Long term protection against cervical infection with the human papillomavirus: Review of currently available vaccines

Romanowski, Barbara

doi:10.4161/hv.7.2.13690

Cited by 104 publications

(76 citation statements)

References 43 publications

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“…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)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

The known unknowns of HPV natural history

Gravitt¹

2011

J. Clin. Invest.

318

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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Section: Introductionmentioning

confidence: 99%

The known unknowns of HPV natural history

Gravitt¹

2011

J. Clin. Invest.

318

228

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“…In October, 2009, the FDA approved HPV vaccination of girls and women, aiming to reduce cervical cancer incidences. The vaccines are known to protect the vaccinated individuals against persistent cervical HPV infection for up to 5-8 years, and effectively prevents precancerous to cancerous change of cervical cells due to HPV infection [26,27]. An HPV vaccine was recently approved (the Gardasil Ò vaccine) for use in boys and men due to convincing epidemiologically link to HPV-related cancers in males (including HPV/OPSCC, anal and penile cancers.).…”

Section: Hpv Vaccinesmentioning

confidence: 99%

Primary Chemotherapy and Radiation as a Treatment Strategy for HPV-Positive Oropharyngeal Cancer

Lui

Grandis

2012

Head and Neck Pathol

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The incidence of human papillomaviruspositive oropharyngeal cancer (HPV/OPSCC) is rapidly increasing, which will represent a major public health burden for decades to come. Although HPV/OPSCC is generally associated with a better prognosis than HPV-negative OPS-CC, the survival rate of individuals with higher-risk clinical and pathologic features remains unchanged. Emerging evidence suggests that HPV/OPSCC is pathologically and molecularly distinct from HPV-negative OPSCC. This review focuses on summarizing treatment strategies for HPV/OPSCC by reviewing the peer-reviewed literature and noting ongoing and planned clinical trials in this disease. We also discuss the potential of designing targeted therapy based on the recent genomic findings of HPV/OPSCC.Keywords HPV/OPSCC Á Chemotherapy Á Radiation HPV-Related Head and Neck Cancer (HNC) and Related-Deaths on the RiseThe incidence of oropharyngeal squamous cell carcinoma (OPSCC), a site for head and neck cancer (HNC), is rising in developed countries including the US and Europe. In the past 2 decades, reports indicate that up to 70-80 % of OPSCC (the most common type of head and neck SCC in year 2010 [1]) in these developed countries are HPVpositive [2]. In fact, the number of HPV-positive OPSCC (hereafter named as HPV/OPSCC) is expected to continue to rise (due to oral sex, multiple sex partners, and premarital sex), while that of HPV-negative OPSCC has been decreasing since 1991 (which parallels the drop in smoking in the US). In fact, the total annual cases of HPV/OPSCC alone are predicted to outnumber that of all cervical cancer cases in the US by 2020 [1].HPV/OPSCC patients are treated with standard chemoradiation therapy or surgery with a generally high response rate [3]. However, treatment is often complicated by morbidities and the positive prognostic benefit of HPV can be mitigated by negative prognostic factors, such as smoking and lymph node metastases [4,5]. Recurrence, metastasis, and second primary cancer still account for the majority of deaths from HPV/OPSCC. The appreciable number of deaths from recurrence or treatment failure (*15 to 18/100, even with the most aggressive current treatment [6,7]), coupled with a dramatic surge in total number of HPV/OPSCC suggests that the total number of deaths from both HPV-positive and HPV-negative OPSCCs will be comparable. More strikingly, a recent study revealed that the highest-risk HPV/OPSCC patients had a 3-year overall survival of only 70.8 %, while the overall survival for the highest-risk HPV-negative OPSCC was 46 % [8] (original data can be found in Fig.

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“…men who have sex with men [11]). In addition, the vaccines available differ in licensed indication, efficacy, levels of cross-protection and long term immunogenicity [12], as well as price and the required number of doses.…”

Section: Introductionmentioning

confidence: 99%