir for latent KSHV infection, and differentiation of these cells also triggers lytic KSHV induction [15, 16] . KSHV endothelial and B cell tumors express the LANA, v-cyclin, and v-FLIP latency proteins, and vIRF3 is also detected as a latency protein in primary-effusion lymphoma cells. In addition, a small percentage of tumor cells express lytic cycle proteins such as the v-IL6 and the viral G-protein coupled receptor (v-GPCR), suggesting that KSHV lytic infection may contribute to the tumorigenic phenotype [17] .