Globally, the array analyses revealed a stark contrast between antibody responses to EBV and KSHV in the same patients. Multiple EBV proteins were consistently recognized by plasma IgG at the dilutions examined, whereas only the LANA (ORF73), ORF38, and K8.1 proteins of KSHV were detected with any consistency, even in patients with KS. This difference carried over to serum IgA responses where 2 latency EBV proteins and 5 lytic proteins were detected by the majority of the sera, while the only KSHV antigen detected by IgA was LANA, and that was seen only rarely. These observed differences may reflect the biology of in vivo persistence. Both viruses latently infect B cells, and both viruses are secreted into saliva [42, 43] . However, EBV can be routinely detected in circulating latently infected B cells of healthy seropositive individuals, whereas detection of KSHV in blood is rare [44] [45] [46] . The preferential ability to detect serum IgA responses against EBV vs KSHV on the protein arrays may also be related to in vivo infection of mucosal epithelial cells by EBV because the most frequently observed antigens were latency proteins or lytic replicative proteins known to be expressed in epithelial cells [47] [48] [49] [50] . KSHV infects endothelial cells as well as B cells, but the contribution of endothelial cells to in vivo viral persistence is not well understood.