Abstract

Infection caused by the human papillomavirus (HPV) is common among the sexually active population worldwide. With 200 known genotypes, 15 of them are considered highrisk oncogenic, with types 16 and 18 being most associated with anogenital and head/ neck cancers. The cell cycle, consisting of the G1, S, G2, and M phases, is regulated by tumor suppressor genes such as Rb and p53, whose dysregulation can result in continuous replication of damaged cells. High-risk HPVs are related to anogenital neoplasias, and the immune response typically eliminates the initial infection, but HPV avoids immune responses during the productive phase of the infection. Viral proteins, including E1, E2, E5, E6, and E7, play critical roles in virus replication and evasion of the immune system. E1 and E2 affect the immune response, while E6 and E7 interact with tumor suppressor genes, promoting viral replication and inhibiting apoptosis.

Keywords

cervical cancer, HPV infection, early detection, immune response, pap smear, cytopathology.