The aim of this paper was to evaluate the factors that predict regression of untreated CIN 2 and 3. A total of 93 patients with colposcopic persistent CIN 2 and 3 lesions after biopsy were followed for 6 months. Human papillomavirus (HPV) types were determined by polymerase chain reaction at enrolment. We analysed the biologic and demographic predictors of natural regression using univariate and multivariate methods. The overall regression rate was 52% (48 out of 93), including 58% (22 out of 38) of CIN 2 and 47% (26 out of 55) of CIN 3 lesions (P ¼ 0.31 for difference). Human papillomavirus was detected in 84% (78 out of 93) of patients. In univariate analysis, 80% (12 out of 15) of lesions without HPV regressed compared to 46% (36 out of 78) of lesions with HPV infection (P ¼ 0.016). Women without HPV and those who had a resolution of HPV had a four-fold higher chance of regression than those with persistent HPV (relative odds ¼ 3.5, 95% CI ¼ 1. 4 -8.6). Women with five or fewer lifetime sexual partners had higher rates of regression than women with more than five partners (P ¼ 0.003). In multivariate analysis, HPV status and number of sexual partners remained as significant independent predictors of regression. In conclusion, HPV status and number of lifetime sexual partners were strongly predictive of regression of untreated CIN 2 and 3. Cervical cancer continues to be the most deadly female cancer in developing countries. (Ponten et al, 1995) The dramatic decrease in mortality rates in Western countries is attributed to cervical cancer screening. (Harlan et al, 1991) The successful implementation of these screening programmes is based on the underlying model that cervical intraepithelial lesions (CIN) behave as progressive stages of a biologic continuum towards the development of invasive cervical cancer (Richart and Barron, 1969;Campion et al, 1986).Genital human papillomavirus (HPV) infection has been established as the critical step in the development of most cervical cancers (IARC, 1995). The cervical carcinogenesis model involves HPV infection, intraepithelial neoplasia, and invasion. Human papillomavirus infection is found in over 40% of young, sexually active, college students (Ho et al, 1998). However, the incidence of cervical cancer is uncommon compared to the lifetime cumulative incidence of viral infection. Thus, there must be essential biological mechanisms and associated risk factors other than HPV infection that are responsible for the progression of precursor lesions to invasive cervical cancer (Schiffman & Brinton, 1995).The aetiology and risk factors involved with cervical carcinogenesis are amenable to study as invasive cervical cancer typically arises after many years from a morphologically defined precancerous lesion. However, since untreated high-grade lesions can progress to invasive cancer, most women with CIN 2 or 3 are treated promptly. Accordingly, there are few reports on the natural history of high-grade dysplasia. On the other hand, not all CIN lesions progress to invasive canc...