ArticleThe open virology journal2012
The invisible enemy - how human papillomaviruses avoid recognition and clearance by the host immune system.
Article in The open virology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed.
- Molecular insights and therapeutic innovations in low-risk human papillomavirus-associated cutaneous wart.Molecular biology reports · 2026Review
- The current landscape of therapeutic vaccination approaches for treatment of HPV-dependent malignancies.NPJ vaccines · 2026Review
- TTV Load Mirrors Local Immunity and Tracks HPV Positivity in the Anogenital Tract.Journal of medical virology · 2026Article
- Human papillomavirus-related oral lesions in people with HIV: A 20-year multinational cohort analysis.Journal of dental sciences · 2026Article
- Emerging Therapeutic Strategies for HPV-Related Cancers: From Gene Editing to Precision Oncology.Current issues in molecular biology · 2025Review
- Intralesional Immunotherapy for Non-Genital Viral Warts: A Review of Current Evidence and Future Perspectives.International journal of molecular sciences · 2025Review
- Novel bioinformatic approaches show the role of driver genes in the progression of cervical cancer: An in-silico study.Heliyon · 2024Article
- Navigating therapeutic strategies: HPV classification in head and neck cancer.British journal of cancer · 2024Review
- Identification and Functional Implications of the E5 Oncogene Polymorphisms of Human Papillomavirus Type 16.Tropical medicine and infectious disease · 2024Article
- Oral and periodontal manifestation related during human papilloma virus infections: Update on early prognostic factors.Heliyon · 2024Review
- Association of Human Papilloma Virus, Cytomegalovirus, and Epstein-Barr Virus with Breast Cancer in Jordanian Women.Medicina (Kaunas, Lithuania) · 2024Article
- HPV related p16BMC oral health · 2024Article
- The HPV viral regulatory mechanism of TLRs and the related treatments for HPV-associated cancers.Frontiers in immunology · 2024Review
- Advancing Immunotherapies for HPV-Related Cancers: Exploring Novel Vaccine Strategies and the Influence of Tumor Microenvironment.Vaccines · 2023Review
- Brachytherapy for targeting the immune system in cervical cancer patients.BMC immunology · 2023Article
- Article
- Oral human papillomavirus prevalence, persistence, and risk-factors in HIV-positive and HIV-negative adults.Tumour virus research · 2022Article
- Infection by High-Risk Human Papillomaviruses, Epithelial-to-Mesenchymal Transition and Squamous Pre-Malignant or Malignant Lesions of the Uterine Cervix: A Series of Chained Events?International journal of molecular sciences · 2021Review
- Unravelling the Immunomodulatory Effects of Viral Ion Channels, towards the Treatment of Disease.Viruses · 2021Review
- Type 2 human papillomavirus E7 attenuates E-cadherin expression in human keratinocytes.Journal of microbiology (Seoul, Korea) · 2021Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human papillomavirus (HPV) needs to persist in squamous epithelia for a certain amount of time to complete its reproductive cycle. Therefore, the virus has evolved multiple immune evasion strategies. The interplay of these immune evasion mechanisms with the host immune system decides whether a HPV infection is cleared or becomes persistent. Clearance of HPV-induced lesions is mediated by a cellular immune response, consisting of both cytotoxic T lymphocyte and T helper cell responses. Persistent HPV infection, on the other hand, is the single most important risk factor for the development of HPV-associated premalignant lesions and HPV-driven cancers. This article reviews the immune evasion mechanisms employed by high-risk HPVs to escape host immune recognition and attack.
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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.