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Human Papillomavirus (HPV) is the most common cause of sexually transmitted diseases and causes a wide range of pathologies including cervical carcinoma. Integration of the HR-HPV DNA into the host genome plays a crucial role in cervical carcinoma. An alteration of the pRb pathways by the E7 proteins is one of the mechanisms that’s account for the transforming capacity of high-risk papillomavirus. For the proper understanding of the underline mechanism of the progression of the disease, the present study investigate the correlation of concentration of host pRb protein, viral E7 oncoprotein and viral load in early and advanced stages of cervical carcinoma. It was found that the viral load in early stages (stage I & II) was less (log10 transformed mean value 2.6 and 3.0) compared to advanced stages (stage III & IV) (Log10 transformed value 5.0 and 5.8) having high expression of HPV E7 onco-protein and reduced level of pRb protein, signifying the role of viral load and expression level of E7 oncoprotein in the progression of cervical cancer.

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<abstract> <p>Cervical cancer is the sequel of a multi-factorial, long-term unresolved disease that includes genetic, epigenetic, and viral components responsible for its development and progression. It is the second most common cancer of females in India. Human papillomavirus (HPV) is considered the primary causative agent of pre-neoplastic and cancerous lesions and 90% of all cervical carcinomas are linked to high-risk HPV type 16 and type 18. Although most HR-HPV infections are asymptomatic, transient, and self-limiting, the persistent infection with a high risk (HR-HPV) may cause precancerous lesions that can progress to cervical cancer. HPV type 16 is the most common HPV in India associated with more than 75% of cervical cancer, followed by HPV type 18 and other high-risk types. Infection with HPV alone is not sufficient for the development of cervical cancer but there is the involvement of some host genetic factors also that are responsible for the development and progression of cervical cancer. This article briefly reviews molecular pathogenesis, viral load, and the interaction of HPV oncoprotein E6 and E7 with host cellular markers in the progression of cervical cancer.</p> </abstract>