Human papillomavirus (HPV) is divided into 2 categories: 1) oncogenic and 2) non-oncogenic. Infection with oncogenic (or high-risk) HPV is a necessary but not sufficient condition for the development of cervical intraepithelial neoplasia. Therefore, only a small percentage of women infected with HPV will develop severe cervical lesions or cervical cancer. Cervical cancer is currently thought to occur as a result of HPV infection, which can be transient or persistent. Most HPV infections are transient and have a low risk of progression. Only a small proportion of infections are persistent, but persistent infection for 1 and 2 years strongly predicts the risk of progression to CIN 3 or cervical cancer, regardless of age. It is not entirely clear what factors contribute to persistent HPV infection. HPV-16 has the strongest oncogenic potential and is associated with approximately 55-60% of all cervical cancer cases worldwide; HPV-18 is second, with 10-15% of patients associated with it. The remaining cervical cancers are associated with approximately 12 additional HPV subtypes. Co-factors known to cause persistent HPV infection include smoking, immune system deficiency, and HIV infection. HPV infection is often seen in adolescents and women in their 20s, with infection rates decreasing with age. Most young women, especially those younger than 21 years of age, are able to clear HPV infection through an effective immune response within an average of 8 months, or 85-90% of women have reduced their viral load to a negative test within 8-24 months. In this population, most cervical lesions regress spontaneously as the infection clears. For women aged 30-65 years, the natural course of HPV infection does not change with age. For women aged 30 years and older, persistent infection after new HPV infection is unlikely. However, women older than 30 years of age are more likely to present with persistent infection. This is consistent with an increase in the incidence of high-grade squamous intraepithelial lesions (HSILs) with increasing age. Considering that low-grade cervical lesions (or CIN1), a manifestation of acute HPV infection, have a high probability of regression to normal tissue, it is recommended that expectant treatment is feasible. In contrast, the clinical management of CIN2 is currently controversial, and the problem lies in the difficulty of accurate diagnosis and ideal treatment. The prognosis of CIN2 appears to be a mixture of low- and high-grade lesions, which are difficult to distinguish simply by histology, rather than just being a separate intermediate lesion. Considering the limitations of the CIN2 classification, the ASCCP and the American Academy of Pathology adopted a revised 2-level histologic classification (low-grade squamous intraepithelial lesions (LSILs] and HSILs), eliminating CIN2 as a separate classification. In a cohort study of untreated CIN3 patients, the cumulative incidence of 30-year invasive cervical cancer was 30.1%, indicating that CIN3 is at great risk of progression to cancer. The time required for disease progression needs to be considered when assessing the appropriate screening interval. Most HPV-associated cervical lesions progress very slowly, and the exact time to progression from CIN 3 to cancer is not known, but the time to progression from CIN 3 to cancer varies by age of diagnosis and screening and remains lengthy. Therefore, less frequent screening is appropriate for this slower disease process.