HHV-8 infection induced the expression of ICAM-1 in HMECs but not in HMEC-AS and enhanced leukocytes adhesion that correlated with the expression of PAX2 by HMECs. (A) The expression of ICAM-1 by HMECs and HMEC-AS 3 days after infection with HHV-8 was evaluated by fluorescent-activated cell sorter (FACS) analysis and compared with control uninfected HMECs. Cells were detached with nonenzymatic solution and incubated with specific primary antibody for 30 minutes and finally with PE goat anti–mouse IgG for 20 minutes. FACS histograms are representative of 3 independent experiments with similar results. (B) The adhesion of leukocytes to endothelium was evaluated. Labeled lymphocytes were added to a monolayer of uninfected HMECs and r-HMECs or HMECs, r-HMEC-AS, and HMEC-AS infected with HHV-8 after 3 days and were incubated for 30 minutes at 37°C, 5% CO₂ in a humidified atmosphere in static condition. After washing, adherent cells were counted in each well. In some experiments, endothelial monolayers were incubated with an anti-ICAM-1 blocking antibody to verify whether enhanced leukocytes adhesion depended on HHV-8–induced expression of ICAM-1. Data are means plus or minus SD of 3 independent experiments performed in triplicate. Analysis of variance with Newman-Keuls multiple comparison test was performed (*P < .005, infected HMECs vs uninfected HMEC; #P < .05, infected r-HMECs vs uninfected r-HMECs).