Hannah Shilling1, Suzanne M Garland2, Steph Atchison1, Alyssa M Cornall2, Julia M L Brotherton3, Deborah Bateson4, Kathleen McNamee5, John M Kaldor6, Jane S Hocking7, Marcus Y Chen8, Christopher K Fairley8, Anna McNulty9, Charlotte Bell10, Lewis Marshall11, Catriona Ooi12, S Rachel Skinner13, Gerald Murray1, Monica Molano1, Sepehr Tabrizi1, Dorothy A Machalek14. 1. Centre for Women's Infectious Diseases, The Royal Women's Hospital, Melbourne, Australia; Molecular Microbiology Group, Infection and Immunity Theme, Murdoch Children's Research Institute, Melbourne, Australia. 2. Centre for Women's Infectious Diseases, The Royal Women's Hospital, Melbourne, Australia; Molecular Microbiology Group, Infection and Immunity Theme, Murdoch Children's Research Institute, Melbourne, Australia; Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria, Australia. 3. Melbourne School of Population and Global Health, University of Melbourne, Victoria, Australia; VCS Population Health, VCS Foundation, East Melbourne, Victoria, Australia. 4. Family Planning New South Wales, Australia; Discipline of Obstetrics, Gynaecology and Neonatology, The University of Sydney, Australia. 5. Family Planning Victoria, Australia; Department of Obstetrics and Gynaecology, Monash University, Melbourne, Victoria, Australia. 6. The Kirby Institute for Infection and Immunity in Society, University of New South Wales, Sydney, Australia. 7. Melbourne School of Population and Global Health, University of Melbourne, Victoria, Australia. 8. Melbourne Sexual Health Centre, Alfred Health, Melbourne, Victoria, Australia; Central Clinical School, Monash University, Melbourne, Victoria, Australia. 9. Sydney Sexual Health Centre, New South Wales, Australia. 10. Adelaide Sexual Health Clinic, South Australia, Australia. 11. South Terrace Clinic, Fremantle Hospital, Western Australia, Australia. 12. Western Sydney Sexual Health Centre, New South Wales, Australia; Northern Sydney Local Health District Sexual Health Service, New South Wales, Australia; Northern Clinical School, Faculty of Health and Medicine, University of Sydney, New South Wales, Australia. 13. Discipline of Child and Adolescent Health, Faculty of Medicine and Health, University of Sydney, Australia. 14. Centre for Women's Infectious Diseases, The Royal Women's Hospital, Melbourne, Australia; Melbourne School of Population and Global Health, University of Melbourne, Victoria, Australia; The Kirby Institute for Infection and Immunity in Society, University of New South Wales, Sydney, Australia. Electronic address: dorothy.machalek@thewomens.org.au.
Abstract
BACKGROUND: In Australia, high and widespread uptake of the quadrivalent human papillomavirus (HPV) vaccine has led to substantial population-level reductions in the prevalence of quadrivalent vaccine targeted HPV genotypes 6/11/16/18 in women aged ≤ 35 years. We assessed risk factors for HPV detection among 18-35 year old women, 9-12 years after vaccine program introduction. METHODS: Women attending health services between 2015 and 2018 provided a self-collected vaginal specimen for HPV genotyping (Roche Linear Array) and completed a questionnaire. HPV vaccination status was validated against the National Register. Adjusted odds ratios (aORs) and 95% confidence intervals (CI) were calculated for factors associated with HPV detection. RESULTS: Among 1564 women (median age 24 years; IQR 21-27 years), Register-confirmed ≥ 1-dose vaccine coverage was highest at 69.3% and 68.1% among women aged 18-21 and 22-24 years respectively, decreasing to 42.9% among those aged 30-35 years. Overall prevalence of quadrivalent vaccine-targeted HPV types was very low (2.0%; 95% CI: 1.4-2.8%) and influenced only by vaccination status (5.5% among unvaccinated compared with 0.7% among vaccinated women; aOR = 0.13 (95% CI: 0.05-0.30)). Prevalence of remaining HPV types, at 40.4% (95% CI: 38.0-42.9%), was influenced by established risk factors for HPV infection; younger age-group (p-trend < 0.001), more recent (p < 0.001) and lifetime sexual partners (p-trend < 0.001), but not vaccination status. Prevalence of HPV31/33/45, which shared risk factors with that of non-vaccine targeted HPV types, was also lower among vaccinated (4%) compared with unvaccinated (7%) women (aOR = 0.51; 95% CI: 0.29-0.89), indicative of cross-protection. CONCLUSION: Vaccination has changed the epidemiology of HPV infection in Australian women, having markedly reduced the prevalence of vaccine-targeted types, including amongst women with known risk factors for infection. Vaccinated women appear to be benefiting from modest cross-protection against types 31/33/45 afforded by the quadrivalent HPV vaccine. These results reinforce the importance of HPV vaccination.
BACKGROUND: In Australia, high and widespread uptake of the quadrivalent human papillomavirus (HPV) vaccine has led to substantial population-level reductions in the prevalence of quadrivalent vaccine targeted HPV genotypes 6/11/16/18 in women aged ≤ 35 years. We assessed risk factors for HPV detection among 18-35 year old women, 9-12 years after vaccine program introduction. METHODS:Women attending health services between 2015 and 2018 provided a self-collected vaginal specimen for HPV genotyping (Roche Linear Array) and completed a questionnaire. HPV vaccination status was validated against the National Register. Adjusted odds ratios (aORs) and 95% confidence intervals (CI) were calculated for factors associated with HPV detection. RESULTS: Among 1564 women (median age 24 years; IQR 21-27 years), Register-confirmed ≥ 1-dose vaccine coverage was highest at 69.3% and 68.1% among women aged 18-21 and 22-24 years respectively, decreasing to 42.9% among those aged 30-35 years. Overall prevalence of quadrivalent vaccine-targeted HPV types was very low (2.0%; 95% CI: 1.4-2.8%) and influenced only by vaccination status (5.5% among unvaccinated compared with 0.7% among vaccinated women; aOR = 0.13 (95% CI: 0.05-0.30)). Prevalence of remaining HPV types, at 40.4% (95% CI: 38.0-42.9%), was influenced by established risk factors for HPV infection; younger age-group (p-trend < 0.001), more recent (p < 0.001) and lifetime sexual partners (p-trend < 0.001), but not vaccination status. Prevalence of HPV31/33/45, which shared risk factors with that of non-vaccine targeted HPV types, was also lower among vaccinated (4%) compared with unvaccinated (7%) women (aOR = 0.51; 95% CI: 0.29-0.89), indicative of cross-protection. CONCLUSION: Vaccination has changed the epidemiology of HPV infection in Australian women, having markedly reduced the prevalence of vaccine-targeted types, including amongst women with known risk factors for infection. Vaccinated women appear to be benefiting from modest cross-protection against types 31/33/45 afforded by the quadrivalent HPV vaccine. These results reinforce the importance of HPV vaccination.