Abstract: Objective To investigate the pathogenic role of high risk HPVs and genomic integration of HPV 16/18 DNA in vulvar intraepithelial neoplasia (VIN) patients. Methods Hybrid Capture HPV DNA assay and PCR were performed to detect high-risk HPVs and HPV 16/18 positive samples. Then RT-PCR, nested PCR and Southern blotting analysis were used in HPV 16/18 positive samples for the amplification and analysis of papillomavirus oncogene transcripts. Results In 32 cases of VIN patients, 24(75%) high-risk HPVs were detected, 23 were HPV 16, and only 1 was HPV 18. Genomic integration of HPV 16/18 was observed in 8 cases of VIN Ⅲ (7 HPV 16 and 1 HPV 18). Except 1 case of VIN Ⅱ, 15 of 23 HPV-16 positive specimens displayed HPV16 episomal transcripts, 7 displayed integrated transcripts. Conclusions HPV 16 is positive in most cases of VIN Ⅱ and VIN Ⅲ. Integration of HPV 16/18 oncogene only occurs in VIN Ⅲ. It is concluded that the integration of high-risk HPVs oncogene is related with the occurrence, and the development to vulvar cancer, of VIN.

Key words: Papillomavirus, human, Vulvar intraepithelial neoplasia, Virus integration