Relationship between HPV-16 infection and the progression of vaginal intraepithelial neoplasia

To explore the relationship between infection with human papillomavirus (HPV)-16 and the development of vaginal intraepithelial neoplasia (VaIN).

This is a retrospective study. 78 patients with suspected VaIN admitted to the gynecologic clinic of Affiliated Hospital of Guilin Medical College from August 2016 to December 2020 who were confirmed to have HPV-16 infection by HPV rapid flow-through hybridization method were selected as the research subjects. The copy numbers of HPV-16 early genes E2 and E6 were detected by quantitative real-time PCR amplification to analyze the integration status of the virus.

The episomal form of HPV-16 exists in all levels of VaIN. As the pathological level of VaIN increased, the episomal form of HPV-16 gradually decreased, and a disruption of the E2 gene became more frequent. However, there was no significant difference between different levels of VaIN (P>0.05). With the increased severity of cytology results, the percentage of the episomal form of HPV-16 decreased from 76.47% in atypical squamous cells of undetermined significance (ASC-US) to 44.44% in the high-grade squamous intraepithelial lesion (HSIL) (χ =4.780, P<0.05). However, the integrated form of HPV-16 did not increase significantly as the severity of cytology increased (χ²=2.215, P>0.05).

HPV gene integration may occur before the onset of VaIN. However, the occurrence of HPV-16 integration is not a risk factor leading to the malignant progression of VaIN. An E2 gene disruption is more common in the early events after HPV-16 infection. HPV-16 gene integration may be the main reason for persistent HPV-16 infection.