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

ABSTRACT: Human Papillomavirus Genomes Associate with Active Host Chromatin during Viral Genome Maintenance [Hi-C]

PROVIDER: PRJNA1247936 | ENA |

REPOSITORIES: ENA

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

Project description: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. 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.

2025-07-07 | GSE294037 | GEO

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

Project description:Human Papillomavirus Genomes Associate with Active Host Chromatin during Viral Genome Maintenance [ATAC-seq]

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

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

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

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Recurrent Integration of Human Papillomavirus Genomes at Transcriptional Regulatory Hubs

Project description:Oncogenic human papillomavirus (HPV) genomes are often integrated into host chromosomes in HPV-associated cancers. HPV genomes are integrated either as a single copy, or as tandem repeats of viral DNA interspersed with, or without, host DNA. Integration occurs frequently in common fragile sites susceptible to tandem repeat formation, and the flanking or interspersed host DNA often contains transcriptional enhancer elements. When co-amplified with the viral genome, these enhancers can form super-enhancer-like elements that drive high viral oncogene expression. Here, we compiled highly curated datasets of HPV integration sites in cervical (CESC) and head and neck squamous cell carcinoma (HNSCC) cancers and assessed the number of breakpoints, viral transcriptional activity, and host genome copy number at each insertion site. Tumors frequently contained multiple distinct HPV integration sites, but often only one “driver” site that expressed viral RNA. Since common fragile sites and active enhancer elements are cell-type specific, we mapped these regions in cervical cell lines using FANCD2 and Brd4/H3K27ac ChIP-seq, respectively. Large enhancer clusters, or super-enhancers, were also defined using the Brd4/H3K27ac ChIP-seq dataset. HPV integration breakpoints were enriched at both FANCD2-associated fragile sites, and enhancer-rich regions, and frequently showed adjacent focal DNA amplification in CESC samples. We identified recurrent integration “hotspots” that were enriched for super-enhancers, some of which function as regulatory hubs for cell-identity genes. We propose that during persistent infection, extrachromosomal HPV minichromosomes associate with these transcriptional epicenters, and accidental integration could promote viral oncogene expression and carcinogenesis.

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