Figure 8A

<b>A. </b>THP-1 cells were infected by spinoculation with an MOI of 20 with either nonfluorescent TB40/E, UL88-STOP, or UL88-Rev, the latter two of which express GFP driven from the IE2 promoter or were left uninfected. GFP fluorescence was measured by flow cytometry at d5 post infection. <b>B.</b> Schematic representation of the experiment methodology for <b>C</b> and <b>D</b>.<b> </b>At day 3, 2.5 x 10⁵ THP-1, of which ~ 2.5 x 10⁴ were HCMV-infected, were transferred onto a monolayer of ~ 2.5 x 10⁵ HDFs and virus spread was monitored every three days by confocal imaging up to day 15. <b>C</b>. Representative images of TB40/E-GFP and UL88-STOP from day 3 and day 7 are shown. <b>D.</b> The spread of infection was quantified as the area of fluorescence using the NIS element software.<b> </b>Graph shows fold change in area of fluorescence for each virus. <b>E. </b>MRC-5 cells were infected with TB40/E-mCh or UL88-STOP-mCh virus at MOI of 0.05. Cells were harvested for RNA isolation at 7 dpi. Antiviral gene expression was profiled using a set of 84 ISGs by qPCR. Results are plotted as volcano plot depicting the modulated genes as compared between TB40/E WT HCMV and UL88-STOP HCMV infection. <b>F</b>. ISGs known to be modulated in HCMV infection are shown with their relative fold change in mRNA levels (normalized to GAPDH) between TB40/E WT and UL88-STOP virus infection. The graph shows the genes that remained unchanged (green box), downregulated (red box), or upregulated (blue box), in TB40/E WT vs UL88-STOP HCMV-infected cells. Results are from biological triplicates.