Pin18 Projected Clinical Benefits and Costeffectiveness of an HPV 16/18 Vaccine

Goldie, SJ; Kohli, MA; Grima, Daniel; Weinstein, MC; Wright, TC; Bosch, FX; Franco, E

doi:10.1016/s1098-3015(10)61915-8

Cited by 26 publications

(36 citation statements)

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“…Differences in duration were of a lesser magnitude for other HPV types evaluated. As some natural history models used in policy analyses have modeled persistent HPV infection in the absence of CIN as a separate health state from transient infection (44), it is also interesting to note that persistent HPV infections without detected CIN were generally not found to exist beyond 18 months for HPV-6 and HPV-11 infections or beyond 36 months for HPV-16 and HPV-18 infections.…”

Section: Discussionmentioning

confidence: 99%

Incidence and Duration of Cervical Human Papillomavirus 6, 11, 16, and 18 Infections in Young Women: An Evaluation from Multiple Analytic Perspectives

Insinga¹,

Dasbach²,

Elbasha³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Objective: To estimate the incidence and duration of cervical human papillomavirus (HPV)-6, HPV-11, infections in a population of young American women. Methods: The study population consisted of U.S. women who at baseline were 16 to 23 years of age, reported zero to five lifetime sexual partners, never having been pregnant, and never having had a prior abnormal Papanicolaou test and were enrolled in the placebo arm of a randomized multicenter clinical trial of a HPV-16 L1 virus-like particle vaccine. Women underwent type-specific endocervical/ ectocervical swab HPV DNA testing at f6-month intervals for up to 48 months of follow-up. To contribute persontime in the analyses of type-specific HPV incidence, a woman must have had at least three satisfactory swab specimens available and been negative for the relevant HPV type (HPV-6, HPV-11, HPV-16, or HPV-18) on her first two trial swabs. The duration of incident HPV infections was estimated using Kaplan-Meier survival analysis methods.Results: Person-years of exposure ranged by type-specific analysis from 2,645 to 3,188, with an incidence rate per 100 person-years of 3.6 for HPV-6, 0.4 for HPV-11, 5.4 for HPV-16, and 2.1 for HPV-18. With censoring at the time of treatment for cervical intraepithelial neoplasia, where done, the mean duration of incident infections was 9.3, 8.4, 18.2, and 16.4 months, respectively, for HPV-6 (n = 103), HPV-11 (n = 13), HPV-16 (n = 142), and HPV-18 (n = 62). When the duration of HPV infections was truncated at the time of cervical intraepithelial neoplasia detection (any grade), where applicable, mean duration figures were 8.4, 8.1, 14.0, and 15.1 months for HPV-6, HPV-11, HPV-16, and HPV-18 infections, respectively. Conclusions: Previous studies of the mean duration of cervical HPV infection have been based on prevalent infections and/or featured relatively short duration of follow-up. This study tested women for HPV infection over a period of up to 48 months and observed a mean duration of incident HPV-16/ HPV-18 infections approximately twice that of HPV-6/ HPV-11. (Cancer Epidemiol Biomarkers Prev 2007;16(4):709-15)

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Section: Discussionmentioning

confidence: 99%

Incidence and Duration of Cervical Human Papillomavirus 6, 11, 16, and 18 Infections in Young Women: An Evaluation from Multiple Analytic Perspectives

Insinga¹,

Dasbach²,

Elbasha³

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…and (b) does a DNA-negative state represent complete virologic clearance or immunologic control of infection below detection limits of current HPV assays (i.e., viral latency)? Because of the uncertainty around these parameters, decision models often involve sensitivity analyses in which assumptions about natural immunity and, to a lesser extent, viral latency are varied, and most have found that the prediction from the models is highly sensitive to these assumptions (34)(35)(36).…”

Section: Introductionmentioning

confidence: 99%

The known unknowns of HPV natural history

Gravitt¹

2011

J. Clin. Invest.

313

228

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The discovery that certain high-risk strains of human papillomavirus (HR-HPV) cause nearly 100% of invasive cervical cancer has spurred a revolution in cervical cancer prevention by promoting the development of viral vaccines. Although the efficacy of these vaccines has already been demonstrated, a complete understanding of viral latency and natural immunity is lacking, and solving these mysteries could help guide policies of cervical cancer screening and vaccine use. Here, we examine the epidemiological and biological understanding of the natural history of HPV infection, with an eye toward using these studies to guide the implementation of cervical cancer prevention strategies. IntroductionThe discovery that certain high-risk strains of human papillomavirus (HR-HPV) cause nearly 100% of invasive cervical cancer (1) has spurred a revolution in cervical cancer prevention. Randomized controlled trials (RCTs) have evaluated the efficacy of two prophylactic vaccines: Gardasil (also known as HPV4 or quadrivalent vaccine) targets two of the most carcinogenic HPV genotypes (HPV16 and HPV18), as well as two types responsible for more than 90% of anogenital warts (HPV6 and HPV11), and Cervarix (also known as HPV2 or bivalent vaccine) targets HPV16 and HPV18 alone. The results of the vaccine trials have been summarized in detail elsewhere (2-10), demonstrating nearly complete protection against cervical disease caused by the targeted genotypes in previously uninfected women for up to 8 years (11). In secondary prevention, primary screening using HPV DNA testing alone has been found to have performance comparable or superior to Pap smear-based screening in several large RCTs in Canada and Europe (12-16). The high predictive value of a negative HPV DNA test allows for safe extension of screening intervals to at least once every 3-5 years (17-19), which if broadly adopted would increase the efficiency of cervical cancer screening with minimal impact on cancer risk.The RCTs have demonstrated clear efficacy of HPV-based screening and vaccination, but questions about best practices for implementation remain (20,21). Many of the policy debates stem from specific uncertainties in our understanding of the natural history of HPV infection across the lifespan, and particularly in older women. The current model of HPV and cervical cancer natural history that anchors the decision models used in policy development is outlined in Figure 1 (reviewed in refs. 22, 23). Briefly, women acquire HPV through sexual intercourse with an infected partner, and thus HPV prevalence is high around the age of sexual debut, when exposure is high in the absence of immunity. Infections "clear" within 2 years in more than 90% of individuals (24)(25)(26). Approximately 60% of these infections will induce type-specific seroconversion, and if cervical samples are collected during productive viral infection, they may be associated with mild cervical abnormalities (i.e., low-grade squamous intraepithelial lesions [LSILs] or cervical intraepithelial neoplasia ...

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“…Vaccines for HPV types 16 and 18, which are implicated in f70% of cervical cancers, as well as types 6 and 11, which cause genital warts, have been shown to be effective and may be licensed within the next 12 months (1,2). Modeling studies have indicated that an HPV vaccine could be cost-effective, even alongside existing screening programs (3). Ideally, girls should be vaccinated before the onset of sexual activity, and estimates suggest that introducing HPV vaccination at age 12 alongside the current U.S. screening program could reduce lifetime cervical cancer incidence by up to 94% (3).…”

Section: Introductionmentioning

confidence: 99%

“…Modeling studies have indicated that an HPV vaccine could be cost-effective, even alongside existing screening programs (3). Ideally, girls should be vaccinated before the onset of sexual activity, and estimates suggest that introducing HPV vaccination at age 12 alongside the current U.S. screening program could reduce lifetime cervical cancer incidence by up to 94% (3).…”

Section: Introductionmentioning

confidence: 99%

Mothers' Attitudes towards Preventing Cervical Cancer through Human Papillomavirus Vaccination: A Qualitative Study

Waller

Marlow

Wardle

2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

138

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Prophylactic vaccines against human papillomavirus (HPV) types causing cervical cancer will soon be available. Success of the vaccine relies on parents' willingness to vaccinate their prepubescent daughters. We explored mothers' attitudes towards vaccination. Twenty-four mothers of girls ages 8 to 14 years took part in four focus groups. Discussions covered attitudes to vaccination in general, cancer vaccines, vaccines for sexually transmitted infections (STI), and the HPV vaccine. Discussions were recorded, transcribed, and analyzed thematically. Mothers were broadly provaccination. Some were excited about a cancer vaccine, although there were fears that it might lead to unhealthy behaviors (e.g., smoking). STI vaccines got a mixed reception. Enthusiasm was moderated by concerns about an increase in risky sexual behavior. When provided with information about the HPV vaccine, women were in favor of protecting their daughters from cervical cancer, abnormal Papanicolaou results and, potentially, from cervical screening. Some worried about an increase in promiscuity and risk of other STIs. There was disagreement about the age at which girls should be vaccinated. Although some women thought this question should be medically driven, others were concerned about discussing the vaccine with young girls and preferred to wait until they were older. In conclusion, mothers were broadly in favor of HPV vaccination but had reservations, particularly about vaccinating girls as young as 10. Larger-scale quantitative work is needed to assess acceptability at the population level. If the vaccine is introduced, information provision is likely to be key to ensuring parents understand the rationale for vaccinating at a young age. (Cancer Epidemiol Biomarkers Prev 2006;15(7):1257 -61)

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Pin18 Projected Clinical Benefits and Costeffectiveness of an HPV 16/18 Vaccine

Cited by 26 publications

References 0 publications

Incidence and Duration of Cervical Human Papillomavirus 6, 11, 16, and 18 Infections in Young Women: An Evaluation from Multiple Analytic Perspectives

Incidence and Duration of Cervical Human Papillomavirus 6, 11, 16, and 18 Infections in Young Women: An Evaluation from Multiple Analytic Perspectives

The known unknowns of HPV natural history

Mothers' Attitudes towards Preventing Cervical Cancer through Human Papillomavirus Vaccination: A Qualitative Study

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