The impact of Human Papillomavirus vaccination on cervical cancer prevention efforts

Division of Gynecologic Oncology, Washington University School of Medicine, St Louis, MO 63110, USA.
Gynecologic Oncology (Impact Factor: 3.77). 05/2009; 114(2):360-4. DOI: 10.1016/j.ygyno.2009.04.005
Source: PubMed


To review concepts, information, obstacles, and approaches to cervical cancer screening and prevention as vaccination against human papillomavirus (HPV) types 16 and 18 is adopted.
Expert forum, conducted September 12-13, 2008, hosted by the Society of Gynecologic Oncologists, including 56 experts in cervical cancer and titled Future Strategies of Cervical Cancer Prevention: What Do We Need to Do Now to Prepare?
The current approach to cervical cancer screening in the U.S. is limited by its opportunistic nature. If given to women before exposure, a vaccine against HPV 16,18 can decrease cervical cancer risk by up to 70%. The impact on abnormal cytology and cervical intraepithelial neoplasia (CIN) will be less but still substantial. As the prevalence of high-grade CIN falls, fewer women with positive screening tests will have truly preinvasive disease. To minimize harm from false positive tests in women who are at low risk for cancer because of early vaccination, later initiation of and longer intervals between screenings are ideal. However, the vaccine is less effective when administered after first intercourse, and delivering and documenting HPV vaccination to girls at optimal ages may prove difficult.
Until population-based data on the performance of cytology, HPV testing, and alternate screening or triage interventions become available, modifying current screening guidelines is premature. Current recommendations to initiate screening as late as age 21 and to screen less often than annually are appropriate for young women known to have been vaccinated before first intercourse.

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Available from: Mark H Einstein, Dec 10, 2014
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    • "Forty different HPV types infect the anogenital mucosa; 15 have been associated with carcinogenesis. HPV-16 and 18 account for most of the invasive cervical and anal cancers, although co-infection with other carcinogenic genotypes occurs (Armstrong, 2010; Massad et al., 2009; Schiller et al., 2012). Gardasil Ò , a quadrivalent vaccine (types 6, 11, 16 and 18), and Cervarix Ò , a bivalent vaccine (types 16 and 18), prevent new HPV infections (Schiller et al., 2012). "
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    ABSTRACT: Commercial vaccines against human papillomavirus (HPV) have low uptake due to parental autonomy, dosing regimen, cost, and cold chain storage requirements. Carrageenan (CG)-based formulations prevent HPV infection in vitro and in vivo but data are needed on the durability of anti-HPV activity and the effect of seminal plasma (SP). The Population Council’s PC-515 gel and the lubricant Divine 9 were tested for their physicochemical properties and anti-HPV activity against HPV16, 18, and 45 pseudoviruses (PsVs). Anti-PsV activity was estimated using the luciferase assay in HeLa cells and the HPV PsV luciferase mouse model. Formulations were applied intravaginally either 2 h pre/2 h post (-2 h/+2 h) or 24 h pre (-24 h) relative to challenge with HPV16 or 45 PsV in PBS or SP/PBS. Both formulations showed broad-spectrum anti-HPV activity in vitro (IC50: 1-20ng/ml), significantly decreasing HPV PsV infection in the mouse model (-2h/+2h, p<0.0001). PC-515 protected better than Divine 9 in the -24 h dosing regimen (p<0.0001) and comparable to Divine 9 in the -2 h/+2 h regimen (p=0.9841). PC-515 retained full activity in the murine model when PsV solutions contained human SP. The durable, potential broad-spectrum anti-HPV activity of CG formulations in the presence of SP supports their further development to prevent HPV acquisition.
    Antiviral Research 06/2014; 108:88-93. DOI:10.1016/j.antiviral.2014.05.018 · 3.94 Impact Factor
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    • "Although current vaccines protect against two of the HPV types which cause around 70% of cervical cancers, another 13 types are established high-risk and a further 3 are probably high-risk [5]. Because of these other types, as well as the fact that no vaccine is 100% effective, cervical cancer screening programmes need to continue in some form, regardless of vaccination programmes [5,17]. Implementation of such “competing” programmes (in the sense that they may compete for the attention and compliance of women at risk) may harm some groups if, post-vaccination, behavioural changes either increase the risk of acquisition of non-vaccine oncogenic HPV types, or reduce the uptake of effective screening and follow-up treatment of pre-clinical abnormalities. "
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    ABSTRACT: Background The global and within-country epidemiology of cervical cancer exemplifies health inequity. Public health programs may reduce absolute risk but increase inequity; inequity may be further compounded by screening programs. In this context, we aimed to explore what the impact of human papillomavirus (HPV) vaccine might have on health equity allowing for uncertainty surrounding the long-term effect of HPV vaccination programs. Methods A simple static multi-way sensitivity analysis was carried out to compare the relative risk, comparing after to before implementation of a vaccination program, of infections which would cause invasive cervical cancer if neither prevented nor detected, using plausible ranges of vaccine effectiveness, vaccination coverage, screening sensitivity, screening uptake and changes in uptake. Results We considered a total number of 3,793,902 scenarios. In 63.9% of scenarios considered, vaccination would lead to a better outcome for a population or subgroup with that combination of parameters. Regardless of vaccine effectiveness and coverage, most simulations led to lower rates of disease. Conclusions If vaccination coverage and screening uptake are high, then communities are always better off with a vaccination program. The findings highlight the importance of achieving and maintaining high immunization coverage and screening uptake in high risk groups in the interest of health equity.
    BMC Public Health 10/2012; 12(1):935. DOI:10.1186/1471-2458-12-935 · 2.26 Impact Factor
  • CytoJournal 09/2009; 6:17. DOI:10.4103/1742-6413.55885
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