Fig. 1: Replication of two high-risk oncogenic HCMV strains in HAs cultures, the activation of oncogenic pathways, and reduced apoptosis rates.

a Time-course of the viral titer in the supernatant of HAs infected with HCMV-DB and BL as measured by IE1-qPCR. b Immunoblotting data of IE1 and pp65 in uninfected HAs lysates and HAs infected with HCMV-DB and BL (day 5 post-infection). β-actin was used as loading control. c Confocal microscopic images of HCMV-IE1, pp65, and late antigen staining in HAs infected with HCMV-DB and BL (day 1 post-infection). Uninfected HAs and MRC5-DB cells were used as negative and positive controls, respectively. Nuclei were counterstained with DAPI; magnification ×63, scale bar 10 μm. d IE1 and UL69 transcripts detection by RT-qPCR in uninfected HAs, HAs-DB and BL as well as HAs infected with UV-treated HCMV. e Myc and EZH2 protein expression as measured by western blot (day 5 post-infection) and FACS (day 3 post-infection) in uninfected HAs and HAs infected with HCMV-DB and BL. β-actin was used as loading control. f Myc and EZH2 transcripts detection by RT-qPCR. g Early apoptosis assessment in HAs-DB and BL (MOI = 1). UI HAs were used as a control. h Akt, and pAkt-Ser473 protein expression as measured by western blot and FACS in uninfected HAs and HAs infected with HCMV-DB and BL. β-actin was used as loading control. Data are represented as mean ± SD of two independent experiments.