Authors

Louiza S. Velentzis, The Daffodil Centre, The University of Sydney, a Joint venture with Cancer Council NSW, Sydney, NSW, Australia; Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia.Follow
David Hawkes, Australian Centre for the Prevention of Cervical Cancer, 265 Faraday Street, Carlton South, Victoria, Australia; Department of Biochemistry and Pharmacology, University of Melbourne, Victoria, Australia; Department of Pathology, University of Malaya, Kuala Lumpur, Malaysia.
Michael Caruana, The Daffodil Centre, The University of Sydney, a Joint venture with Cancer Council NSW, Sydney, NSW, Australia.
Julia MI Brotherton, Melbourne School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia; Australian Centre for the Prevention of Cervical Cancer, 265 Faraday Street, Carlton South, Victoria, Australia; Department of Obstetrics and Gynaecology, University of Malaya, Kuala Lumpur 50603, Malaysia.
Megan A. Smith, The Daffodil Centre, The University of Sydney, a Joint venture with Cancer Council NSW, Sydney, NSW, Australia.
Lara Roeske, Royal Australian College of General Practitioners, East Melbourne, Victoria, Australia.
Khurram A. Karim, Australian Centre for the Prevention of Cervical Cancer, 265 Faraday Street, Carlton South, Victoria, Australia.
Suzanne M. Garland, Infection and Immunity, Murdoch Children's Research Institute, Parkville, Victoria, Australia; Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, Victoria, Australia; Centre Women's Infectious Diseases Research, Royal Women's Hospital, Melbourne, Victoria, Australia.
C David Wrede, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, Victoria, Australia; Department of Oncology & Dysplasia, Royal Women's Hospital, Melbourne, Victoria, Australia.
Jeffery Tan, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, Victoria, Australia; Department of Oncology & Dysplasia, Royal Women's Hospital, Melbourne, Victoria, Australia.
Cosette Wheeler, University of New Mexico Cancer Center, Albuquerque, NM, USA.
Philip E. Castle, Division of Cancer Prevention, National Cancer Institute, NIH, Rockville, MD, USA; Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD, USA.
Marion Saville, Australian Centre for the Prevention of Cervical Cancer, 265 Faraday Street, Carlton South, Victoria, Australia; Department of Obstetrics and Gynaecology, University of Malaya, Kuala Lumpur 50603, Malaysia.
Karen Canfell, The Daffodil Centre, The University of Sydney, a Joint venture with Cancer Council NSW, Sydney, NSW, Australia.

Document Type

Article

Publication Date

6-1-2023

Abstract

Australia's cervical screening program transitioned from cytology to HPV-testing with genotyping for HPV16/18 in Dec'2017. We investigated whether program data could be used to monitor HPV vaccination program impact (commenced in 2007) on HPV16/18 prevalence and compared estimates with pre-vaccination benchmark prevalence. Pre-vaccination samples (2005-2008) (n = 1933; WHINURS), from 25 to 64-year-old women had been previously analysed with Linear Array (LA). Post-vaccination samples (2013-2014) (n = 2989; Compass pilot), from 25 to 64-year-old women, were analysed by cobas 4800 (cobas), and by LA for historical comparability. Age standardised pre-vaccination HPV16/18 prevalence was 4.85% (95%CI:3.81-5.89) by LA; post-vaccination estimates were 1.67% (95%CI:1.21-2.13%) by LA, 1.49% (95%CI:1.05-1.93%) by cobas, and 1.63% (95%CI:1.17-2.08%) for cobas and LA testing of non-16/18 cobas positives (cobas/LA). Age-standardised pre-vaccination oncogenic HPV prevalence was 15.70% (95%CI:13.79-17.60%) by LA; post-vaccination estimates were 9.06% (95%CI:8.02-10.09%) by LA, 8.47% (95%CI:7.47-9.47%) by cobas and cobas/LA. Standardised rate ratios between post-vs. pre-vaccination rates were significantly different for HPV16/18, non-16/18 HPV and oncogenic HPV: 0.34 (95%CI:0.23-0.50), 0.68 (95%CI:0.55-0.84) and 0.58 (95%CI:0.48-0.69), respectively. Additional strategies (LA for all cobas positives; combined cobas and LA results on all samples) had similar results. If a single method is applied consistently, it will provide important data on relative changes in HPV prevalence following vaccination.

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