Molecular Mechanisms of Human Papillomavirus-Induced Cervical Carcinogenesis

Approximately 15–20% of all tumors are generally associated with infectious agents and these infectious agents are normally underappreciated. Approximately 85% of all cervical cancer deaths are reported in low–middle-income countries, almost 18% higher than in developed countries. More than a third of cervical cancer cases globally were reported in Asian countries, China, and India. However, Human Papillomavirus (HPV) still remains a very common etiological agent in cervical cancer patients worldwide. As we know, cervical cancer is one of the major causes of death of women globally, and high-risk HPVs (HPV 16 and 18) are associated with cervical carcinogenesis. The present chapter comprehensively emphasized the molecular mechanism of HPVs, their structural organization and etiopathogenesis caused by its early region oncoproteins (E), and their contribution to the progression of cervical carcinogenesis. E proteins are the major contributors to the progression of the disease. Viral integration, its replication, and transcription are mainly the outcomes due to E1, E2, and E4 proteins, while E6 and E7 are important contributors which act as oncoproteins. In this chapter, the structural organization and biological functions of all the E proteins of HPV and their role in the initiation and progression of cervical cancer are comprehensively discussed.