New study shows HPV vaccine is working to reduce rates of genital warts
- Written by Dave Hawkes, Honorary Fellow at Department of Pharmacology and Therapeutics, University of Melbourne
The human papillomavirus (HPV) vaccine was introduced in Australia in 2007 and New Zealand in 2008 to prevent cervical cancer. It is free for women up to age 26 in Australia and to all women under 20 in New Zealand. This is because 99.7% of cervical cancers are associated with the sexually transmissible infection.
There is mounting evidence the HPV vaccination program is preventing cervical disease. This includes both precancerous lesions and cervical cancer. Although it takes 10 to 20 years from HPV infection until cervical cancer develops, the data are already showing a 17% decline in precancerous lesions in women aged 25 to 29.
But the human papillomavirus is also responsible for causing genital warts. Despite a range of questions about the vaccine’s efficacy in this area, a recent New Zealand study has shown a large reduction in genital warts.
In women in the age group offered vaccination, 25% had genital warts diagnosed when attending a sexual health clinic in 2007 (before the vaccine was introduced). In 2013, the rate had dropped to less than 5%.
Although HPV vaccination for males was not added to the New Zealand National Immunisation Schedule until 2017, genital warts in males attending sexual health clinics dropped from 22% in 2007 to less than 5% in 2013.
So how is this possible? It can be attributed to something called “herd immunity”. HPV is a sexually transmitted virus, so if women are vaccinated and can’t be infected with certain HPV types, then their sexual partners won’t be exposed. While genital warts are unpleasant, they are not deadly, unlike cervical cancer.
A 2013 Australian study also showed the impact of the vaccine program on genital warts only a few years after its introduction. The prevalence of genital warts in women under 21 dropped by 92% between 2007 and 2011.
Even though boys were not part of the HPV vaccine program until 2013, by 2011 genital warts had fallen by 81% in males under 21.
This study showed a few other interesting features of the effects of HPV vaccination on genital warts. While a reduction was observed for both females and males in the under 21, and 21 to 30 years age groups, no change was seen in the over 30s – an age group not eligible for the HPV vaccination program.
There was also no difference in genital wart rates in men who have sex with men. This should change with the 2013 introduction of vaccination in males in Australia.
Unfortunately, Aboriginal and Torres Strait Islander women are still twice as likely as non-Indigenous women to be diagnosed with cervical cancer, and four times more likely to die of the disease.
It is well established Indigenous women are more likely to suffer from HPV-related cervical disease. This is despite the fact young Indigenous women are not more likely than their non-Indigenous counterparts to have a HPV infection.
A recent study looked at the effect of HPV vaccination on genital warts in Aboriginal and Torres Strait Islander and other Australian populations. It found a fall in the rate of genital warts in both Indigenous men and women under 30, but not in men and women over 30, or in men who have sex with men.
The Gardasil vaccine, commonly used in the Australian program, protects against four HPV types: 6, 11, 16 and 18. HPV6 and 11 cause genital warts, while HPV16 and 18 are associated with 70% of cervical cancers. Emerging evidence suggests the drop in cervical disease is following the same pattern as observed for genital warts.
These latest data from New Zealand contribute to an already large body of evidence that demonstrates that introducing a population-based HPV vaccination program greatly reduces HPV-related disease, and genital warts in particular. This is in direct contrast to trends for other sexually transmitted infections such as chlamydia, which have steadily increased over the past few years.
Authors: Dave Hawkes, Honorary Fellow at Department of Pharmacology and Therapeutics, University of Melbourne