Cervical cancer causes significant morbidity and mortality worldwide, particularly in areas with limited access to HPV vaccination and screening. Persistent infection with high-risk HPV genotypes, particularly HPV-16 and HPV-18, is the primary initiating event in its development, but does not explain why only a subset of those infected develop the disease. The cervicovaginal microbiome affects the epithelial barrier, local immunity and inflammatory balance. Communities dominated by Lactobacillus crispatus are associated with antiviral states and mucosal stability, while profiles enriched in anaerobes (CST IV) lead to chronic inflammation and more severe lesions. Microbial metabolites interact with HPV oncogenes and host epigenetic regulation. Studies have linked the microbiome to HPV persistence, cervical intraepithelial neoplasia (CIN), and cancer progression. Microbiome biomarkers and interventions such as probiotics have potential, but evidence is limited by methodological heterogeneity.