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Over the past several decades, the concept that human papillomavirus (HPV) can induce tumor formation has become well established. Persistent infection with high-risk HPV (hrHPV) types constitutes the primary risk factor for the development of nearly all cervical cancers, as well as a substantial proportion of malignant tumors of the vagina and vulva. The presence and abundance of certain bacterial species may confer protective effects against HPV infection and facilitate viral clearance, thereby reducing the risk of precancerous lesions in these anatomical sites. Conversely, other bacterial taxa may contribute to the promotion of pathological conditions. Consequently, elucidating the composition of the vaginal microbiota and its dysbiotic alterations in relation to HPV infection and persistence may enhance the predictive accuracy regarding infection outcomes. Furthermore, the precise identification of bacterial components associated with HPV-induced pathology holds potential clinical relevance and may inform alternative therapeutic strategies. Current technological advancements enable rapid, high-throughput analysis of the vaginal microbiome, which can be applied in longitudinal studies to delineate the roles of specific bacterial species in the initiation, prevention, progression, or regression of HPV-related cervical, vaginal, and vulvar lesions. Genetic and environmental factors that underlie the differential outcomes between viral clearance and cancer development remain an active area of investigation, with the microbiome emerging as a critical element that may modulate this balance by either promoting or inhibiting viral infection.
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Fu et al. (2026) studied this question.
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