ArticleJournal of virology2009
Papillomavirus E2 proteins and the host BRD4 protein associate with transcriptionally active cellular chromatin.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 55 citations in OpenAlex.
- Hybrid extrachromosomal DNA in HPV-driven cancers.Journal of virology · 2026Review
- The interaction between virus-bound KLF4 and host-bound PARP1 directs the localization of wild-type adeno-associated virus type 2 (wtAAV2) to cellular sites of DNA damage.Journal of virology · 2026Article
- Association of hepatitis B virus genomes with active chromatin hubs challenges host replication fidelity, leading to DNA damage.Journal of virology · 2025Article
- Human papillomavirus genomes associate with active host chromatin during persistent viral infection.PLoS pathogens · 2025Article
- Human Papillomavirus Genomes Associate with Active Host Chromatin during Persistent Viral Infection.bioRxiv : the preprint server for biology · 2025Article
- Protein-DNA Interactions Regulate Human Papillomavirus DNA Replication, Transcription, and Oncogenesis.International journal of molecular sciences · 2023Review
- Recurrent integration of human papillomavirus genomes at transcriptional regulatory hubs.NPJ genomic medicine · 2021Article
- Review
- Regulation of Human Papillomavirus 18 Genome Replication, Establishment, and Persistence by Sequences in the Viral Upstream Regulatory Region.Journal of virology · 2021Article
- Human Papillomaviruses Target the DNA Damage Repair and Innate Immune Response Pathways to Allow for Persistent Infection.Viruses · 2021Review
- RUNX1-mediated alphaherpesvirus-host trans-species chromatin interaction promotes viral transcription.Science advances · 2021Article
- Persistent Human Papillomavirus Infection.Viruses · 2021Review
- Multiple Roles of Brd4 in the Infectious Cycle of Human Papillomaviruses.Frontiers in molecular biosciences · 2021Review
- The SMC5/6 Complex Represses the Replicative Program of High-Risk Human Papillomavirus Type 31.Pathogens (Basel, Switzerland) · 2020Article
- Hitchhiking of Viral Genomes on Cellular Chromosomes.Annual review of virology · 2019Review
- Mechanisms of persistence by small DNA tumor viruses.Current opinion in virology · 2018Review
- Article
- BET bromodomain inhibitors show anti-papillomavirus activity in vitro and block CRPV wart growth in vivo.Antiviral research · 2018Article
- Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The interaction of papillomavirus E2 proteins with cellular Brd4 protein is important for transcriptional regulation of viral genes and partitioning of viral genomes. Bovine papillomavirus type 1 (BPV-1) E2 binds cellular chromatin in complex with Brd4 in both mitotic and interphase cells. To identify specific sites of E2 interaction on cellular chromatin, a genome-wide chromatin immunoprecipitation-on-chip analysis was carried out using human promoter sequences. Both E2 and Brd4 were found bound to most transcriptionally active promoters in C33A cells. These promoters were also bound by RNA polymerase II and were modified by histone H3 acetylation and K4 trimethylation, all indicators of active transcription. E2 binding strongly correlated with Brd4 and RNA polymerase II occupancy and H3K4me3 modification at all human promoters, indicating that E2 bound to active promoters. E2 binding did not correlate with the presence of consensus E2 binding sites in the promoters. Furthermore, the mRNA levels of E2-bound cellular genes were not significantly changed by E2 expression. Thus, the papillomavirus E2 proteins bind to transcriptionally active cellular genes but do not change their activity. We propose that this may be a way for the virus to ensure that the viral genome is retained in transcriptionally active regions of the nucleus to escape silencing. Therefore, E2-mediated tethering of viral genomes to host chromatin has multiple roles: to partition the viral genome to daughter cells, to ensure that the genomes are retained in the nucleus, and to make certain that the genomes are retained in functionally active nuclear domains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.