Human Papillomavirus Infection and Cervical Cancer

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Table of Contents

Abstract
Introduction
Pathogenesis and Epigenetics of HPV
Incidence and Prevalence of HPV
Methods of Detection
Methods of Prevention
Conclusion
References

Abstract

The paper is devoted to the explanation of links between human papillomavirus (HPV) and cervical cancer. Previous research findings suggest that HPV infection leads to cancerogenesis and impairment of the host’s normal cell cycle, resulting in cervical dysplasia. Besides a description of HPV pathogenesis and epigenetics, the paper provides an overview of the global incidence and prevalence rates pertaining to infection and cervical cancer. In addition, major methods for the detection and prevention of HPV-associated cancer are identified. It is revealed that regular screening with cytology and HPV tests may help to decrease mortality risks and improve treatment outcomes, whereas HPV vaccination can reduce the overall risk of cervical cancer development.

Introduction

Cervical cancer is associated with a significant burden of morbidity and mortality among women worldwide and especially among those living in lower- and middle-income countries. According to Mwaka et al. (2016), 83% of newly diagnosed cervical cancer cases out of the total number of 500,000 occur in less advanced regions. Moreover, over 80% of all diagnoses take place there at late stages of the disease and, therefore, usually result in poor treatment outcomes (Mwaka et al. 2016). One of the major reasons defining both high incidence and late diagnosis of cervical cancer is insufficient awareness of risk factors and early symptoms of the disease. Based on this, the present paper will aim to describe such a major risk of this cancer as HPV infection and explain its effects on the human body. It is worth noting that HPV accounts for about 600,000 cases of cervical, oropharyngeal, anal, and vulvovaginal cancers each year globally (Bansal, Singh, & Rai, 2016). Considering that effective methods for HPV treatment do not exist nowadays, the issue of its prevention is of particular importance, and it will be addressed in this paper as well.

Pathogenesis and Epigenetics of HPV

HPV belongs to the family of non-enveloped DNA viruses, also known as Papillomaviridae. By now, researchers have discovered over a hundred HPV types that can be either low-risk or high-risk, depending on their taxonomic rank and oncogenic potential. Among them all, HPV 16 and 18 genotypes are linked to cancer development more than other types and account for about 70% of all HPV-related cancer diagnoses (Plesa et al., 2016). As for the mode of HPV infection, it usually occurs through sexual contact, yet the cases of non-sexual transmission through fomites have been reported as well (Bansal, Singh, & Rai, 2016). Among the key risk factors contributing to HPV infection are early engagement in sexual activity, multiple sexual partners, and utilization of oral contraceptives (Bansal, Singh, & Rai, 2016). It is observed that in many instances, the infection becomes cleared by the immune system after entering the body (Bansal, Singh, & Rai, 2016). Nevertheless, persistent HPV infection leads to oncogenesis through the mechanism of abnormal cellular transformation and genetic alterations, which are closely interrelated.

To understand, how HPV affects the host cells, it is important to look at the replication and growth mechanisms of the virus. According to Bansal, Singh, and Rai (2016), “the genome of HPV consists of double-stranded cDNA and encodes DNA sequences for six early (E1, E2, E4, E5, E6, and E7) and two late proteins (L1 and L2) (p. 86). E4 and E5 proteins are mainly responsible for virus assembly and growth, whereas E1 and E2 proteins participate in virus replication and regulation of expression of E6 and E7 – oncoproteins contributing to the pathogenesis of cancer (Bansal, Singh, & Rai, 2016). As stated by Plesa et al. (2016), E6 and E7 oncoproteins have to transform properties and actively interact with many host cell proteins. It is also observed that E6 plays a major role in the loss of p53 protein, which functions as a tumor suppressor and is responsible for healthy cell transformation in the human body (Plesa et al., 2016; Bansal, Singh, & Rai, 2016). In this way, the virus reenters the host cell DNA replication cycle and causes progressive genetic damage.

At the molecular level, HPV-associated disruption of the cell cycle and the consequent uncontrolled cell division become manifested as cervical intraepithelial neoplasia (CIN). According to Georgescu et al. (2018), CIN is a precancerous lesion that functions as a precursor of cervical cancer. Different types of CIN, classified by their degree of dysplasia as mild, moderate, and severe, are asymptomatic and can either regress spontaneously or develop into cancer over years (Georgescu et al., 2018). Like in the case of the HPV virus itself, the immune system normally helps to suppress the progression of dysplastic lesions (Georgescu et al., 2018). It means that immunocompromised women bear a greater risk of CIN progression into invasive cancer.

Incidence and Prevalence of HPV

HPV infection is extremely common and is considered to affect almost every sexually active individual at some point in their life (Centers for Disease Control and Prevention, n.d.). At the same time, the prevalence of HPV-related cancers is higher in women than in men. According to de Martel, Plummer, Vignat, and Franceschi (2017), at the global level, the number of cancers attributed to HPV equates to 570,000 in females and only 60,000 in males. Among them, 530,000 new diagnoses are for cervical cancer (de Martel et al., 2017). Noteworthily, approximately 50% of those cases are diagnosed in women under 50 years old and over two-thirds – in less developed countries, particularly in the South-Eastern ones, such as India, as well as sub-Saharan Africa (de Martel et al., 2017).

As for mortality due to HPV-associated cervical cancer, it is higher in countries with a lower Human Development Index (HDI). HDI refers not only to the level of economic development but also to the existence and effectiveness of local policies, infrastructures, and evidence-based practices aimed to promote the healthy lives of individuals and communities (United Nations Development Programme, n.d.). As reported by Forman et al. (2012), the 5-year survival rate in women diagnosed with cervical cancer is “less than 20% in low HDI countries and more than 65% in very high countries” (p. F12). This disparity may be linked to the regularity and quality of screening for HPV and cervical cancer, education about risk factors, and so forth.

Methods of Detection

Cervical cancer screening procedures usually include cytology and molecular HPV tests. According to Hoste, Vossaert, and Poppe (2013), screening with cytology alone, with 2- to 3-year intervals, has proved to reduce mortality due to cervical cancer in countries with fairly good access to high-quality screening. This decline in the number of deaths can be attributed to early detection of cancer and timely implementation of treatment for preinvasive lesions in women (Hoste, Vossaert, & Poppe, 2013). However, it is observed that false-positive cytology results are very common (Hoste, Vossaert, & Poppe, 2013). At the same time, molecular HPV tests are associated with greater sensitivity. They allow a better prediction of whether a woman will develop a severe form of CIN by identifying the presence of HPV, virus type, and consequently, the risk of cervical cancer (Hoste, Vossaert, & Poppe, 2013). It is valid to say that the combination of these two methods within reasonable screening intervals may lead to the more successful identification of cervical cancer at the early stages of its development.

Methods of Prevention

As in the case with many other sexually transmitted infections, HPV can be prevented through educational interventions aimed to reduce risk-taking behaviors in individuals, encourage them to use condoms, and so forth. However, considering that HPV is highly prevalent nowadays, changes in behavior may result only in limited success. It is suggested that HPV vaccination deems to be more promising and successful in terms of infection prevention. As stated by Hoste, Vossaert, and Poppe (2013), “universal vaccination against HPV 16 and 18 might prevent up to 80% of invasive [cervical cancer] worldwide, considering an additional cross protection against HPV strains not included in the HPV 16-18 vaccine” (p. 2). The World Health Organization (2018) claims that HPV vaccines, which are now being marketed across many countries, are very safe and highly effective. Therefore, educational interventions should aim to promote HPV vaccination among individuals and communities in order to ensure a substantial degree of coverage.

Conclusion

HPV and HPV genotypes 16 and 18, in particular, are the major cause of cervical cancer development. As the findings of the literature review demonstrate, the virus leads to cervical dysplasia and cancerogenesis. Thus, it affects the host at both epigenetic and molecular levels. As epidemiological data also make it clear, mortality rates due to HPV-related cervical cancer are much greater in less developed counties with lower access to high-quality care and screening. At the same time, regular performance of screening procedures is essential for early detection of cancer and its timely and successful treatment. In addition, HPV vaccination is regarded as one of the most efficient methods for the prevention of cervical cancer nowadays. For decreasing the prevalence and incidence of both HPV and cervical cancer, vaccination should become a universal practice.

References

Bansal, A., Singh, M. P., & Rai, B. (2016). Human papillomavirus-associated cancers: A growing global problem. International Journal of Applied & Basic Medical Research, 6(2), 84-89.

Centers for Disease Control and Prevention. (n.d.). Human papillomavirus (HPV) statistics. Web.

de Martel, C., Plummer, M., Vignat, J., & Franceschi, S. (2017). Worldwide burden of cancer attributable to HPV by site, country, and HPV type. International Journal of Cancer, 141(4), 664-670.

Forman, D., de Martel, C., Lacey, C. J., Soerjomataram, I., Lortet-Tieulent, J., Bruni, L., … Franceschi, S. (2012). Global burden of human papillomavirus and related diseases. Vaccine, 30, F12-F23.

Georgescu, S. R., Mitran, C. I., Mitran, M. I., Caruntu, C., Sarbu, M. I., Matei, C., … Tampa, M. (2018). New insights in the pathogenesis of HPV infection and the associated carcinogenic processes: The role of chronic inflammation and oxidative stress. Journal of Immunology Research, 2018, pp. 1-10.

Hoste, G., Vossaert, K., & Poppe, W. A. (2013). The clinical role of HPV testing in primary and secondary cervical cancer screening. Obstetrics and Gynecology International, 2013, 1-7.

Mwaka, A. D., Orach, C. G., Were, E. M., Lyratzopoulos, G., Wabinga, H., & Roland, M. (2016). Awareness of cervical cancer risk factors and symptoms: Cross-sectional community survey in post-conflict northern Uganda. Health expectations: An International Journal of Public Participation in Health Care and Health Policy, 19(4), 854-867.

Plesa, A., Iancu, I. V., Botezatu, A., Huica, I., Stoian, M., & Anton, G. (2016). The involvement of epigenetic mechanisms in HPV‐induced cervical cancer. Web.

United Nations Development Programme. (n.d.). Human Development Index (HDI). Web.

World Health Organization. (2018). Human papillomavirus (HPV). Web.

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