pathogenesis of hpv in cervical cancer

Asiaf A., Ahmad S. T., Mohammad S. O., Zargar M. A. It has been suggested that increased methylation of CpG dinucleotides within E2 binding site (E2BS) on the host genome can modify interaction of different factors and result in abnormal cell differentiation with further disease progression [34]. Cervical cancer can be prevented or found early through screening. McLaughlin-Drubin M. E., Munger K. Viruses associated with human cancer. ACOG American College of Gynecologists and Obstetricians. The link between HPV and cervical squamous cell carcinoma has become well established since the early 80s. Many studies confirmed that persistent infection with an oncogenic HPV type is the main risk factor for detecting a cervical intraepithelial neoplasia (CIN) that may range from CIN1 to CIN3 and cancer [12, 13, 15]. PMC7062568 DOI: 10.1080/01443615.2019.1634030 Abstract Cervical cancer is by far the most common HPV-related disease. These events cause overexpression of E6 and E7 proteins that eventually contribute to viral carcinogenesis by altering cellular apoptotic mechanism [5, 10]. One of the international studies found that 10.4% of patients with normal cytology have been detected with either high- or low-risk HPV types. It is a relatively small, non-enveloped virus of about 55 nm diameter. The age-specific HPV prevalence varies in young and advanced age women populations [49]. 06/21/2023. RETRACTED ARTICLE: Molecular mechanisms in progression of HPV Gupta R., Gupta S., Mehrotra R., Sodhani P. Cervical cancer screening in resource-constrained countries: current status and future directions. HPVs can also cause cancer of the vagina, vulva, penis, and anus, as well as some head and neck cancers, anogenital warts, and recurrent respiratory papillomatosis. Williams VM, Filippova M, Soto U, Duerksen-Hughes PJ. E7, on the other hand, binds pRb causing its inactivation and degradation. Skin-to-skin genital contact is a well-established mode of transmission. Li N, Franceschi S, Howell-Jones R, Snijders PJ, Clifford GM. The exceptionally strong and lasting antibody response has been well documented; for example, the 100% seroconversion rate in young healthy women, preadolescent boys, and girls with antibody response remains stable for over a decade [81]. 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. If these prevention strategies can be implemented in both developed and developing countries, many thousands of lives could be saved. If biopsy is negative for CIN, patients will undergo repeat cytology at 12 months. Only those who can attend a cervical cancer screening will find out if they have it. CIN3 is considered a true precancer with the potential to progress to invasive cancer at a rate of 0.2% to 4% within 12months [16, 18]. A., Lee S. S., Thomas M., Banks L., Javier R. Interactions of the PDZ-protein MAGI-1 with adenovirus E4-ORF1 and high-risk papillomavirus E6 oncoproteins. Burgers W. A., Blanchon L., Pradhan S., Launoit Y. d., Kouzarides T., Fuks F. Viral oncoproteins target the DNA methyltransferases. The authors declare that they have no conflicts of interests with respect to this paper. Nearly all cases of cervical cancer are due to chronic HPV infection (Harro et al 2001). These factors or modifiers of HPV activities include: Immune response to HPV infection is cell-mediated and thus conditions that impair cell-mediated responses such as renal transplantation or HIV disease increase the risk of acquisition and progression of HPV [Calore et al 2001, Cubie et al 2000, Torrisi et al 2000). As a result, this hypermethylation event reduces the binding affinity of the viral regulatory protein E2 to E2BS, thus leading to E6 and E7 overexpression and further epigenetic inhibition of tumor suppressor genes [10]. Cancer screening test useUnited States, 2015. Nygrd M., Saah A., Munk C., et al. The E6/E7 oncoproteins are overexpressed after HPV invasion into the host cervical cells in the form of HPV DNA or viral integration into the hosts genome and are closely related to the development of cervical cancers (Munagala et al 2011). Currently, primary approaches to HPV prevention include both risk reduction and development of vaccines against HPV infection. There is also discrepancy in the frequency of the screening tests among countries and age groups [72]. HPV type can be defined as an entity based on the more than 10% difference in the DNA sequence of the L1 gene between two genomes. Retracted: "Correlation between ER, PR, P53, Ki67 expression, and high Deregulation of miRNA expression can occur mostly due to epigenetic methylation of miRNA promoters [34]. HPV cannot be tested for currently in a regular sexual health checkup. Despite the success of these vaccine candidates, there still remains the concern that conventional expression methods when fully developed might result in very expensive products (Giorgi et al 2010, Rybicki 2014) that will be inaccessible to the resource-constraint countries who have the highest incidences of cervical cancer. The binding of E6 to these proteins leads to inactivation and degradation. Self-collection cervical screening gives patients the option to test For example, according to the report of HPV Information Centre (2017), no data on the epidemiology of HPV infection are available in Kazakhstan (which is a Central Asian country), and only a few articles on the epidemiology of HPV infection in Kazakhstan were published in international peer-reviewed journals and several articles in local medical journals [53]. TU and KK contributed information related to HPV genotypes, epidemiology, and cervical cancer pathogenesis. pRb downregulates E2F a transcription factor. Burk R. D., Harari A., Chen Z. Human papillomavirus (HPV) is the most prominent risk factor for cervical carcinogenesis, and more than 90% of cervical cancers are accompanied by high-risk HPV infection, whose types 16 and 18 . The WHO recommends vaccination for girls aged 9-13 years as this is the most cost-effective public health measure against cervical cancer (Burd 2003, WHO 2009, WHO 2014). Frontiers | Drug repositioning via host-pathogen protein-protein A study investigated the prevalence of HPV infection among the adolescent population in Uganda has shown significantly high distribution of high-risk HPV types (16, 18, 31, 52, and 58), which is 51.4% [57]. . 8600 Rockville Pike Therefore, to address this inaccuracy, the recently created HPV FASTER protocols aim at combining both strategies with the purpose of accelerating the reduction of cervical cancer incidence and mortality, making the programs both cost-effective and sustainable [91]. spontaneously within a year or two. However, the development of rapid molecular methods for the detection of HPV DNA is a milestone in cervical cancer screening in these low-resource settings as these may make the test more feasible in the future and reduce the huge infrastructural requirements (Catarino et al 2015). Bruni L., Diaz M., Castellsagu X., Ferrer E., Bosch F. X., de Sanjos S. Cervical human papillomavirus prevalence in 5 continents: meta-analysis of 1 million women with normal cytological findings. Moreover, cervical cancer screening strategies are different between countries. The HPV genome consists of a single molecule of double-stranded, circular DNA (Favre 1975) with all Open Reading Frame (ORF) protein-coding sequences confined to one strand. Worldwide, pooled data from case-control studies indicated that HPV DNA could be detected in 99.7% of women with histologically confirmed squamous cell cervical cancer compared with 13.4% of control women. Most women's bodies are able to fight HPV infection. Lehoux M., DAbramo C. M., Archambault J. Molecular mechanisms of human papillomavirus-induced carcinogenesis. WHO World Health Organization. HUMAN PAPILLOMAVIRUSES AND CERVICAL CANCER. Upon the viral evolution, accumulation of numerous lineage-defining genetic variations in these regions can lead to speciation into separate HPV types. Natural history of genital human papillomavirus infections In Lacey C (ed.). Insinga R. P., Dasbach E. J., Elbasha E. H. Epidemiologic natural history and clinical management of Human Papillomavirus (HPV) Disease: a critical and systematic review of the literature in the development of an HPV dynamic transmission model. FOIA If any repeat cytology shows ASCUS or greater, referral to colposcopy is recommended. Trends and determinants of human papillomavirus concordance among human immunodeficiency virus-positive and -negative heterosexual couples in rakai, Uganda. Diverse intratumoral heterogeneity and immune microenvironment of two This is a significant risk factor for high-grade cervical disease according to some studies (Adam et 2000, Brisson et al 1994). For example, in sub-Saharan Africa, there were 34.8 new cases and 22.5 deaths per 100,000 women, while in Western Asia there were only 4.4 new cases and 1.9 deaths per 100,000 women in 2012 [44]. Virginia A. Campos N. G., Tsu V., Jeronimo J., Mvundura M., Kim J. J. Evidence-based policy choices for efficient and equitable cervical cancer screening programs in low-resource settings. All authors reviewed and approved the final manuscript. The human papillomavirus replication cycle, and its links to cancer If the biopsy confirms CIN, patients are treated per standard protocol for the management of CIN. Natural history of cervical neoplasia and risk of invasive cancer in women with cervical intraepithelial neoplasia 3: a retrospective cohort study. Perlman S, Wamai RG, Bain PA, Welty T, Welty E, Ogembo JG. Inclusion of HPV vaccine in the national immunization schedule: (i) Cervical cytology (conventional Pap smear and liquid-based), Bivalent: 0, 1, 6 months; tetravalent: 0, 2, 6 months, Low-grade squamous intraepithelial lesion, High-grade squamous intraepithelial lesion. The researchers found HPV DNA in 8977 of the samples, which comprise 85% of all specimens. However, the most plausible mechanism is the local tissue damage occurring during vaginal childbirth or cellular oxidative stress with the increased likelihood of DNA damage and HPV integration (Castle 2004, Williams 2011). Possibly high prevalence of HPV among women in sub-Saharan African countries is more prominent due to high exposure of human immunodeficiency virus (HIV) in the country, and cervical cancer may become epidemic if cervical cancer knowledge is not increased and the barriers for early screening services will still exist [56]. Cervical carcinogenesis is strongly associated with persistent HPV infection that can further affect both the host genome and the viral genome methylation process [34]. However, in some women whose infections continue to persist, the risk of developing precancerous conditions is significant. The virus usually infects the mucocutaneous epithelium and produces viral particles in matured epithelial cells and then causes a disruption in normal cell-cycle control and the promotion of uncontrolled cell division leading to the accumulation of genetic damage (Unger et al 2004). Prevalence of cervical disease at age 20 after immunisation with bivalent HPV vaccine at age 12-13 in Scotland: retrospective population study. The second is called the early region (E) and it consists of ORFs E1, E2, E4, E5, E6, and E7, which are involved in viral replication and tumorigenesis. Several epidemiologic studies have clearly shown that the risk of contracting genital high-risk HPV infection and cervical cancer is influenced by sexual activity (Erickson et al 2013, ACOG 2017). In a recent pilot study, HPV16 E6/E7 oncoprotein test has a satisfactory diagnostic value for cervical cancer screening and demonstrated a better sensitivity than cytological test and better specificity than HPV DNA testing (Zhang et al 2018). Administration of the vaccine is carried out by intramuscular injection with three doses of prime/boost series over a 6-month period. Oncogenic viruses can facilitate various stages of carcinogenesis [1]. Each virion capsid contains about 12 copies of the minor capsid protein, L2 (Sapp et al 1995). It has an icosahedral capsid with 72 capsomers and these contain at least two capsid proteins, L1 and L2. Approximately 5.5-11% of all cervical cancers are reported to be HPV-negative, which can be attributed to truly negative and false-negative results. However, there are many recent studies that have generated promising vaccine candidates tested in clinical trials (Vici 2016, Yang 2016, Kim et al 2017). Furthermore, alpha-PV can be classified into nine groups: alpha-5 (HPV23, 51, 69, and 82), alpha-6 (HPV30, 53, 56, and 66), alpha-7 (HPV18, 39, 45, 59, 68, 70, 85, and 97), and alpha-9 (HPV16, 31, 33, 35, 52, 58, and 67), which include mostly the oncogenic high-risk types [7]. Summary Report. Federal government websites often end in .gov or .mil. HPV can also cause cervical cancer. Cancer screening in the United States, 2017: a review of current American Cancer Society guidelines and current issues in cancer screening. However, HPV infection rates continue to persist, especially in developing countries, where cervical cancer incidence and prevalence are still high. 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. However, overexpression of some miRNAs such as miR-203 inhibits HPV amplification. Barcelona, Spain: ICO Information Centre on HPV and Cancer (HPV Information Centre); 2014. HPV is often spread through sexual contact, is . Reid R., Stanhope C. R., Herschman B. R., Booth E., Phibbs G. D., Smith J. P. Genital warts and cervical cancer. Human papillomavirus (HPV) is the commonest viral infection of the reproductive tract and is one of the most common causes of sexually transmitted infection worldwide (Burd 2003). Results of the population-based survey of adults aged 5070 in England suggest that although awareness of the purpose of early detection screening is high, awareness that screening can prevent cancer is low across all demographic groups [74]. H. Wang, Yulan Jin, et al. Cancer incidence and mortality worldwide: sources, methods and major patterns in GLOBOCAN 2012. Surrogate markers therefore have been proposed to determine vaccines' effectiveness on a shorter term, such as population-based continuous monitoring of high-grade precursor lesions such as CIN3 [89]. It is well known that one of the main causative agents for cervical cancer is high-risk HPV strains, and this type of malignancy is preventable. Indian Journal of Pharmaceutical Sciences. 2012 updated consensus guidelines for the management of abnormal cervical cancer screening tests and cancer precursors. https://www.esmo.org/Oncology-News/FDA-Approves-Gardasil-9-for-Prevention-of-Certain-Cancers-Caused-by-Five-Additional-Types-of-HPV. Although, cervical cancer is more common in older women of 35 years and above, thus suggesting that the infection occurs at a younger age with a slow progression to cancer at an older age. On the other hand, even the nonavalent Gardasil vaccine cannot prevent all cervical cancer cases due to type specificity and time of implementation. The most prevalent types detected were HPV16 (18.4%) and HPV18 (9.22%), followed by HPV types 33, 51, and 52 (nearly 5% each) [53]. These women were aged 20 to 24 years in 2017 at the end of our study. Symptoms . The third is referred to as the late region (L) and this encodes the L1 and L2 ORFs for the viral capsid. Ferlay J., Shin H.-R., Bray F., Forman D., Mathers C., Parkin D. M. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. In postmenopausal women who have ASCUS and clinical or cytologic evidence of atrophy, a 6-week course of intravaginal estrogen is recommended if there are no contraindications to estrogen use. Rositch A. F., Burke A. E., Viscidi R. P., Silver M. I., Chang K., Gravitt P. E. Contributions of recent and past sexual partnerships on incident human papillomavirus detection: acquisition and reactivation in older women. Harro CD, Pang Y-YS, Roden RBS, Hildesheim A, Wang Z, Reynolds MJ, et al. Cervical cancer is the second common female malignant tumor globally which seriously threatens female's health. E6, for example, binds with E6-associated binding protein (E6AP), a ubiquitin ligase leading to a structural change in E6 allowing it to bind with p53, the cell cycle control tumor suppressor protein to form a trimeric complex E6/E6AP/p53 (Figure 1). Correlation between ER, PR, P53, Ki67 Expression and High-Risk HPV Infection in Patients with Different Levels of Cervical Intraepithelial Neoplasia. Qiao YL, Sellors JW, Eder PS, Bao YP, Lim JM, Zhao FH Statistical data from the recent years show that utilization of HPV vaccines is very effective for preventing infection and disease related to the specific HPV genotypes [78]. It should be noted that women who develop cervical cancer have often had the same type of high-risk HPV detected in cervical specimens 3 to 5years prior to their cancer incidence. 140: Management of abnormal cervical cancer screening test results and cervical cancer precursors. Cervical cancer is almost always caused by a HPV infection. To date, over 100 . HPV 18. Other recommended preventive interventions against HPV infections that are appropriate for both boys and girls are education about safe sexual practices including delayed onset of sexual activity; promotion and provision of condoms for those already engaged in sexual activity; male circumcision; and warnings about tobacco smoking. Analysis of human papillomavirus 16 E6, E7 genes and Long Control Region in cervical samples from Uruguayan women. Cervical cancer is by far the most common HPV-related disease (Burd 2003). In addition, the age-specific HPV prevalence varies widely across different populations and showed two peaks of HPV positivity in younger and older women. It appears that smoking is the most important risk factor independent of HPV infection for high-grade cervical disease (Adam et al 2000).
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