Abstract
The human papillomavirus (HPV) was the first virus known to induce carcinogenesis and is associated with cancers of the uterine cervix, anogenital tumors and malignancies of the head and neck. This paper reviews the structure and basic genomic characteristics of the virus and outlines the clinical involvement of the main HPV serotypes, focusing on the carcinogenic role of HPV-16 and 18. The mechanisms that occur in the development of cervical neoplasia due to the oncogenic proteins E6 and E7 which interfere with the regulation of the cell cycle through their interaction with p53 and retinoblastoma protein are described. Epidemiological factors, diagnostic tools and the management of the disease are also reviewed, along with the available vaccines to prevent the viral infection. Insights on current research on involvement of oxidative stress and micro-RNAs in cervical carcinogenesis are also explored as they may unlock new means of diagnosis and treatment in the future.
Highlights
The human papillomaviruses (HPVs) are a group of small viruses containing deoxyribonucleic acid (DNA) which belong to the Papillomaviridae family
It has been found that HPV DNA features in over 99% of cervical cancer cases; the most common high-risk serotype varies across countries, ethnicities and socioeconomic statuses
The Role of HPV in Cervical Carcinogenesis HPV is the major risk factor for cervical cancer, many researchers speculate that the actual integration of viral DNA in the host cell is not a common event and, most of the time, HPV infection is resolved relatively quickly by the immune system
Summary
The human papillomaviruses (HPVs) are a group of small viruses containing deoxyribonucleic acid (DNA) which belong to the Papillomaviridae family. Review lesions that can predispose one to malignancy of the uterine cervix.[4] It has been found that HPV DNA features in over 99% of cervical cancer cases; the most common high-risk serotype varies across countries, ethnicities and socioeconomic statuses.
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