<p>Ovarian cancer, an aggressive gynecological tumor, is primarily driven by persistent inflammation and resistance to conventional treatments. High-risk human papillomavirus (HR-HPV) has been identified as a potential contributing factor to disease development. In this narrative review, we integrate current findings on how HPV infection intersects with molecular and immune pathways in OC. The viral oncoproteins E6 and E7 dismantle key tumor suppressors such as p53 and retinoblastoma protein (pRb), while simultaneously activating inflammatory circuits like NF-κB and STAT3, resulting in continuous cytokine release and immune dysfunction. HPV also interferes with innate antiviral defenses, including Toll-like receptor and cGAS–STING pathways, thereby evading immune clearance. In parallel, hormonal regulators such as estrogen further enhance viral activity and amplify pro-inflammatory signaling within ovarian tissues. We argue that HPV-driven inflammation represents a significant but understudied mechanism in ovarian tumor biology. Recognizing this relationship provides new opportunities for therapeutic innovation. Targeted interventions ranging from cytokine inhibitors and STING activators to immune checkpoint therapy and hormone-modulating agents offer promising strategies to interrupt the viral–inflammatory cycle that sustains tumor progression. Ultimately, HPV may not serve as a primary cause of ovarian cancer, but it likely functions as a powerful enhancer of inflammation and oncogenic signaling. Clarifying this contribution reshapes our understanding of ovarian carcinogenesis and points toward novel translational approaches for prevention and treatment.</p>