The evolution of HPV infection → cervical cancer What is the evolution from HPV infection to cervical cancer? (Figure 1) ① HPV infection, especially high-risk HPV persistently infects cervical epithelial cells. (Figure 1) ②Cervical epithelial cells are structurally altered, i.e., heterogeneous proliferative changes, resulting in cervical intraepithelial neoplasia, or CIN. ③Cervical pre-cancerous lesions are classified into CIN grade I, CIN grade II, and CIN grade III according to the extent of the lesions. When the heterogeneous proliferative cells are within 1/3 of the epithelium, we call it CIN grade I. When the heterogeneous proliferative cells reach 1/3 but do not exceed 2/3 of the epithelium, we call it CIN grade II, and when the heterogeneous proliferative cells exceed 2/3 of the entire epithelium, we call it CIN grade III. (As shown in Figure 2) (Figure 2) ④ When the heterogeneous proliferative cells occupy the whole epithelial layer but do not break through the epithelial basal layer, it is called carcinoma in situ. The heterogeneous cells break through the basement membrane of the cervical epithelium and form cervical cancer. (Figure 3) (Figure 3) Regression of cervical precancerous lesions – cervical intraepithelial neoplasia (CIN) How high is the risk of progression to cervical cancer for CIN grade I, CIN grade II, and CIN grade III, respectively? It has been reported in the literature that women with CIN grade I, CIN grade II, and CIN grade III have a 4-fold, 14.5-fold, and 16.5-fold higher risk of developing cervical cancer, respectively, than normal women, meaning that the risk of progression to cervical cancer increases with the progression of CIN lesions. CIN grade I lesions progress in 16% of patients, remain unchanged in 22%, and reverse to normal in 62% of patients! When lesions escalate to CIN grade III, nearly 45% of patients will progress further, 23% will maintain their status quo ante, and 32% will go normal. Eighty percent of HPV-infected patients rely on immunity to clear on their own, which we call transient infection. As we have seen in the evolution of the whole process of cervical cancer, 80% of patients infected with HPV can clear the infection by themselves through their own immune resistance, which is called transient infection. However, when the patient’s immunity is not sufficient to clear HPV, the HPV virus is latent in the body for a long time, which is called persistent infection. When the persistent infection reaches 6 to 18 months, especially when high-risk HPV infection exists, CIN may occur; ② CIN further develops into in situ cancer; ③ when heterotypic cells break through the epithelial basement membrane, it evolves into invasive cancer, that is, cervical cancer in the real sense. Therefore, the whole process from HPV infection to cervical cancer development is a slow and gradual process, which takes about 10~12 years (as shown in Figure 4). In such a long time, we have enough time to detect cervical precancerous lesions (CIN) and stop its further progression in time! (Figure 4)