Figure 1.

Distribution of normal and human papillomavirus (HPV)-infected squamous epithelial cells in normal, precancerous lesions (mild, moderate and severe dysplasia; CIN 1, CIN 2, and CIN 3, respectively) and cancer of the cervix. The initial stage of carcinogenesis is controlled by viral HPV integration and host factors. HPV enters the basal epithelial cells through a micro-wound. Subsequently, the virus integrates its genome into the host genome in the nucleus through nuclear envelope breaks. Once it enters the nucleus, HPV takes over control of the host genome, self-replicates, and spreads throughout the epithelium. Further replication of the viral genome causes the host cells to grow irregularly and in a disorganized manner compared to normal cells. Subsequently, the virions are sloughed off with the dead squamous cells of the host epithelium, facilitating further transmission.