ReviewViruses2025
Regulation and Deregulation of Viral Gene Expression During High-Risk HPV Infection.
Review in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- The Role of Sex Hormone Receptors in the Squamous Cell Carcinoma of the Uterine Ectocervix: A Review and Future Directions.Diagnostics (Basel, Switzerland) · 2026Review
- The current landscape of therapeutic vaccination approaches for treatment of HPV-dependent malignancies.NPJ vaccines · 2026Review
- In Vitro Model Characterizing Carcinogenic Progression of HPV-Positive Oropharyngeal Cancer.Cancers · 2026Article
- Role of E5 from HPV16 in the Evasion of the Immune Response.International journal of molecular sciences · 2026Review
- Cervical Cancer Screening in Transition: Global Challenges and Local Realities.International journal of women's health · 2026Review
- Clinical profile and pattern of second primary tumors in HPV-positive and HPV-negative oropharyngeal cancer.Revista brasileira de epidemiologia = Brazilian journal of epidemiology · 2026Article
- Diagnostic utility and tissue localization of HPV16 and HPV18 E7 immunohistochemistry in cervical lesion progression: a comparative study with PCR.Frontiers in oncology · 2026Article
- High-risk HPV and bacterial STIs in a primary screening population in rural Hainan, China: prevalence, co-infection, and association with cervical abnormalities.Frontiers in public health · 2026Article
- HPV-driven inflammatory pathways in ovarian carcinogenesis: molecular mechanisms and emerging therapeutic interventions.Journal of ovarian research · 2025Review
- Evaluation of systemic inflammation- and nutrition-based indices in the prediction of HPV persistence.BMC women's health · 2025Article
- Human papillomavirus prevalence, genotype distribution, risk factors, and cervical pathology association in women aged 50 years and older: a retrospective cross-sectional study in Xinjiang, China.Frontiers in oncology · 2025Article
- The dual role of vulvovaginal candidiasis in HPV infection: implications for vaginal microecology and cervical lesions.Frontiers in microbiology · 2025Review
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
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
Cervical cancer remains a global health burden, with persistent infection by high-risk human papillomaviruses (HR-HPVs) being the primary etiological factor. HR-HPVs target stem-like cells of the cervical epithelium to establish chronic infections. Upon infection of the cervical transformation zone (TZ)-a region adjacent to the squamocolumnar junction (SCJ)-these viruses drive neoplastic transformation, which is due in part to the unique cellular composition and hormonal responsiveness of the TZ. Reserve cells, which can accumulate at the cervical crypt entrances of the TZ, are thought to be highly susceptible to HR-HPV infection because of their location beneath a single layer of columnar cells. Infection of the stratified ectocervical epithelium, in contrast, requires a wound to allow basal cell infection, replication, and the expression of early genes to adjust epithelial homeostasis while facilitating immune evasion. Persistent infection by HR-HPV types, particularly HPV16 and HPV18, can result in the deregulated expression of viral genes E6 and E7, driving cell cycle disruption, genomic instability, and subsequent viral genome integration. Differences in the microenvironment and transcriptional environment of the ectocervix compared with the TZ could explain the frequent deregulation of E6 and E7 at the latter site, which can drive disease progression towards cancer.
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What Socratic 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 Socratic graph.