EC Gynaecology

Cervical cancer represents a significant public health issue worldwide, particularly prominent among women in low- and middle-income countries. It is the fourth most common malignancy among women globally. It is predominantly caused by a persistent infection with high-risk types of human papillomavirus (HPV). Out of the more than 200 types identified, approximately 14 are considered high-risk for the development of cervical cancer [8]. HPV types 16 and 18 are the most dangerous, responsible for about 70% of all cervical cancer. The virus infects the basal cells of the epithelium, where it usually remains in a non-replicative state. As the infected cells differentiate and move towards the surface, the virus begins to replicate, completing its life cycle without causing cell death [10]. This non-lytic lifecycle allows the virus to persist unnoticed by the host immune system which has an oncogenic potential. In a small fraction of infections, HPV DNA integrates into the host genome. This integration disrupts the usual virus lifecycle and the regulation of viral oncogenes, E6 and E7. These genes are pivotal in the progression to cancer; they encode proteins that can inactivate tumor suppressor pathways involving p53 and retinoblastoma (Rb) proteins, eventually leading to malignant transformation. Understanding the virology of HPV and its interaction with the host factors provides crucial insights into the mechanisms of cervical cancer development. This knowledge is fundamental in guiding the development of preventive strategies, such as vaccines and targeted therapies, and improving screening methods to detect precancerous changes early.

 Keywords: Virology; Carcinoma of Cervix; Human Papillomavirus (HPV); Retinoblastoma (Rb)

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