ArticleJournal of virology2008
The E8--E2 gene product of human papillomavirus type 16 represses early transcription and replication but is dispensable for viral plasmid persistence in keratinocytes.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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
52 citing papers in PubMed.
- Article
- Differentiation-independent Activation of HPV Genome Replication by the lncRNA DINO.bioRxiv : the preprint server for biology · 2026Article
- Inhibition of high risk HPV31 E8^E2 repressor activity enables differentiation-independent genome amplification and E4 expression.PLoS pathogens · 2026Article
- Chromatin assembly by the histone chaperone HIRA facilitates Human Papillomavirus replication.bioRxiv : the preprint server for biology · 2025Article
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Article
- Experimental Support for Human Papillomavirus Genome Amplification Early after Infectious Delivery.Journal of virology · 2023Article
- Protein-DNA Interactions Regulate Human Papillomavirus DNA Replication, Transcription, and Oncogenesis.International journal of molecular sciences · 2023Review
- Human Papillomavirus Genome Copy Number Is Maintained by S-Phase Amplification, Genome Loss to the Cytosol during Mitosis, and Degradation in GJournal of virology · 2023Article
- Transcription Properties of Beta-HPV8 and HPV38 Genomes in Human Keratinocytes.Journal of virology · 2022Article
- Review
- Restriction of viral gene expression and replication prevents immortalization of human keratinocytes by a beta-human papillomavirus.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Human Papillomaviruses Target the DNA Damage Repair and Innate Immune Response Pathways to Allow for Persistent Infection.Viruses · 2021Review
- EXPRESSION OF E8^E2 IS REQUIRED FOR WART FORMATION BY MOUSE PAPILLOMAVIRUS 1 IN VIVO.Journal of virology · 2021Article
- Use of Cap Analysis Gene Expression to detect human papillomavirus promoter activity patterns at different disease stages.Scientific reports · 2020Article
- High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis.Cancers · 2020Review
- Whole Genomic Analysis and Comparison of Two Canine Papillomavirus Type 9 Strains in Malignant and Benign Skin Lesions.Viruses · 2020Article
- Epigenetic Regulation of the Human Papillomavirus Life Cycle.Pathogens (Basel, Switzerland) · 2020Review
- Hitchhiking of Viral Genomes on Cellular Chromosomes.Annual review of virology · 2019Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A conserved E8(wedge)E2 spliced mRNA is detected in keratinocytes transfected with human papillomavirus type 16 (HPV-16) plasmid DNA. Expression of HPV-16 E8--E2 (16-E8--E2) is independent of the major early promoter, P97, and is modulated by both specific splicing events and conserved cis elements in the upstream regulatory region in a manner that differs from transcriptional regulation of other early viral genes. Mutations that disrupt the predicted 16-E8--E2 message also increase initial HPV-16 plasmid amplification 8- to 15-fold and major early gene (P97) transcription 4- to 5-fold over those of the wild type (wt). Expressing the 16-E8--E2 gene product from the cytomegalovirus (CMV) promoter represses HPV-16 early gene transcription from P97 in a dose-dependent manner, as detected by RNase protection assays. When expressed from the CMV promoter, 16-E8--E2 also inhibits the amplification of an HPV-16 plasmid and a heterologous simian virus 40 (SV40) ori plasmid that contains E2 binding sites in cis. In contrast, cotransfections with HPV-16 wt genomes that express physiologic levels of 16-E8--E2 are sufficient to repress HPV-16 plasmid amplification but are limiting and insufficient for the repression of SV40 amplification. 16-E8--E2-dependent repression of HPV-16 E1 expression is sufficient to account for this observed inhibition of initial HPV-16 plasmid amplification. Unlike with other papillomaviruses, primary human keratinocytes immortalized by the HPV-16 E8 mutant genome contain more than eightfold-higher levels of unintegrated plasmid than the wt, demonstrating that 16-E8(wedge)E2 limits the viral copy number but is not required for plasmid persistence and maintenance.
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