A cross-sectional analysis about bacterial vaginosis, high-risk human papillomavirus infection, and cervical intraepithelial neoplasia in Chinese women Original paper
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Dr. Umar
Read MoreClinical Pharmacist and Clinical Pharmacy Master’s candidate focused on antibiotic stewardship, AI-driven pharmacy practice, and research that strengthens safe and effective medication use. Experience spans digital health research with Bloomsbury Health (London), pharmacovigilance in patient support programs, and behavioral approaches to mental health care. Published work includes studies on antibiotic use and awareness, AI applications in medicine, postpartum depression management, and patient safety reporting. Developer of an AI-based clinical decision support system designed to enhance antimicrobial stewardship and optimize therapeutic outcomes.
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
What was studied?
This cross-sectional study investigated the BV HPV CIN microbiome relationship by examining how bacterial vaginosis (BV), high-risk human papillomavirus (HR-HPV) infection, and cervical intraepithelial neoplasia (CIN) jointly shape the vaginal microbial ecosystem. Using 16S rRNA sequencing, the research assessed microbial diversity, community structure, and dominant taxa across clinical states in Chinese women. The goal was to identify microbial patterns that mark dysbiosis, illuminate pathways linking BV and HPV persistence, and evaluate whether microbiome composition contributes to CIN risk.
Who was studied?
The study enrolled 624 women aged 25–65 years attending a Beijing hospital, ultimately analyzing 423 qualifying vaginal secretion samples after excluding participants with candidiasis, trichomoniasis, sexually transmitted infections, recent antibiotic use, or insufficient DNA yield. Women were categorized by BV status, HR-HPV infection, and CIN grade. The cohort included 193 HPV-negative and 230 HR-HPV-positive samples; of these, 94 HR-HPV-positive women had biopsy-confirmed CIN. Careful stratification allowed comparison of microbiome patterns across normal, BV-only, HPV-only, BV+HPV, CIN-only, and BV+HPV+CIN groups.
Most important findings
The study found that vaginal microbiome composition shifted substantially with BV, HPV, and CIN. Lactobacillus crispatus dominated in healthy women, but BV and HPV infections each reduced Lactobacillus abundance and increased microbial complexity. Lactobacillus iners was markedly enriched in HPV-positive women, often replacing L. crispatus and defining a transition toward dysbiosis. Women with BV exhibited CST IV patterns characterized by depleted Lactobacillus and increased anaerobes such as Gardnerella, Prevotella, Sneathia, and Megasphaera. Microbial diversity rose sharply in BV, HPV, and co-infected groups, while CIN alone increased compositional complexity without significantly altering richness. Logistic regression identified both BV and HR-HPV as independent CIN risk factors. LEfSe analysis showed strong L. iners enrichment in HPV infection and Prevotellaceae expansion during BV. PICRUSt functional prediction suggested that BV+HPV co-infection enhanced pathways related to transporters, transcription factors, and carbohydrate metabolism, while HPV alone depleted functions involved in amino acid biosynthesis, folate metabolism, and oxidative pathways.
Key implications
These findings highlight that vaginal dysbiosis—particularly loss of Lactobacillus dominance and expansion of anaerobic BV-associated taxa—may amplify HPV persistence and increase CIN risk. L. iners appears central to this transition: adaptable, resilient, and often thriving in intermediate or dysbiotic states, it may facilitate conditions that impair HPV clearance. The study reinforces BV as a clinically meaningful risk factor for CIN and emphasizes the potential value of microbiome-informed screening, prognostication, and therapeutic strategies in gynecologic practice.
Citation
Xu X, Zhang Y, Yu L, et al. A cross-sectional analysis about bacterial vaginosis, high-risk human papillomavirus infection, and cervical intraepithelial neoplasia in Chinese women.Scientific Reports. 2022;12:6609. doi:10.1038/s41598-022-10532-1. s41598-022-10532-1
Bacterial vaginosis (BV) is caused by an imbalance in the vaginal microbiota, where the typically dominant Lactobacillus species are significantly reduced, leading to an overgrowth of anaerobic and facultative bacteria.