Fig. 3
From: A review of the carcinogenic potential of human papillomavirus (HPV) in urological cancers
HPV and developing cancer. High-potential viruses have fine-tuned adaptations that allow them to take advantage of the host’s basal cells in the cutaneous and mucosal epithelium. Once the viral replication cycle is complete, the viral particles are released during cell division by desquamation from infected cells, which serve as a reservoir for the virus. Cervical epithelial cells in the transformation zone develop lesions when infected with HR-HPV for an extended period. Due to viral integration and cell change, lesions can disappear or advance to the first, second, and third phases of cervical intraepithelial neoplasia (CIN) (CIN1, CIN2, and CIN3). The CIN lesions are categorized according to their degree of severity. Invasive carcinoma develops from low-grade squamous intraepithelial lesions (LSIL), progressing to high-grade intraepithelial lesions (HSIL) [62]