Evidence map›Paper›PMID 40065022›Full record

ArticleScientific reports2025

Analysis of HPV-16 viral load, integration status, and p16 expression in relation to EBV co-infection and cervical lesion severity.

Azam Khamseh, Ali Farhadi, Somayeh Jalilvand, Fariba Yarandi, Narges Izadi-Mood, Saied Ghorbani, Hassan Saadati, Elham Shirali, Seyed Mohammad Jazayeri, Jamal Sarvari

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Azam KhamsehDepartment of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran.
Ali FarhadiDepartment of Medical Laboratory Sciences, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
Somayeh JalilvandDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Fariba YarandiDepartment of Obstetrics and Gynecology, Yas Hospital, Tehran, Iran.
Narges Izadi-MoodDepartment of Pathology, Yas Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Saied GhorbaniDepartment of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran.
Hassan SaadatiDepartment of Epidemiology and Biostatistics, School of Health, North Khorasan University of Medical Sciences, Bojnurd, Iran.
Elham ShiraliYas Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Seyed Mohammad JazayeriResearch Center for Clinical Virology, Tehran University of Medical Sciences, Tehran, Iran. jazayeri42@gmail.com.
Jamal SarvariDepartment of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Science, Shiraz, Iran. sarvarij@sums.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer, one of the most common cancers in women, is primarily driven by high-risk human papillomaviruses (HPV) infections, particularly HPV-16. Co-infection with Epstein-Barr virus (EBV) has been reported to exacerbate disease progression by influencing HPV genome integration. This study examines HPV-16 integration status, p16INK4a expression, and their relationship with EBV co-infection and viral load in cervical cancer cases. In this study, 134 HPV-16-positive formalin-fixed, paraffin-embedded cervical samples were collected and analyzed for HPV-16 viral load, genome integration and EBV co-infection, followed by p16INK4a immunohistochemistry. Statistical analysis was performed to examine the association between viral markers and cervical cancer progression. HPV-16 viral loads varied significantly by histological grade, with the highest loads observed in cervical intraepithelial neoplasia 2 (CIN 2) lesions. HPV integration status revealed episomal forms in 32.8% of samples, mixed forms in 56%, and fully integrated forms in 11.2%. p16INK4a expression correlated with disease progression, increasing with CIN grade and in squamous cell carcinoma (SCC). EBV was detected in 13.4% of samples, but no significant associations were found between EBV infection and HPV integration, viral load, or p16INK4a expression levels. HPV-16 viral load and integration status are strongly associated with cervical lesion severity, while p16INK4a expression increases with lesion grade, indicating its utility as a diagnostic marker. EBV co-infection did not significantly impact lesion progression, suggesting that its role in cervical cancer remains unclear.

Indexed as

CoinfectionCyclin-Dependent Kinase Inhibitor p16Epstein-Barr Virus InfectionsHerpesvirus 4, HumanHuman papillomavirus 16Papillomavirus InfectionsUterine Cervical NeoplasmsViral LoadVirus IntegrationAdultAgedFemaleHumansMiddle AgedUterine Cervical DysplasiaCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16Cervical cancerCINEBVHPV-16Integrationp16INK4a

Identifiers

PMID40065022
PMCPMC11893773

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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.