FIG. 8.

Effect of inhibition of HDAC activity on growth and viral gene expression in cells infected with ORF66p kinase-deficient VZV. (A) MeWo cells were mock treated or pretreated with 1 mM sodium butyrate for 6 h. Following treatment, cells were infected with cell-free wild-type (VZV-WT) or ORF66p kinase-deficient (VZV-ORF66KD) VZV at a multiplicity of infection of 0.0001. Cells were maintained in medium with or without 1 mM sodium butyrate as indicated, and medium was replaced daily. At 24-h intervals postinfection, cell-associated virus titers were measured by titration on fresh monolayers of MeWo cells. Five days postinfection, monolayers were fixed and stained and plaques were counted to calculate the titers of infectious centers. Each datum point represents the average from two independent experiments, and the error bars indicate standard deviations. Stars identify P values [t_(pval) < 0.006] for VZV-ORF66KD at 72, 96, and 120 hpi, as determined by t test. (B) MeWo cells were pretreated as described previously and infected with cell-free wild-type (VZV-WT) or ORF66p kinase-deficient (VZV-ORF66KD) VZV at a multiplicity of infection of 0.0001. Postinfection, cells were maintained as described above. At the indicated time points postinfection, cells were harvested and equal amounts of total protein (20 μg) were analyzed by Western blotting using antisera specific for ORF4p, ORF61p, ORF62p, ORF63p, and actin.