FIG. 5.

Cells infected with MCMVs lacking m38.5 show increased sensitivity to virus- and drug-induced cell death compared to cells infected with wt MCMV. (A to C) 10.1 fibroblasts (A), SVEC4-10 endothelial cells (B), and NIH 3T3 fibroblasts (C) were infected with the indicated viruses, and levels of cell viability at 24 and 96 hpi were measured by an MTT assay. No difference in viability among the cell types at 24 hpi was detected (data not shown in panels B and C). m38.5HA, MCMV-m38.5HA; Δm38.5HA, MCMVΔm38.5HA; ΔM37-m39, MCMVΔM37-m39. (D) The premature death of MCMVΔm38.5-infected cells was largely blocked by an inhibitor of viral DNA replication (PAA, 250 μg/ml) but not by the calpain inhibitor z-LLY-fmk (zLLY). −, control; Δm38.5, MCMVΔ38.5. (E) The addition of the pancaspase inhibitor z-VAD-fmk (zVAD), but not the solvent dimethyl sulfoxide (DM), also reduced premature cell death. (F) 10.1 cells infected with wt MCMV were resistant to cell death induced by STS, MG132, and TNF-α, but MCMVΔm38.5-infected cells were sensitive to STS- and MG132-induced cell death, and ΔM36-infected cells were sensitive to TNF-α-induced apoptosis. In all experiments, the 24-hpi values for untreated cells were normalized to 100%.