ArticlePLoS genetics2018
HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 98 citations in OpenAlex.
- The cervicovaginal microbiome: an emerging determinant of HPV infection and disease.Journal of virology · 2026Review
- Biology-aligned cervical cancer screening: target-centric biomarkers and next-generation diagnostic platforms.Biomarker research · 2026Review
- HPV in oropharyngeal squamous papillomas: a missing link in head and neck viral pathogenesis.Virchows Archiv : an international journal of pathology · 2026Article
- Impact of Tau overexpression on DNA replication dynamics in centromeres of human neural progenitor cells.iScience · 2026Article
- HPV Integration in Head and Neck Cancer: Downstream Splicing Events and Expression Ratios Linked with Poor Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Molecular heterogeneity of HPV-associated cancers and strategies to overcome treatment resistance.Cancer heterogeneity and plasticity · 2026Article
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- Epigenetic profiling reveals key super-enhancer networks driving oncogenesis in HPV-positive HNSCC.iScience · 2025Article
- HPVPool-Seq: a genotype-guided pooling strategy for cost-effective next-generation sequencing detection of HPV integration in cervical samples.Microbiology spectrum · 2025Article
- Article
- From Viral Infection to Genome Reshaping: The Triggering Role of HPV Integration in Cervical Cancer.International journal of molecular sciences · 2025Review
- Human Papillomavirus Integration Induces Oncogenic Host Gene Fusions in Oropharyngeal Cancers.Cancer discovery · 2025Article
- Human papillomavirus genomes associate with active host chromatin during persistent viral infection.PLoS pathogens · 2025Article
- Nuclear keratin 6A upregulates human papillomavirus oncogene expression through TEAD1 interaction.Virology journal · 2025Article
- Rearrangements of viral and human genomes at human papillomavirus integration events and their allele-specific impacts on cancer genome regulation.Genome research · 2025Article
- Human Papillomavirus-Related Cancer Vaccine Strategies.Vaccines · 2024Review
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- The application of organoids in cancers associated with pathogenic infections.Clinical and experimental medicine · 2024Review
- Structure and transcription of integrated HPV DNA in vulvar carcinomas.NPJ genomic medicine · 2024Article
- Cis-regulatory effect of HPV integration is constrained by host chromatin architecture in cervical cancers.Molecular oncology · 2024Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
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Abstract
Integration of human papillomavirus (HPV) genomes into cellular chromatin is common in HPV-associated cancers. Integration is random, and each site is unique depending on how and where the virus integrates. We recently showed that tandemly integrated HPV16 could result in the formation of a super-enhancer-like element that drives transcription of the viral oncogenes. Here, we characterize the chromatin landscape and genomic architecture of this integration locus to elucidate the mechanisms that promoted de novo super-enhancer formation. Using next-generation sequencing and molecular combing/fiber-FISH, we show that ~26 copies of HPV16 are integrated into an intergenic region of chromosome 2p23.2, interspersed with 25 kb of amplified, flanking cellular DNA. This interspersed, co-amplified viral-host pattern is frequent in HPV-associated cancers and here we designate it as Type III integration. An abundant viral-cellular fusion transcript encoding the viral E6/E7 oncogenes is expressed from the integration locus and the chromatin encompassing both the viral enhancer and a region in the adjacent amplified cellular sequences is strongly enriched in the super-enhancer markers H3K27ac and Brd4. Notably, the peak in the amplified cellular sequence corresponds to an epithelial-cell-type specific enhancer. Thus, HPV16 integration generated a super-enhancer-like element composed of tandem interspersed copies of the viral upstream regulatory region and a cellular enhancer, to drive high levels of oncogene expression.
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