ReviewBiochimica et biophysica acta2012
Hitchhiking on host chromatin: how papillomaviruses persist.
Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 57 citations in OpenAlex.
- HPV, HBV, and HIV-1 Viral Integration Site Mapping: A Streamlined Workflow from NGS to Genomic Insights of Carcinogenesis.Viruses · 2024Article
- Article
- Human Papillomavirus 16 E2 Interaction with TopBP1 Is Required for E2 and Viral Genome Stability during the Viral Life Cycle.Journal of virology · 2023Article
- Interaction with TopBP1 Is Required for Human Papillomavirus 16 E2 Plasmid Segregation/Retention Function during Mitosis.Journal of virology · 2022Article
- HPV Integration Site Mapping: A Rapid Method of Viral Integration Site (VIS) Analysis and Visualization Using Automated Workflows in CLC Microbial Genomics.International journal of molecular sciences · 2022Article
- A Critical Role for p53 during the HPV16 Life Cycle.Microbiology spectrum · 2022Article
- Human Beta Papillomavirus Type 8 E1 and E2 Proteins Suppress the Activation of the RIG-I-Like Receptor MDA5.Viruses · 2022Article
- Article
- Human Papillomavirus 16 (HPV16) E2 Repression of TWIST1 Transcription Is a Potential Mediator of HPV16 Cancer Outcomes.mSphere · 2020Article
- Clinicopathological characteristics and papillomavirus types in cutaneous warts in bovine.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2020Article
- Viral microRNA effects on persistent infection of human lymphoid cells by polyomavirus SV40.PloS one · 2018Article
- Phosphorylation of the Bovine Papillomavirus E2 Protein on Tyrosine Regulates Its Transcription and Replication Functions.Journal of virology · 2017Article
- Post-Transcriptional Regulation of KLF4 by High-Risk Human Papillomaviruses Is Necessary for the Differentiation-Dependent Viral Life Cycle.PLoS pathogens · 2016Article
- Failure to interact with Brd4 alters the ability of HPV16 E2 to regulate host genome expression and cellular movement.Virus research · 2016Article
- Human papillomaviruses activate and recruit SMC1 cohesin proteins for the differentiation-dependent life cycle through association with CTCF insulators.PLoS pathogens · 2015Article
- Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.Journal of clinical medicine · 2015Article
- Altering murine leukemia virus integration through disruption of the integrase and BET protein family interaction.Nucleic acids research · 2014Article
- The viral E8^E2C repressor limits productive replication of human papillomavirus 16.Journal of virology · 2014Article
- Virion factors that target Daxx to overcome intrinsic immunity.Journal of virology · 2013Review
- The papillomavirus E2 proteins.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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent viruses need mechanisms to protect their genomes from cellular defenses and to ensure that they are efficiently propagated to daughter host cells. One mechanism by which papillomaviruses achieve this is through the association of viral genomes with host chromatin, mediated by the viral E2 tethering protein. Association of viral DNA with regions of active host chromatin ensures that the virus remains transcriptionally active and is not relegated to repressed heterochromatin. In addition, viral genomes are tethered to specific regions of host mitotic chromosomes to efficiently partition their DNA to daughter cells. Vegetative viral DNA replication also initiates at specific regions of host chromatin, where the viral E1 and E2 proteins initiate a DNA damage response that recruits cellular DNA damage and repair proteins to viral replication foci for efficient viral DNA synthesis. Thus, these small viruses have capitalized on interactions with chromatin to efficiently target their genomes to beneficial regions of the host nucleus. This article is part of a Special Issue entitled: Chromatin in time and space.
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.