This review explores the molecular mechanisms by which human papillomavirus (HPV), particularly high-risk HPV (HR-HPV), contributes to the development of cervical cancer (CaCU). The study highlights ten key mechanisms associated with at least seven of the fourteen hallmarks of cancer, as defined by Hanahan and Weinberg. These mechanisms include HPV infection, cellular tropism, genetic predisposition, viral load, viral physical state, epigenetic regulation, loss of E2 function, deregulated expression of E6/E7 oncogenes, regulation of host cell protein function, and acquisition of the mesenchymal phenotype. The review emphasizes the role of HR-HPVs in inducing genomic instability, promoting uncontrolled cell proliferation, and facilitating tumor progression. It also discusses the importance of understanding these mechanisms for the development of new diagnostic and therapeutic strategies for cervical cancer. The study underscores the need for further research to identify clinically relevant biomarkers that can improve the early detection and treatment of cervical cancer. The review also highlights the significance of HPV vaccination in reducing the global burden of cervical cancer, particularly in low- and middle-income countries. The findings suggest that targeting the molecular pathways involved in HPV-induced carcinogenesis could lead to more effective interventions for the prevention and treatment of cervical cancer.This review explores the molecular mechanisms by which human papillomavirus (HPV), particularly high-risk HPV (HR-HPV), contributes to the development of cervical cancer (CaCU). The study highlights ten key mechanisms associated with at least seven of the fourteen hallmarks of cancer, as defined by Hanahan and Weinberg. These mechanisms include HPV infection, cellular tropism, genetic predisposition, viral load, viral physical state, epigenetic regulation, loss of E2 function, deregulated expression of E6/E7 oncogenes, regulation of host cell protein function, and acquisition of the mesenchymal phenotype. The review emphasizes the role of HR-HPVs in inducing genomic instability, promoting uncontrolled cell proliferation, and facilitating tumor progression. It also discusses the importance of understanding these mechanisms for the development of new diagnostic and therapeutic strategies for cervical cancer. The study underscores the need for further research to identify clinically relevant biomarkers that can improve the early detection and treatment of cervical cancer. The review also highlights the significance of HPV vaccination in reducing the global burden of cervical cancer, particularly in low- and middle-income countries. The findings suggest that targeting the molecular pathways involved in HPV-induced carcinogenesis could lead to more effective interventions for the prevention and treatment of cervical cancer.