ReviewBiochimica et biophysica acta
Papillomavirus interaction with cellular chromatin.
Review in Biochimica et biophysica acta. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- HPV in oropharyngeal squamous papillomas: a missing link in head and neck viral pathogenesis.Virchows Archiv : an international journal of pathology · 2026Article
- HPV11 targeting KDM4A regulates the polarization of macrophage MCell communication and signaling : CCS · 2024Article
- The SETD2 Methyltransferase Supports Productive HPV31 Replication through the LEDGF/CtIP/Rad51 Pathway.Journal of virology · 2023Article
- BRD4S interacts with viral E2 protein to limit human papillomavirus late transcription.Journal of virology · 2021Article
- From Merkel Cell Polyomavirus Infection to Merkel Cell Carcinoma Oncogenesis.Frontiers in microbiology · 2021Review
- Epigenetic Regulation of the Human Papillomavirus Life Cycle.Pathogens (Basel, Switzerland) · 2020Review
- Review
- Acetylation of E2 by P300 Mediates Topoisomerase Entry at the Papillomavirus Replicon.Journal of virology · 2019Article
- SETD2-dependent H3K36me3 plays a critical role in epigenetic regulation of the HPV31 life cycle.PLoS pathogens · 2018Article
- BET bromodomain inhibitors show anti-papillomavirus activity in vitro and block CRPV wart growth in vivo.Antiviral research · 2018Article
- High prevalence of co-infection between human papillomavirus (HPV) 51 and 52 in Mexican population.BMC cancer · 2017Article
- Histone H3 Acetyl K9 and Histone H3 Tri Methyl K4 as Prognostic Markers for Patients with Cervical Cancer.International journal of molecular sciences · 2017Article
- Therapeutics Targeting Protein Acetylation Perturb Latency of Human Viruses.ACS chemical biology · 2016Review
- The Nuclear DNA Sensor IFI16 Acts as a Restriction Factor for Human Papillomavirus Replication through Epigenetic Modifications of the Viral Promoters.Journal of virology · 2015Article
- Article
- Oncogenic processes.BioMed research international · 2014Article
- Evaluation of HPV infection and smoking status impacts on cell proliferation in epithelial layers of cervical neoplasia.PloS one · 2014Article
- Article
- Targeting the JMJD2 histone demethylases to epigenetically control herpesvirus infection and reactivation from latency.Science translational medicine · 2013Article
- Snapshots: chromatin control of viral infection.Virology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
High-risk human papillomavirus (HPV) infection is the primary risk factor for cervical cancer. HPVs establish persistent infection by maintaining their genomes as extrachromosomal elements (episomes) that replicate along with host DNA in infected cells. The productive life cycle of HPV is intimately tied to the differentiation program of host squamous epithelium. This review examines the involvement of host chromatin in multiple aspects of the papillomavirus life cycle and the malignant progression of infected host cells. Papillomavirus utilizes host mitotic chromosomes as vehicles for transmitting its genetic materials across the cell cycle. By hitchhiking on host mitotic chromosomes, the virus ensures accurate segregation of the replicated viral episomes to the daughter cells during host cell division. This strategy allows persistent maintenance of the viral episome in the infected cells. In the meantime, the virus subverts the host chromatin-remodeling factors to promote viral transcription and efficient propagation of viral genomes. By associating with the host chromatin, papillomavirus redirects the normal cellular control of chromatin to create a cellular environment conducive to both its own survival and malignant progression of host cells. Comprehensive understanding of HPV-host chromatin interaction will offer new insights into the HPV life cycle as well as chromatin regulation. This virus-host interaction will also provide a paradigm for investigating other episomal DNA tumor viruses that share a similar mechanism for interacting with host chromatin.
Indexed as
Identifiers
What OpenQuestion holds
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.