Correlation between HPV-16 integration status and cervical intraepithelial neoplasia and cervical cancer in patients infected with HIV

Abstract

Background

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

Methods

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.

Results

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.

Conclusions

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.