Figure 1.
The HPV-microbiome-biofilm triad. Schematic representation of bidirectional interactions between HPV infection (including E6/E7-driven oncogenic activity), cervicovaginal dysbiosis, and bacterial biofilm formation (e.g., Gardnerella). These interconnected processes modulate host immune and inflammatory signaling (e.g., IL-36g, NF-kB), promoting HPV persistence, treatment failure/recurrence, and progression to cervical intraepithelial neoplasia and cancer. Co-infections are shown as additional modulators of the system.
