The ‘Why and How’ of Cervical Cancers and Genital HPV Infection

Knowing about the virology of human papillomavirus (HPV) including its structure, functions and mechanism of infection, helps in understanding the disease process and morphology of precancerous lesions for cervical cancer. Two types of HPV, low- and high-risk type, adopt different mechanisms of infection which cannot be differentiated on morphological basis. In addition to HPV infection, many other factors such as genetic predisposition, hormonal factors, host immune response, and multiple sexual partners can modify the course and progression of the disease. The viral genome comprises early and late proteins. These early and late genes are expressed in particular course of time after initial infection. Various products of early genes (E1–E7) coordinate for completion of viral life cycle in maturing squamous epithelium by utilizing replication factors and DNA polymerase enzyme of the host cell nucleus. The late genes are mainly concerned with packaging of the viral particles and their release through mature squamous cells. The episomal form of infection seen in the low-risk group of viruses results in productive infection whereas the integrated form seen in high-risk group of viruses is the basis of disruption of host cell growth cycle by inactivating two important tumor suppressor genes p53 and Rb gene by products of E6 and E7 genes. Cervical precancerous lesions and cancer are the resultant effect of the accumulation of mutations. This article discusses the virology of HPV, pathogenesis of HPV infection, and various other factors modifying the disease course.