Human Papillomavirus Infection and Cervical Cancer: Epidemiology, Screening, and Vaccination-Review of Current Perspectives

Abstract

Viral infections contribute as a cause of 15-20% of all human cancers. Infection by oncogenic viruses can promote different stages of carcinogenesis. Among many types of HPV, around 15 are linked to cancer. In spite of effective screening methods, cervical cancer continues to be a major public health problem. There are wide differences in cervical cancer incidence and mortality by geographic region. In addition, the age-specific HPV prevalence varies widely across different populations and showed two peaks of HPV positivity in younger and older women. There have been many studies worldwide on the epidemiology of HPV infection and oncogenic properties due to different HPV genotypes. However, there are still many countries where the population-based prevalence has not yet been identified. Moreover, cervical cancer screening strategies are different between countries. Organized cervical screening programs are potentially more effective than opportunistic screening programs. Nevertheless, screening programs have consistently been associated with a reduction in cervical cancer incidence and mortality. Developed countries have achieved such reduced incidence and mortality from cervical cancer over the past 40 years. This is largely due to the implementation of organized cytological screening and vaccination programs. HPV vaccines are very effective at preventing infection and diseases related to the vaccine-specific genotypes in women with no evidence of past or current HPV infection. In spite of the successful implementation of the HPV vaccination program in many countries all over the world, problems related to HPV prevention and treatment of the related diseases will continue to persist in developing and underdeveloped countries.

Figure 1

Progression of cervical cancerogenesis which involves HPV gene integration, leading to sustained expression of E6 and E7, impacting and dysregulating the various pathways including the inactivation and degradation of p53 and pRB that lead to uncontrolled cellular division, proliferation, tumor suppressor evasion, and other features of tumorigenicity.