Fig. 2: Viral gene expression is dysregulated after PARP inhibition.

A Principal component analysis (PCA) separating type I EBV latency (Mutu) and type III EBV latency (LCL) human B-cells by treatment (control or 2.5 µM olaparib). Data derived from RNA-seq dataset utilizing biological duplicates. B Volcano plot illustrating dysregulated gene expression after olaparib treatment in Mutu cell line, with the left of the dashed line representing genes downregulated after PARP inhibition and the right representing genes upregulated after PARP inhibition. Genes displayed are dysregulated at p < 0.05 and FDR < 0.05. Genes with 2-fold change and q < 0.01 after correction for multiple testing (FDR) were considered as significantly differentially expressed. C Volcano plot illustrating dysregulated gene expression after olaparib treatment in LCL, as described in (B). Genes with 2-fold change and q < 0.01 after correction for multiple testing (FDR) were considered as significantly differentially expressed. D RT-qPCR validation of genes shown to be dysregulated by RNA-seq in LCL after PARP inhibition. Bar graph represents the average expression of three biological duplicates per treatment, each normalized to 18S expression, respectively. (N = 3, mean ± SD). Groups were compared by paired student’s t test assuming equal variance (two-tailed). (*=p ≤ 0.05, **=p ≤ 0.01, ***p =≤0.001) Source data are provided as a Source Data file. E RT-qPCR validation of RPMS1 expression using five separate primer sets, spanning various exons in the gene. Source data are provided as a Source Data file. The bar graph represents the average expression of three biological replicates per treatment (N = 3, mean ± SD). Groups were compared by paired student’s t test assuming equal variance (two-tailed). (*=p ≤ 0.05, **=p ≤ 0.01, ***p =≤0.001).