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      Projections of human papillomavirus (HPV) vaccination impact in Ethiopia, India, Nigeria and Pakistan: a comparative modelling study

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          Abstract

          Introduction

          Cervical cancer is the second most common cancer among women in Ethiopia, India, Nigeria and Pakistan. Our study objective was to assess similarities and differences in vaccine-impact projections through comparative modelling analysis by independently estimating the potential health impact of human papillomavirus (HPV) vaccination.

          Methods

          Using two widely published models (Harvard and Papillomavirus Rapid Interface for Modelling and Economics (PRIME)) to estimate HPV vaccination impact, we simulated a vaccination scenario of 90% annual coverage among 10 cohorts of 9-year-old girls from 2021 to 2030 in Ethiopia, India, Nigeria and Pakistan. We estimated potential health impact in terms of cervical cancer cases, deaths and disability-adjusted life years averted among vaccinated cohorts from the time of vaccination until 2100. We harmonised the two models by standardising input data to comparatively estimate HPV vaccination impact.

          Results

          Prior to harmonising model assumptions, the range between PRIME and Harvard models for number of cervical cancer cases averted by HPV vaccination was: 262 000 to 2 70 000 in Ethiopia; 1 640 000 to 1 970 000 in India; 330 000 to 3 36 000 in Nigeria and 111 000 to 1 33 000 in Pakistan. When harmonising model assumptions, alignment on HPV type distribution significantly narrowed differences in vaccine-impact estimates.

          Conclusion

          Despite model differences, the Harvard and PRIME models yielded similar vaccine-impact estimates. The main differences in estimates are due to variation in interpretation around data on cervical cancer attribution to HPV-16/18. As countries make progress towards WHO targets for cervical cancer elimination, continued explorations of underlying differences in model inputs, assumptions and results when examining cervical cancer prevention policy will be critical.

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          Most cited references36

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          Efficacy of human papillomavirus (HPV)-16/18 AS04-adjuvanted vaccine against cervical infection and precancer caused by oncogenic HPV types (PATRICIA): final analysis of a double-blind, randomised study in young women

          The Lancet, 374(9686), 301-314
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            Epidemiologic classification of human papillomavirus types associated with cervical cancer.

            Infection with human papilloma virus (HPV) is the main cause of cervical cancer, but the risk associated with the various HPV types has not been adequately assessed. We pooled data from 11 case-control studies from nine countries involving 1918 women with histologically confirmed squamous-cell cervical cancer and 1928 control women. A common protocol and questionnaire were used. Information on risk factors was obtained by personal interviews, and cervical cells were collected for detection of HPV DNA and typing in a central laboratory by polymerase-chain-reaction-based assays (with MY09/MY11 and GP5+/6+ primers). HPV DNA was detected in 1739 of the 1918 patients with cervical cancer (90.7 percent) and in 259 of the 1928 control women (13.4 percent). With the GP5+/6+ primer, HPV DNA was detected in 96.6 percent of the patients and 15.6 percent of the controls. The most common HPV types in patients, in descending order of frequency, were types 16, 18, 45, 31, 33, 52, 58, and 35. Among control women, types 16, 18, 45, 31, 6, 58, 35, and 33 were the most common. For studies using the GP5+/6+ primer, the pooled odds ratio for cervical cancer associated with the presence of any HPV was 158.2 (95 percent confidence interval, 113.4 to 220.6). The odds ratios were over 45 for the most common and least common HPV types. Fifteen HPV types were classified as high-risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82); 3 were classified as probable high-risk types (26, 53, and 66); and 12 were classified as low-risk types (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and CP6108). There was good agreement between our epidemiologic classification and the classification based on phylogenetic grouping. In addition to HPV types 16 and 18, types 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82 should be considered carcinogenic, or high-risk, types, and types 26, 53, and 66 should be considered probably carcinogenic. Copyright 2003 Massachusetts Medical Society
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              Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study.

              Knowledge about the distribution of human papillomavirus (HPV) genotypes in invasive cervical cancer is crucial to guide the introduction of prophylactic vaccines. We aimed to provide novel and comprehensive data about the worldwide genotype distribution in patients with invasive cervical cancer. Paraffin-embedded samples of histologically confirmed cases of invasive cervical cancer were collected from 38 countries in Europe, North America, central South America, Africa, Asia, and Oceania. Inclusion criteria were a pathological confirmation of a primary invasive cervical cancer of epithelial origin in the tissue sample selected for analysis of HPV DNA, and information about the year of diagnosis. HPV detection was done by use of PCR with SPF-10 broad-spectrum primers followed by DNA enzyme immunoassay and genotyping with a reverse hybridisation line probe assay. Sequence analysis was done to characterise HPV-positive samples with unknown HPV types. Data analyses included algorithms of multiple infections to estimate type-specific relative contributions. 22,661 paraffin-embedded samples were obtained from 14,249 women. 10,575 cases of invasive cervical cancer were included in the study, and 8977 (85%) of these were positive for HPV DNA. The most common HPV types were 16, 18, 31, 33, 35, 45, 52, and 58 with a combined worldwide relative contribution of 8196 of 8977 (91%, 95% CI 90-92). HPV types 16 and 18 were detected in 6357 of 8977 of cases (71%, 70-72) of invasive cervical cancer. HPV types 16, 18, and 45 were detected in 443 of 470 cases (94%, 92-96) of cervical adenocarcinomas. Unknown HPV types that were identified with sequence analysis were 26, 30, 61, 67, 69, 82, and 91 in 103 (1%) of 8977 cases of invasive cervical cancer. Women with invasive cervical cancers related to HPV types 16, 18, or 45 presented at a younger mean age than did those with other HPV types (50·0 years [49·6-50·4], 48·2 years [47·3-49·2], 46·8 years [46·6-48·1], and 55·5 years [54·9-56·1], respectively). To our knowledge, this study is the largest assessment of HPV genotypes to date. HPV types 16, 18, 31, 33, 35, 45, 52, and 58 should be given priority when the cross-protective effects of current vaccines are assessed, and for formulation of recommendations for the use of second-generation polyvalent HPV vaccines. Our results also suggest that type-specific high-risk HPV-DNA-based screening tests and protocols should focus on HPV types 16, 18, and 45. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                BMJ Glob Health
                BMJ Glob Health
                bmjgh
                bmjgh
                BMJ Global Health
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2059-7908
                2021
                1 November 2021
                : 6
                : 11
                : e006940
                Affiliations
                [1 ]departmentCenter for Health Decision Science , Harvard University T H Chan School of Public Health , Boston, Massachusetts, USA
                [2 ]departmentDepartment of Infectious Disease Epidemiology , London School of Hygiene & Tropical Medicine , London, UK
                [3 ]Public Health Foundation of India , New Delhi, India
                [4 ]Vitalant Research Institute , San Francisco, California, USA
                [5 ]departmentSchool of Public Health , The University of Hong Kong , Hong Kong, Hong Kong
                Author notes
                [Correspondence to ] Dr Allison Portnoy; aportnoy@ 123456mail.harvard.edu
                Author information
                http://orcid.org/0000-0002-8467-1324
                http://orcid.org/0000-0003-0563-1576
                http://orcid.org/0000-0001-6658-8255
                Article
                bmjgh-2021-006940
                10.1136/bmjgh-2021-006940
                8562528
                34725040
                6507d0f5-23f7-4739-a811-3d87186b0baa
                © Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.

                This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See:  https://creativecommons.org/licenses/by/4.0/.

                History
                : 19 July 2021
                : 18 October 2021
                Funding
                Funded by: Bill & Melinda Gates Foundation;
                Award ID: INV-009125
                Categories
                Original Research
                1506
                Custom metadata
                unlocked

                health policy,public health,vaccines,cancer
                health policy, public health, vaccines, cancer

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