ReviewViruses2015
High-risk human papillomavirus targets crossroads in immune signaling.
Review in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- HPV in breast cancer: prevalence and comparison with healthy tissue-a systematic review and meta-analysis.Cancer causes & control : CCC · 2026Pooled it
- Cytokine response following perturbation of the cervicovaginal milieu during HPV genital infection.Immunologic research · 2021Trial
- Role of E5 from HPV16 in the Evasion of the Immune Response.International journal of molecular sciences · 2026Review
- Review
- Virtual Screening, Molecular Docking and Molecular Dynamics Simulation of Bioactive Compounds from Various Indonesian Medicinal Plants as Potential Inhibitors of Human Papillomavirus Type 16 E6 Protein in Cervical Cancer Development.Tropical life sciences research · 2025Article
- Deciphering the roles of myeloid derived suppressor cells in viral oncogenesis.Frontiers in immunology · 2023Review
- Human Papillomaviruses as Infectious Agents in Gynecological Cancers. Oncogenic Properties of Viral Proteins.International journal of molecular sciences · 2022Review
- Persistent Human Papillomavirus Infection.Viruses · 2021Review
- Digital RNA Sequencing of Human Epidermal Keratinocytes Carrying Human Papillomavirus Type 16 E7.Frontiers in genetics · 2020Article
- HPV Induces Changes in Innate Immune and Adhesion Molecule Markers in Cervical Mucosa With Potential Impact on HIV Infection.Frontiers in immunology · 2020Article
- Human papilloma virus-specific T cells can be generated from naïve T cells for use as an immunotherapeutic strategy for immunocompromised patients.Cytotherapy · 2018Article
- HPV11 E6 mutation by overexpression of APOBEC3A and effects of interferon-ω on APOBEC3s and HPV11 E6 expression in HPV11.HaCaT cells.Virology journal · 2017Article
- Oncogenic human papillomaviruses.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- The Mouse Papillomavirus Infection Model.Viruses · 2017Review
- Host cell restriction factors that limit transcription and replication of human papillomavirus.Virus research · 2017Review
- Article
- TRAF3 signaling: Competitive binding and evolvability of adaptive viral molecular mimicry.Biochimica et biophysica acta · 2016Review
- Comment on 'The incidence of leukaemia in women with BRCA1 and BRCA2 mutations: an International Prospective Cohort Study'.British journal of cancer · 2016Article
- Effect of human papillomavirus 16 oncoproteins on oncostatin M upregulation in oral squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2016Article
- Human Papillomavirus Downregulates the Expression of IFITM1 and RIPK3 to Escape from IFNγ- and TNFα-Mediated Antiproliferative Effects and Necroptosis.Frontiers in immunology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent infections with a high-risk type human papillomavirus (hrHPV) can progress to cancer. High-risk HPVs infect keratinocytes (KCs) and successfully suppress host immunity for up to two years despite the fact that KCs are well equipped to detect and initiate immune responses to invading pathogens. Viral persistence is achieved by active interference with KCs innate and adaptive immune mechanisms. To this end hrHPV utilizes proteins encoded by its viral genome, as well as exploits cellular proteins to interfere with signaling of innate and adaptive immune pathways. This results in impairment of interferon and pro-inflammatory cytokine production and subsequent immune cell attraction, as well as resistance to incoming signals from the immune system. Furthermore, hrHPV avoids the killing of infected cells by interfering with antigen presentation to antigen-specific cytotoxic T lymphocytes. Thus, hrHPV has evolved multiple mechanisms to avoid detection and clearance by both the innate and adaptive immune system, the molecular mechanisms of which will be dealt with in detail in this review.
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.