Abstract:

Persistent infection with high-risk human papilloma virus (HPV) is the key prerequisite for cervical carcinogenesis. However, most infections are cleared by the host immunity system, indicating that additional factors collaborate to drive the oncogenic process. The reproductive tract microbiome primarily inhabits the vaginal and cervical mucosa, where it maintains microenvironmental homeostasis and resists pathogen invasion through mechanisms such as metabolite production and competitive exclusion. Studies indicate that throughout the disease progression from simple HPV infection to cervical intraepithelial neoplasia (CIN) and ultimately to invasive cervical cancer, the reproductive tract microbiome undergoes dynamic remodeling, characterized by Lactobacillus depletion and a significant increase in anaerobic diversity. This dysbiosis not only disrupts the cervical-vaginal mucosal barrier to facilitate HPV integration, but also promotes malignant transformation by inducing persistent chronic inflammation and releasing specific metabolites. Therefore, microbiome-based intervention strategies hold translational promise for blocking HPV infection progression, aiding cervical cancer diagnosis, and enhancing the efficacy while reducing the toxicity of chemoradiotherapy.

Key words: Uterine cervical neoplasms, Carcinoma, Vagina, Cervix uteri, Reproductive tract, Microbiota, Papillomaviridae