Human papillomavirus (HPV) infection is the major cause of cervical cancer and its precursor, cervical intraepithelial neoplasia (CIN), and HPV testing has therefore been proposed for improved triaging and follow-up of women treated for CIN. We compared two common HPV DNA detection tests (Hybrid Capture II [HCII] and PCR-enzyme immunosorbent assay (EIA) using the primers GP5؉/GP6؉ followed by HPV typing with reverse dot blot hybridization) for sensitivity and specificity for detection of CIN and of CIN recurrence after treatment. Two hundred and thirty-nine women referred to the Department of Obstetrics and Gynaecology in Västerås, Sweden, were enrolled because of atypical Pap smears; 177 of these were later treated for dysplasia by conization or loop diathermy. Samples for HPV DNA testing were taken before and 4 to 6 months after treatment. There was substantial agreement between the HCII and PCR-EIA (kappa, 0.70 before treatment and 0.72 after treatment). The sensitivity for histopathologically confirmed CIN III was 100.0% for PCR-EIA and 95.6% for HCII. For patients with CIN II or worse (CIN II؉), the sensitivities were 92.9% (PCR-EIA) and 91.8% (HCII). The specificities for CIN II؉ in the pretreatment setting were 30.4% for PCR-EIA and 24.1% for HCII. After treatment, the sensitivities for CIN III in cytology were 100.0% by both methods, and for CIN II؉, sensitivities were 80.0% by both methods. The specificities for CIN II؉ in the posttreatment setting were 83.5% for PCR and 85.4% for HCII. In conclusion, the sensitivities of both PCR-EIA and HCII are high and almost equal, suggesting that both methods are suitable as tools for detection and posttreatment follow-up of CIN II-III.Cancer of the cervix is the third most common form of cancer among women worldwide, with almost 400,000 new cases each year (28). The principal cause of invasive cervical cancer and its precursor lesions is infection with oncogenic types of human papillomavirus (HPV) (3,4,15,21,24,34,40), which is found in close to 100% of cancers (39). A recent case control study reported that HPV types 16,18,31,33,35,39, 45, 51, 52, 56, 58, 59, 68, 73, and 82 conferred increased risk for cervical cancer and that HPV types 6,11,40, 42, 43, 44, 54, 61, 70, 72, and 81 did not increase the cervical cancer risk (23). A meta analysis of all studies of cervical cancer found that the most important HPV type in squamous cell carcinomas is HPV 16, followed by HPV 18, 45, 31, and 33 (7). In adenocarcinomas, the most common type is HPV 18 followed by HPV 16 and 45 (7).In young women, the incidence of HPV infection is high, but the infection is often of short duration (16). The prevalence of high-risk (HR) HPV DNA is highest among sexually active teenagers, declining in women 20 to 30 years of age, and is still lower in women over the age of 30 (4, 19). Persistent HR HPV infections, which are more common in older women, greatly increase the risk of cervical intraepithelial neoplasia (CIN) (33) or cervical cancer, especially if the viral load is high (15,16,3...