Progression Pathways of Human Papillomavirus-Associated Cancer

Human Papillomavirus (HPV) accounts for approximately 30% of all cancers caused by infectious agents. HPV consists of small, non-enveloped DNA viruses belonging to the Papillomaviridae family. To date, over 200 types of HPV, classified into five genera—Alphapapillomavirus, Betapapillomavirus, Gammapapillomavirus, Mupapillomavirus, and Nupapillomavirus—have been identified. The Alphapapillomavirus genus, particularly HPV 16 and 18, is responsible for nearly 5% of all human cancers globally. This includes the majority of cervical carcinoma cases, other anogenital disorders, and an increasing number of oral cancers. Moreover, the Betapapillomavirus genus encompasses HPVs linked to malignant skin tumors in immunocompromised individuals and those with epidermodysplasia verruciformis. High-risk HPVs associated with tumors express proteins that exhibit oncogenic potential by disrupting the cell cycle through interactions with tumor suppressor proteins, thereby facilitating cancer progression. Additionally, these viral proteins significantly influence host immune regulation, aiding in the evasion of immune detection and furthering cancer development. This review will also cover the impact of omics data on understanding how viral oncogenes contribute to malignant transformation.