ArticleJournal of virology2002
Long-term effect of interferon on keratinocytes that maintain human papillomavirus type 31.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 55 citations in OpenAlex.
- Trial
- The roles of DNA damage repair and innate immune surveillance pathways in HPV pathogenesis.Virology · 2024Review
- APOBEC3: Friend or Foe in Human Papillomavirus Infection and Oncogenesis?Annual review of virology · 2022Review
- Review
- Apoptotic caspases suppress an MDA5-driven IFN response during productive replication of human papillomavirus type 31.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The interesting relationship between APOBEC3 deoxycytidine deaminases and cancer: a long road ahead.Open biology · 2020Article
- Vesicular trafficking permits evasion of cGAS/STING surveillance during initial human papillomavirus infection.PLoS pathogens · 2020Article
- Article
- Human Papillomavirus 16 E5 Inhibits Interferon Signaling and Supports Episomal Viral Maintenance.Journal of virology · 2020Article
- Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression.Viruses · 2017Review
- Interferon Gamma Prevents Infectious Entry of Human Papillomavirus 16 via an L2-Dependent Mechanism.Journal of virology · 2017Article
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
- Evasion of host immune defenses by human papillomavirus.Virus research · 2017Review
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Interferon Kappa Inhibits Human Papillomavirus 31 Transcription by Inducing Sp100 Proteins.Journal of virology · 2016Article
- The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016Review
- Review
- Activation of NF-κB by human papillomavirus 16 E1 limits E1-dependent viral replication through degradation of E1.Journal of virology · 2015Article
- Viral load, gene expression and mapping of viral integration sites in HPV16-associated HNSCC cell lines.International journal of cancer · 2015Article
- Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.Journal of clinical medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The long-term effects of interferon treatment on cell lines that maintain human papillomavirus type 31 (HPV-31) episomes have been examined. High doses and prolonged interferon treatment resulted in growth arrest of HPV-positive cells, with a high percentage of cells undergoing apoptosis. These effects were not seen with interferon treatment of either normal human keratinocytes or cells derived from HPV-negative squamous carcinomas, which exhibited only slight decreases in their rates of growth. Within 2 weeks of the initiation of treatment, a population of HPV-31-positive cells that were resistant to interferon appeared consistently and reproducibly. The resistant cells had growth and morphological characteristics similar to those of untreated cells. Long-term interferon treatment of HPV-positive cells also resulted in a reduction in HPV episome levels but did not significantly decrease the number of integrated copies of HPV. Cells that maintained HPV genomes lacking E5 were sensitive to interferon, while cells expressing only the E6/E7 genes were resistant. In contrast, cells that expressed E2 from a tetracycline-inducible promoter were found to be significantly more sensitive to interferon treatment than parental cells. This suggests that at least a portion of the sensitivity to interferon could be mediated through the E2 protein. These studies indicate that cells maintaining HPV episomes are highly sensitive to interferon treatment but that resistant populations arise quickly.
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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.