Human papillomavirus prevalence among indigenous and non-indigenous Australian women prior to a national HPV vaccination program
- Equal contributors
1 Regional World Health Organisation Human Papillomavirus Laboratory Network, Department of Microbiology and Infectious Diseases, The Royal Women's Hospital, Locked Bag 300, Parkville, Victoria 3052, Australia
2 Department of Obstetrics and Gynaecology, University of Melbourne, Parkville, Victoria 3052, Australia
3 Department of Microbiology, Royal Children's Hospital, Locked Bag 300, Parkville, Victoria 3052, Australia
4 Murdoch Childrens Research Institute, Parkville, Victoria 3052, Australia
5 National Centre for Immunisation Research and Surveillance, University of Sydney and The Children's Hospital at Westmead, Locked Bag 4001, Westmead, NSW 2145, Australia
6 Registries, Victorian Cytology Service, PO Box 310, East Melbourne, Victoria 8002, Australia
7 Menzies School of Health Research, Box 41096, Casuarina, Northern Territory 0811, Australia
8 PathWest Laboratory Medicine WA, Locked Bag 2009, Nedlands, Western Australia 6909, Australia
BMC Medicine 2011, 9:104 doi:10.1186/1741-7015-9-104Published: 13 September 2011
Indigenous women in Australia have a disproportionate burden of cervical cancer despite a national cervical screening program. Prior to introduction of a national human papilloma virus (HPV) vaccination program, we determined HPV genotype prevalence by Indigenous status and residence in remote areas.
We recruited women aged 17 to 40 years presenting to community-based primary health services for routine Pap screening across Australia. A liquid-based cytology (LBC) cervical specimen was tested for HPV DNA using the AMPLICOR HPV-DNA test and a PGMY09/11-based HPV consensus PCR; positive specimens were typed by reverse hybridization. We calculated age-adjusted prevalence by weighting to relevant population data, and determined predictors of HPV-DNA positivity by age, Indigenous status and area of residence using logistic regression.
Of 2152 women (655 Indigenous), prevalence of the high-risk HPV genotypes was similar for Indigenous and non-Indigenous women (HPV 16 was 9.4% and 10.5%, respectively; HPV 18 was 4.1% and 3.8%, respectively), and did not differ by age group. In younger age groups, the prevalence of other genotypes also did not differ, but in those aged 31 to 40 years, HPV prevalence was higher for Indigenous women (35% versus 22.5%; P < 0.001), specifically HPV clades α5 (OR = 2.1, 95% CI 1.1 to 4.3) and α7, excluding type 18 (OR 1.9, 95% CI 1.1 to 3.3). In multivariate analysis, detection of any HPV genotype was strongly associated with smoking and Pap-test abnormalities, with both risk factors more common among Indigenous women.
Although we found no difference in the prevalence of HPV16/18 among Australian women by Indigenous status or, for Indigenous women, residence in remote regions, differences were found in the prevalence of risk factors and some other HPV genotypes. This reinforces the importance of cervical screening as a complement to vaccination for all women, and the value of baseline data on HPV genotype prevalence by Indigenous status and residence for the monitoring of vaccine impact.