Tuesday, 13th of November 2012 |
J Infect Dis. (2012) doi: 10.1093/infdis/jis590
First published online: October 19, 2012
Fall in Human Papillomavirus Prevalence Following a National Vaccination Program
1. Sepehr N. Tabrizi1,2,3,4,
3. John M. Kaldor9,
5. Eleanor Cummins4,
8. Kathleen McNamee6,7,
9. Maria Garefalakis11 and
10. Suzanne M. Garland1,2,3,4
+ Author Affiliations
1. 1Regional World Health Organization Human Papillomavirus Laboratory Network, Department of Microbiology and Infectious Diseases, The Royal Women's Hospital, Victoria, Australia
2. 2Department of Obstetrics and Gynecology, University of Melbourne, Australia
3. 3Department of Microbiology
4. 4Murdoch Children's Research Institute, Royal Children's Hospital, Parkville, Australia
5. 5Registries, Victorian Cytology Service, East Melbourne, Australia
6. 6Family Planning Victoria, Box Hill
7. 7Department of Obstetrics and Gynecology, Monash University, Clayton, Victoria, Australia
8. 8Sydney University Discipline of Pediatrics and Child Health, Children's Hospital Westmead, Australia
9. 9The Kirby Institute, University of New South Wales, Darlinghurst
10. 10Family Planning New South Wales, Ashfield
11. 11Family Planning Western Australia, Northbridge, Western Australia
1. Correspondence: Sepehr N. Tabrizi, PhD, Department of Microbiology and Infectious Diseases, The Royal Women's Hospital, Locked Bag 300, Parkville, Victoria 3052, Australia (sepehr.tabrizi@thewomens.org.au).
Abstract below; full text is at http://jid.oxfordjournals.org/content/early/2012/10/24/infdis.jis590.long
Background. In April 2007, Australia became the first country to introduce a national government-funded human papillomavirus (HPV) vaccination program. We evaluated the program's impact on genotype-specific HPV infection prevalence through a repeat survey of women attending clinical services.
Methods. HPV genoprevalence in women aged 18–24 years attending family planning clinics in the prevaccine period (2005–2007) was compared with prevalence among women of the same age group in the postvaccine period (2010–2011). The same recruitment and testing strategies were utilized for both sets of samples, and comparisons were adjusted for potentially confounding variables.
Results. The prevalence of vaccine HPV genotypes (6, 11, 16, and 18) was significantly lower in the postvaccine sample than in the prevaccine sample (6.7% vs 28.7%; P < .001), with lower prevalence observed in both vaccinated and unvaccinated women compared with the prevaccine population (5.0% [adjusted odds ratio, 0.11; 95% confidence interval, 0.06–0.21] and 15.8% [adjusted odds ratio, 0.42; 95% confidence interval, 0.19–0.93], respectively). A slightly lower prevalence of nonvaccine oncogenic HPV genotypes was also found in vaccinated women (30.8% vs 37.6%; adjusted odds ratio, 0.68; 95% confidence interval, 0.46–0.99).
Conclusions. Four years after the commencement of the Australian HPV vaccination program, a substantial decrease in vaccine-targeted genotypes is evident and should, in time, translate into reductions in HPV-related lesions.
An updated file was supplied to correctly reflect author Julia M. L. Brotherton's affiliations.
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