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Human Papillomavirus Genomes Associate with Active Host Chromatin during Viral Genome Maintenance [4C-seq]

GSE294036 Homo sapiens (human) Other 7 samples Submitted 2025/07/07 Platform GPL24676
At a glance

human · 7 samples

Organism
Homo sapiens (human)
Samples
7 samples: 4 × 9E cells, extrachromosomal HPV31, biol vs 3 × 6E cells, integrated HPV31, biolGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI.
Paper
Human papillomavirus genomes associate with active host chromatin during persistent viral infectionPLoS pathogens · 2025
Summary (written by the submitters)
Human papillomaviruses (HPVs) maintain their genomes as minichromosomes in the nuclei of infected keratinocytes. This study investigates the association of HPV31 genomes with host chromatin using both HiC and 4C-seq chromosome conformation capture techniques. We show that HPV31 genomes preferentially associate with transcriptionally active A compartments of host chromatin, regions of open chromatin defined by ATAC-seq, and super-enhancers defined by Brd4 and H3K27ac ChIP-seq.
Read the full summary ↓
The viral genome association sites were also highly correlated with genomic loci previously identified as common HPV integration sites in cervical cancers. Recent studies have shown that transcriptionally active sites are prone to dsDNA breaks, and we find a strong correlation among dsBREAK datasets with transcriptionally active and open regions of host chromatin and the HPV31 genome association sites defined in our study. These findings suggest that HPV genomes associate with cellular transcriptional epicenters to maintain active viral gene expression during persistent infection, but also indicate that the susceptibility of these regions to dsDNA breaks could explain their propensity for viral DNA integration in HPV-associated cancers.
Published in
Human papillomavirus genomes associate with active host chromatin during persistent viral infection
Warburton A, Markowitz TE, Miranda JL et al. · PLoS pathogens 2025 · PMID 40892869 · doi:10.1371/journal.ppat.1013454
This dataset
Download · which file do I need?

Direct links to NCBI, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need.

All supplementary files ↗
3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE294036_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Also filed as BioProject PRJNA1247935. Searching any of these in the dataset finder brings you back here.

Study design
4 × 9E cells, extrachromosomal HPV31, biol vs 3 × 6E cells, integrated HPV31, biol

Supports a between-group comparison across 7 samples.

How we read this: 2 replicated groups read from 7 sample titles; they account for 7 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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