Fig. 3

HPV integration disrupts local host epigenome and transcriptome. a Genomic assay signal for an HPV integration site of SiHa (chr13:73,513,424). Top: RNA expression FPM; middle: ATAC-seq FPM; bottom: CTCF ChIP-seq RPM. Pink bars: signal from SiHa; blue bars: signal from 4 other HPV⁺ cell lines without integration at this position. Red dashed line: HPV integration site. Inset at top right of each panel shows signal within the hybrid genomic window including the host genome upstream of the integration site, full-length HPV16 (red shading) beginning at the integration site, a gap representing uncertainty in the end of the integrated HPV genome, and the host genome downstream of the integration site. b ATAC-seq peaks in a 1-Mbp window centered on SiHa’s integration site. Each column shows a 200-bp genomic window overlapping a peak. We generated all 200-bp genomic windows with a stride of 50 bp which overlapped a peak in any of the 5 cell lines. (Top): ATAC-seq FPM and CTCF ChIP-seq \(\log _{2}\) fold enrichment over control for each cell line divided by the cell line’s corresponding maximum value in chromosome 13. (Middle): Difference in the epigenome of SiHa and the most extreme value in the other 4 cell lines when SiHa had the most extreme value among the cell lines. When SiHa did not have the most extreme value, we used white. (Bottom): Physical location of peaks. Black lines map every 100 kbp to the corresponding peak. Red dashed line: HPV integration site. c Similar to (b), but for CTCF ChIP-seq instead of ATAC-seq