This study aimed to explore the mechanism by which HIV infection promotes cervical cancer and precancerous lesions.

This was a retrospective observational study including 96 patients with high-risk HPV-16 infection who underwent cervical biopsy, cervical conization, or hysterectomy. Among them, 43 patients were diagnosed with both HIV and cervical cancer or precancerous lesions. High-risk HPV infection (HPV16+) positive samples were collected, and total RNA was extracted and amplified by fluorescence quantitative PCR. The expression of HPV E2 and E6 in cervical tissues of HIV-infected and non-HIV-infected patients with high-risk HPV was determined.

As the degree of cervical tissue lesions increased, the proportions of integrated HPV-16 increased significantly within both HIV-negative (P=0.008) and HIV-positive groups (P=0.027). In comparison to the HIV-positive group, although the HIV-negative group had a higher proportion of free type HPV-16 infection (64.3% vs. 35.7%) and a lower proportion of integrated type infection (41.7% vs. 58.3%), the differences were not statistically significant (P=0.117). The lower the CD4+ T lymphocyte level, the greater the possibility of HPV-16 integrated infection.

Patients with HIV and HPV-16 infection exhibit a significantly higher rate of integrated HPV-16 infection, which is closely linked to HIV-induced immunosuppression, particularly the depletion of CD4+ T lymphocytes. This integration accelerates the progression of cervical lesions, increasing the risk of developing high-grade cervical intraepithelial neoplasia or cervical cancer. These findings underscore the need for targeted screening and therapeutic strategies in HIV-positive women to prevent HPV-related malignancies.