FIG. 5.

Accumulation of E2FBP1 or ICP0 in HSV-1-infected cells is affected by the level of the other. (A) Hep-2 cells were transformed with a control (vector) expression plasmid or with expression plasmids for wild-type (WT) or ΔA HA-E2FBP1. The cells were then grown on glass coverslips and infected with HSV-1 at an MOI of 10. After infection, cells were further cultivated for the indicated times and then fixed and stained with anti-E2FBP1 (DRIL1; red), anti-ICP0 (5H7; green), and DAPI (gray). (B) hTERT-BJ1 cells were infected with recombinant lentiviruses encoding either HA-E2FBP1 or its ΔA mutant driven by an MMTV LTR promoter. The cells were then grown on glass coverslips, treated with 2 μM dexamethasone (Dex) to induce expression of HA-E2FBP1 for 18 h, infected with HSV-1 at an MOI of 5 in the presence of Dex, and maintained in the presence of Dex until fixation at 120 mpi. Cells were stained with anti-HA (red), anti-ICP0 (green) (left panels), and DAPI (gray). (C) Colocalization of E2FBP1 proteins and ICP0 in HSV-1-infected hTERT-BJ1-derived cells. hTERT-BJ1 cells were infected with recombinant lentiviruses encoding the indicated mutants of HA-E2FBP1 driven by an MMTV LTR promoter. The cells were then infected with HSV-1 and treated as described above. Cells were stained at 120 mpi with anti-HA (red), anti-ICP0 (green), and DAPI (gray).