The cervicovaginal microbiome (CVMB) is pivotal in maintaining the homeostasis of the lower female genital tract and has emerged as a significant modulator of cervical carcinogenesis. Although persistent infection with high-risk human papillomavirus (HR-HPV) is a prerequisite for the development of cervical intraepithelial neoplasia (CIN) and subsequent cervical carcinoma, it remains insufficient alone to drive oncogenesis. Accumulating evidence suggests that alterations in the CVMB composition profoundly impact HPV persistence, local immune responses, and disease progression. A vaginal microbiota dominated by Lactobacillus species, most notably Lactobacillus crispatus, correlates with low microbial diversity, robust immune regulation, and facilitated HPV clearance. Conversely, microbial dysbiosis—characterized by Lactobacillus depletion and a concomitant proliferation of anaerobic taxa, typical of Community State Type (CST) IV and Lactobacillus iners-dominated profiles—is strongly associated with chronic inflammation, oxidative stress, epithelial barrier compromise, and an elevated risk of CIN progression. This review synthesizes current evidence regarding the multifaceted interactions among the cervicovaginal microbiome, HPV pathogenesis, immune dysregulation, and oxidative stress in the etiology of CIN. Elucidating these intricate host–microbiome dynamics may precipitate the discovery of novel microbiome-derived biomarkers, ultimately informing innovative prophylactic and therapeutic interventions for cervical cancer.
Knap-Wielgus et al. (Tue,) studied this question.