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Association between Quantitative High-Risk Human Papillomavirus DNA Load and Cervical Intraepithelial Neoplasm Risk

¹ Department of Nursing of Tatung Hospital, Kaohsiung Municipal United Hospital; ² Graduate Institute of Basic Medicine, Departments of ³ Gynaecology and Obstetrics and ⁴ Occupational and Environmental Medicine and Family Medicine, Kaohsiung Medical University; ⁵ Bureau of Health; ⁶ Department of Family Medicine, I-Shou University and Hospital, Kaohsiung, Taiwan; and ⁷ Department of Family Medicine, China Medical University and Hospital, Taichung, Taiwan

Requests for reprints: Ming-Tsang Wu, Graduate Institute of Occupational Safety and Health, Kaohsiung Medical University, Building CS 917, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan. Phone: 886-7-312-1101, ext. 2315; Fax: 886-7-322-1806. E-mail: mingtsangwu{at}yahoo.com

Human papillomavirus (HPV) infection is a high-risk factor for cervical intraepithelial neoplasm (CIN) but the association between the quantitative HPV DNA load and the severity of CIN remains controversial. We conducted a community study to investigate the correlation between the two. Potential study subjects were selected through Pap smear screening in Kaohsiung County, Taiwan. Ninety-one subjects with either their first case of inflammation or CIN1 by biopsy confirmation were assigned to a case group; 175 normal subjects with negative findings by Pap smears or biopsies were assigned to a control group. Cervical HPV load was detected with Hybrid Capture II assay for high-risk HPV infection, with nested PCR for high- and low-risk HPV infection, and with type-specific PCR for HPV type 16 (HPV-16). Individuals with positive high-risk HPV infection had an increased risk of developing CIN. Compared with HPV-negative subjects, the odds ratios were 32.2 [95% confidence interval (95% CI), 10.4-99.5] for subjects with CIN1, 37.2 (95% CI, 7.4-187.6) for subjects with CIN2, and 68.3 (95% CI, 14.1-328.5) for subjects with CIN3 after adjusting for other confounding factors. The similar trend was also found among the HPV-16–negative individuals. In addition, high-risk HPV DNA load levels were highly correlated with the different grades of CINs in the overall population (Spearman's correlation coefficient r = 0.67, P < 0.0001, n = 266) and the HPV-16–negative population (Spearman's correlation coefficient r = 0.58, P < 0.0001, n = 234). We concluded that high-risk HPV infection, irrespective of HPV-16 infection, was highly and positively associated with the development of CIN.

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