Authors
Maryam Mashhadi Abolghasem Shirazi
Published in
International reviews of immunology. Pages 1-19. Sep 28, 2026. Epub Sep 28, 2026.
Abstract
Persistent infection with high-risk human papillomavirus (HPV) is the essential precursor to cervical carcinogenesis and remains a major global health challenge despite advances in vaccination and screening. While most cervical HPV infections are spontaneously cleared, a subset persists and progresses to cervical intraepithelial neoplasia (CIN) and ultimately invasive cervical cancer. Emerging evidence identifies nuclear factor kappa B (NF-κB) as a central regulator linking antiviral immunity, chronic inflammation, epithelial survival, and disease progression. In this hybrid review, we systematically synthesize clinical evidence regarding NF-κB activation in persistent cervical high-risk HPV infection and integrate mechanistic insights from molecular studies to develop a translational framework for therapeutic intervention. Current data suggest that HPV oncoproteins E6 and E7 selectively reprogram NF-κB signaling, attenuating antiviral interferon responses while maintaining inflammatory pathways that favor viral persistence and immune dysregulation. A stage-dependent model emerges in which early suppression of antiviral signaling is followed by chronic low-grade NF-κB activation, promoting epithelial survival, microenvironmental remodeling, and progression toward high-grade CIN. We further discuss pathway-specific therapeutic opportunities, including selective NF-κB modulation and integration with therapeutic E6/E7 vaccination. Collectively, NF-κB represents a promising biomarker and therapeutic target for host-directed strategies aimed at viral clearance and prevention of cervical cancer progression.
PMID:
42804243
Bibliographic data and abstract were imported from PubMed on 29 Sep 2026.
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