Abstract
Human papillomaviruses (HPV) are the first viruses to have been acknowledged to prompt carcinogenesis, and they are linked with cancers of the uterine cervix, anogenital tumors, and head and neck malignancies. This paper examines the structure and primary genomic attributes of HPV and highlights the clinical participation of the primary HPV serotypes, focusing on the roles that HPV-16 and 18 play in carcinogenesis. The mechanisms that take place in the progression of cervical neoplasia are described. The oncogenic proteins E6 and E7 disrupt control of the cell cycle by their communication with p53 and retinoblastoma protein. Epidemiological factors, diagnostic tools, and management of the disease are examined in this manuscript, as are the vaccines currently marketed to protect against viral infection. We offer insights into ongoing research on the roles that oxidative stress and microRNAs play in cervical carcinogenesis since such studies may lead to novel methods of diagnosis and treatment. Several of these topics are surfacing as being critical for future study. One particular area of importance is the study of the mechanisms involved in the modulation of infection and cancer development at cervical sites. HPV-induced cancers may be vulnerable to immune therapy, offering the chance to treat advanced cervical disease. We propose that oxidative stress, mRNA, and the mechanisms of HPV infection will be critical points for HPV cancer research over the next decade.
Highlights
Specialty section: This article was submitted to Infectious Diseases, a section of the journal Frontiers in MicrobiologyReceived: 25 April 2018 Accepted: 12 November 2018 Published: 28 November 2018Citation: Wang X, Huang X and Zhang Y (2018) Involvement of Human Papillomaviruses in Cervical Cancer.Front
Human papillomaviruses (HPV) infection is a risk factor for malignancy of the uterine cervix as it has a pivotal role in carcinogenesis via the activation of its genomic products (Cubie, 2013)
In a study featuring over 30,000 cervical cancers, International Agency for Research on Cancer (IARC) showed that of the most frequent HPV serotypes that lead to cervical malignancy (16, 18, 58, 33, 45, 31, 52, 35, 59, 39, 51, and 56), HPV 16 induces more than 50% of cervical cancers, while HPV 16 and 18 together lead to over 70% of cases across the globe (Burd, 2016)
Summary
Specialty section: This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology. As the infected basal cells move up and differentiate, the viral late genes L1 and L2 are transcribed, prompting the vegetative stage of the life cycle distinguished by dramatic amplification of the genome (Narisawasaito and Kiyono, 2007) It appears that control over the expression of late genes depends on the state of differentiation of the host cell (Howley, 2006). While HPV is the greatest risk factor for cervical cancer, many researchers propose that the specific integration of viral DNA in the host cell does not frequently happen, and in the majority of the time, HPV infection is removed quite speedily by the immune system. HPV is able to promote immune evasion through the expression of the E5 oncogene, which is responsible for modulation of several immune mechanisms, including antigen presentation and inflammatory pathways (de Freitas et al, 2017)
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