Molecular, immunological and oncogenic mechanisms of cervical cancer mediated by HPV/HIV co-infection, clinical implication and management

Abstract

Human papillomavirus (HPV) and human immunodeficiency virus (HIV) co-infection pose a major public health challenge, especially in regions with high HIV prevalence. HIV-induced immunosuppression increased the persistence of high-risk HPV infection to cervical cancer. HPV E6 and E7 oncoproteins inhibit p53 and pRB, the major tumor suppressor proteins. HIV proteins Tat and Nef promote oncogenic processes and immune depletion. This leads to persistent inflammation and immunological exhaustion, which accelerate cervical cancer development in HIV/HPV co-infection. The clinical implication is significant, with higher risks of cervical intraepithelial neoplasia (CIN) and cervical cancer, highlighting the significance of integrated care. To reduce the burden of cervical cancer in HIVpositive women, integrated strategies are needed, including regular screening per WHO guidelines, expanded vaccination, improved access to treatment (surgery, chemoradiation, and emerging immunotherapies), and contextspecific research into therapeutic vaccines and biomarkers. Future research should focus on integrating cervical cancer screening and HPV testing into HIV care. While incorporating AI-assisted triage tools into routine cervical screening programs to enhance early detection, optimize resource utilization, and improve patient outcomes in high-risk populations.