HPV and cervical cancer: an investigative review into molecular biology, immune evasion and the implications in carcinogenesis

• DOI: 10.15406/jcpcr.2024.15.00560
• Publication Date: 2024-10-19T06:38:05Z
• Authors: Diogo José Horst; Axel Baumgarten O...; Jaime Antônio Mac...
• Keywords: Evasion (ethics); Surgical oncology; Psycho-oncology; Gynecologic oncology

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