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INTERNATIONAL CONGRESS OF

CancerGenetics

• The Vaginal Microbiome and HPV-Driven Carcinogenesis: A Structured Review

• Maryam Dehghani,^1,* Seyedeh Sogand Majidi,²
  1. Midwifery student -Islamic Azad University -Tehran Medical Branch
  2. Midwifery student -Islamic Azad University -Tehran Medical Branch
  
  
  
• Introduction: Persistent infection with high-risk human papillomavirus (hrHPV) is necessary but not sufficient for cervical carcinogenesis. Most HPV infections clear spontaneously, yet a subset progresses to high-grade cervical intraepithelial neoplasia (CIN) or cancer, suggesting additional cofactors influence viral persistence and malignant transformation. The vaginal microbiome (VMB) has emerged as a critical determinant of HPV outcomes. Community state types (CSTs) dominated by Lactobacillus spp., particularly L. crispatus, are generally protective, promoting mucosal integrity, local immunity, and viral clearance. In contrast, diverse, anaerobe-enriched CSTs (CST IV), featuring taxa such as Gardnerella vaginalis, Sneathia/Fannyhessea, Prevotella, and Atopobium vaginae, are associated with elevated vaginal pH, chronic inflammation, epithelial barrier disruption, and increased risk of persistent HPV infection and lesion progression.
• Methods: We performed a narrative structured review of peer-reviewed literature indexed in PubMed and Web of Science (ISI) from 2011 to 2025. Search terms included “vaginal microbiome/microbiota,” "HPV,” “cervical intraepithelial neoplasia,” “persistence,” and “cervical cancer.” Eligible studies comprised observational cohorts, longitudinal analyses, interventional trials, and systematic reviews emphasizing omics-based approaches. Extracted data included sequencing platform (16S rRNA vs. shotgun metagenomics), CST classification, taxonomic composition, microbial metabolites, immune correlates, and clinical outcomes such as HPV persistence, clearance, and CIN progression or regression.
• Results: Across multiple populations, hrHPV persistence and high-grade lesions consistently correlate with reduced Lactobacillus abundance—especially L. crispatusd enrichment of anaerobic bacteria. Mechanistic studies indicate that dysbiosis alters the vaginal microenvironment by raising pH, reducing lactic acid and bacteriocin production, disrupting epithelial barriers, and promoting a pro-inflammatory milieu rich in cytokines such as IL-6 and TNF-α. Multi-omics analyses reveal that microbial metabolites can influence host DNA methylation, epithelial gene expression, and HPV oncogene activity, collectively contributing to lesion progression. Longitudinal studies demonstrate that vaginal microbiome instability predisposes women to persistent infection, whereas stable Lactobacillus-dominated communities are associated with spontaneous viral clearance. Early interventional studies suggest that restoration of Lactobacillus dominance, via probiotics or targeted microbiome modulation, can reduce inflammation and potentially enhance HPV clearance. However, evidence from controlled trials with CIN endpoints remains limited, emphasizing the need for rigorous clinical evaluation.
• Conclusion: The vaginal microbiome functions as a biological gatekeeper in HPV natural history. Lactobacillus-dominated CSTs protect against persistent infection and lesion progression, while dysbiotic, anaerobe-enriched communities increase susceptibility to CIN and cervical cancer. Integrating microbiome profiling into HPV screening and vaccination programs could refine risk stratification, identifying women at highest risk despite negative cytology or immunization. Future priorities include standardized CST reporting, longitudinal multi-omics studies to understand mechanistic pathways, and randomized controlled trials evaluating microbiome-targeted interventions for prevention and management of HPV-related disease.
• Keywords: Vaginal microbiome, HPV, Cervical neoplasia, Dysbiosis, Lactobacillus