Epidemiologic Approaches to Evaluating the Potential for Human Papillomavirus Type Replacement Postvaccination

Tota, Joseph E.; Ramanakumar, Agnihotram V.; Jiang, Mengzhu; Dillner, Joakim; Walter, Stephen D.; Kaufman, Jay S.; Coutlée, François; Villa, Luisa L.; Franco, Eduardo L.

doi:10.1093/aje/kwt018

Cited by 91 publications

(121 citation statements)

References 70 publications

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“…It was previously discussed that the relatively higher prevalence of HPV16 may result in under detection of low-copy HPV co-infections, particularly when the same amplification primers are used for HPV16 and other HPV types (50). Using an epidemiological approach, Tota et al (51) hypothesized that eradicating vaccine-targeted HPV16 and 18 enhances the chance of other HPV types not targeted by the vaccine to occupy the ecological niche created by the extinction of HPV16 and 18. Due to cross-protection against other HPV types with current vaccines and the upcoming implementation of novel multivalent vaccines against the majority of the HR-HPV types diminishes the risk of type replacement (52).…”

Section: Discussionmentioning

confidence: 99%

Shift in prevalence of HPV types in cervical cytology specimens in the era of HPV vaccination

Fischer

Bettstetter²,

Becher

et al. 2016

Oncology Letters

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Abstract. The aim of the present population-based cohort study was to analyze the association between the prevalence of 32 types of human papilloma virus (HPV) in 615 female patients with abnormal cervical cytopathology findings. In total, 32 HPV types were screened by DNA array technology. HPV infection was detected in 470 women (76.42%), 419 of whom (89.15%) were infected with ≥1 high-risk (HR)-HPV type. HPV16, which is recognized as the main HR-HPV type responsible for the development of cervical cancer, was observed in 32.98% of HPV + participants, followed by HPV42 (18.09%), HPV31 (17.66%), HPV51 (13.83%), HPV56 (10.00%), HPV53 (8.72%) and HPV66 (8.72%). The prevalence of HR-HPV types, which may be suppressed directly (in the case of HPV16 and 18), or possibly via cross-protection (in the case of HPV31) following vaccination, was considerably lower in participants ≤22 years of age (HPV16, 28.57%; HPV18, 2.04%; HPV31, 6.12%), compared with participants 23-29 years of age (HPV16, 45.71%; HPV18, 7.86%; HPV31, 22.86%), who were less likely to be vaccinated. Consequently, the present study hypothesizes that there may be a continuous shift in the prevalence of HPV types as a result of vaccination. Furthermore, the percentage of non-vaccine HR-HPV types was higher than expected, considering that eight HPV types formerly classified as 'low-risk' or 'probably high-risk' are in fact HR-HPV types. Therefore, it may be important to monitor non-vaccine HPV types in future studies, and an investigation concerning several HR-HPV types as risk factors for the development of cervical cancer is required.

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Section: Discussionmentioning

confidence: 99%

Shift in prevalence of HPV types in cervical cytology specimens in the era of HPV vaccination

Fischer

Bettstetter²,

Becher

et al. 2016

Oncology Letters

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“…Rapid evaluation of which vaccination strategies work best to reduce the spread of the HPV infection is therefore potentially useful for exchanging experiences of which HPV vaccination strategies that work best. Finally, there is a possibility that eradication of HPV vaccine types may result in an increase of nonvaccine HPV types, socalled type replacement (9). Conversely, cross-protection against HPV types not included in the vaccine may result in declines also of nonvaccine types (10).…”

Section: Introductionmentioning

confidence: 99%

Change in Population Prevalences of Human Papillomavirus after Initiation of Vaccination: The High-Throughput HPV Monitoring Study

Söderlund-Strand

Uhnoo

Dillner

2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Organized human papillomavirus (HPV) vaccination was introduced in Sweden in 2012. On-demand vaccination was in effect from 2006 to 2011. We followed the HPV prevalences in Southern Sweden from 2008 to 2013.Methods: Consecutive, anonymized samples from the Chlamydia trachomatis screening were analyzed for HPV DNA for two low-risk types and 14 high-risk types using PCR with genotyping using mass spectrometry. We analyzed 44,146 samples in 2008, 5,224 in 2012, and 5,815 in 2013.Results: Registry-determined HPV vaccination coverages of the population in Southern Sweden increased mainly among 13-to 22-year-old women. Most analyzed samples contained genital swabs from women and the HPV6 prevalence in these samples decreased from 7.0% in 2008 to 4.2% in 2013 [À40.0%; P < 0.0005 (c 2 test)].

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“…One possible explanation was a potential bias against the vaccine due to technicalities in the PCR methodology used for HPV DNA testing (15). The broad-spectrum L1-based SPF 10 PCR-DEIA system has 10 primers that target relatively well-conserved genomic sequences, permitting the simultaneous amplification of at least 64 HPV genotypes in a single test.…”

Section: Discussionmentioning

confidence: 99%

“…The present analysis investigated the hypothesis that the discrepant efficacy results for persistent infection versus lesional endpoints for some nonvaccine HPV types might be due to a technical issue in the PCR methodology used for HPV DNA detection (15). The protocol-specified testing algorithm for PATRICIA included the broad-spectrum L1-based SPF 10 PCR DNA immunoassay (DEIA) line probe assay (LiPA 25 ) system (here referred to as SPF 10 PCR-DEIA/LiPA 25 ) and type-specific PCRs for HPV-16 and HPV-18 (16, 17) but did not include type-specific PCRs for nonvaccine HPV types.…”

mentioning

confidence: 99%

Post Hoc Analysis of the PATRICIA Randomized Trial of the Efficacy of Human Papillomavirus Type 16 (HPV-16)/HPV-18 AS04-Adjuvanted Vaccine against Incident and Persistent Infection with Nonvaccine Oncogenic HPV Types Using an Alternative Multiplex Type-Specific PCR Assay for HPV DNA

Struyf

Colau

Wheeler

et al. 2015

Clin Vaccine Immunol

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; GlaxoSmithKline Vaccines, King of Prussia, Pennsylvania, USA bb The efficacy of the human papillomavirus type 16 (HPV-16)/HPV-18 AS04-adjuvanted vaccine against cervical infections with HPV in the Papilloma Trial against Cancer in Young Adults (PATRICIA) was evaluated using a combination of the broad-spectrum L1-based SPF 10 PCR-DNA enzyme immunoassay (DEIA)/line probe assay (LiPA 25 ) system with type-specific PCRs for HPV-16 and -18. Broad-spectrum PCR assays may underestimate the presence of HPV genotypes present at relatively low concentrations in multiple infections, due to competition between genotypes. Therefore, samples were retrospectively reanalyzed using a testing algorithm incorporating the SPF 10 PCR-DEIA/LiPA 25 plus a novel E6-based multiplex type-specific PCR and reverse hybridization assay (MPTS12 RHA), which permits detection of a panel of nine oncogenic HPV genotypes (types 16, 18, 31, 33, 35, 45, 52, 58, and 59). For the vaccine against HPV types 16 and 18, there was no major impact on estimates of vaccine efficacy (VE) for incident or 6-month or 12-month persistent infections when the MPTS12 RHA was included in the testing algorithm versus estimates with the protocol-specified algorithm. However, the alternative testing algorithm showed greater sensitivity than the protocol-specified algorithm for detection of some nonvaccine oncogenic HPV types. More cases were gained in the control group than in the vaccine group, leading to higher point estimates of VE for 6-month and 12-month persistent infections for the nonvaccine oncogenic types included in the MPTS12 RHA assay (types 31, 33, 35, 45, 52, 58, and 59). This post hoc analysis indicates that the per-protocol testing algorithm used in PATRICIA underestimated the VE against some nonvaccine oncogenic HPV types and that the choice of the HPV DNA testing methodology is important for the evaluation of VE in clinical trials. (This study has been registered at ClinicalTrials.gov under registration no. NCT00122681.) P ersistent infection with oncogenic human papillomavirus (HPV) is a necessary prerequisite for the development of invasive cervical cancer (ICC) (1). HPV type 16 (HPV-16) and HPV-18 are found in approximately 70% of cases (2-5). Other common oncogenic HPV types causing ICC include types 31, 33, 35, 45, 52, and 58 (2-5). GlaxoSmithKline Vaccines has developed a prophylactic vaccine against HPV types 16 and 18, formulated with the AS04 adjuvant system. This vaccine has been shown to be immunogenic and efficacious and to have a clinically acceptable safety profile (6)(7)(8)(9)(10)(11)(12)(13)(14).In the large, randomized, double-blind, controlled Papilloma Trial against Cancer in Young Adults (PATRICIA) (ClinicalTrials.gov registration no. NCT00122681), the HPV-16/18 AS04-adjuvanted vaccine prevented persistent infections and highgrade cervical lesions associated with HPV types 16 and/or 18 (11-13) and showed high efficacy against cervical intraepithelial

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Epidemiologic Approaches to Evaluating the Potential for Human Papillomavirus Type Replacement Postvaccination

Cited by 91 publications

References 70 publications

Shift in prevalence of HPV types in cervical cytology specimens in the era of HPV vaccination

Shift in prevalence of HPV types in cervical cytology specimens in the era of HPV vaccination

Change in Population Prevalences of Human Papillomavirus after Initiation of Vaccination: The High-Throughput HPV Monitoring Study

Post Hoc Analysis of the PATRICIA Randomized Trial of the Efficacy of Human Papillomavirus Type 16 (HPV-16)/HPV-18 AS04-Adjuvanted Vaccine against Incident and Persistent Infection with Nonvaccine Oncogenic HPV Types Using an Alternative Multiplex Type-Specific PCR Assay for HPV DNA

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