The article discusses the mechanisms by which human papillomavirus (HPV) induces oncogenesis. It begins with historical context, noting that HPV was long suspected as the cause of warts, and provides early experimental evidence supporting this theory. The article then explains that HPV is a small, nonenveloped virus that infects squamous epithelia and causes warts. It describes the classification of HPV into mucosal and cutaneous types, with high-risk and low-risk categories based on their potential to cause malignant progression. High-risk HPV types, such as HPV-16, are associated with cervical cancer and other anogenital malignancies. The article details the genomic structure of HPV, its life cycle, and the role of key viral proteins, particularly E6 and E7. These proteins are central to the oncogenic process, as they inactivate tumor suppressor proteins like p53 and pRB, leading to uncontrolled cell proliferation. The integration of the HPV genome into the host chromosome is a critical step in the transformation process, leading to the expression of E6 and E7 genes and the loss of other viral genes. The article also explores the role of telomerase activation in HPV-induced immortalization and the contribution of HPV oncoproteins to genomic instability. The article highlights the mechanisms by which HPV E6 and E7 proteins contribute to oncogenesis, including their ability to destabilize the retinoblastoma (pRB) protein and inactivate p53, which are essential for cell cycle regulation. It also discusses the role of HPV in inducing centrosome abnormalities, which can lead to mitotic defects and aneuploidy. The article concludes with a comparison of high-risk and low-risk HPV types, noting that high-risk HPV is more likely to cause malignant progression due to its ability to maintain infected cells in a stem cell-like state, facilitating long-term persistence. The study emphasizes the importance of understanding the molecular interactions of HPV oncoproteins in the context of cancer development and progression.The article discusses the mechanisms by which human papillomavirus (HPV) induces oncogenesis. It begins with historical context, noting that HPV was long suspected as the cause of warts, and provides early experimental evidence supporting this theory. The article then explains that HPV is a small, nonenveloped virus that infects squamous epithelia and causes warts. It describes the classification of HPV into mucosal and cutaneous types, with high-risk and low-risk categories based on their potential to cause malignant progression. High-risk HPV types, such as HPV-16, are associated with cervical cancer and other anogenital malignancies. The article details the genomic structure of HPV, its life cycle, and the role of key viral proteins, particularly E6 and E7. These proteins are central to the oncogenic process, as they inactivate tumor suppressor proteins like p53 and pRB, leading to uncontrolled cell proliferation. The integration of the HPV genome into the host chromosome is a critical step in the transformation process, leading to the expression of E6 and E7 genes and the loss of other viral genes. The article also explores the role of telomerase activation in HPV-induced immortalization and the contribution of HPV oncoproteins to genomic instability. The article highlights the mechanisms by which HPV E6 and E7 proteins contribute to oncogenesis, including their ability to destabilize the retinoblastoma (pRB) protein and inactivate p53, which are essential for cell cycle regulation. It also discusses the role of HPV in inducing centrosome abnormalities, which can lead to mitotic defects and aneuploidy. The article concludes with a comparison of high-risk and low-risk HPV types, noting that high-risk HPV is more likely to cause malignant progression due to its ability to maintain infected cells in a stem cell-like state, facilitating long-term persistence. The study emphasizes the importance of understanding the molecular interactions of HPV oncoproteins in the context of cancer development and progression.