An earlier study of young women attending a UK sexual health clinic reported a much lower prevalence: 12% HPV prevalence in cervical samples from 15 to 19 year old women recruited at a sexual health clinic to a longitudinal study in Birmingham between 1988 and 1992 [27]. Jit M et al. reported less than 5% of girls under 14 years of age to have serological evidence of HPV 6, 11, 16 or 18 infection, rising to over 20% in women aged 18 years and over

[6]. As our study sampled sexually active young women, and was based on HPV DNA detection, it is not surprising that we found a substantially higher prevalence of HPV in the youngest teenagers sampled [28]. However, in common with the seroprevalence data, even amongst our sexually active sample of young women, there was a steep trend to increasing HPV prevalence OSI-906 datasheet with increasing age, from 13 years up to at least 16 years. HPV vaccines do not impact on infections Raf inhibitor present at the time of immunisation [29]. The steep increase in HR HPV prevalence between the ages of 13 and 16 years supports the decision to deliver routine HPV immunisation at age 12–13 years. At age 14 years, assuming 8% of 14 year olds have had sexual intercourse [18] and an HPV 16/18 prevalence in these girls of up to 9%, then an estimated maximum 0.7% of 14 year old girls had existing infection

with either HPV 16 or 18 at the time of immunisation. The percentage of 12 year olds (routine cohort) infected with HPV 16 or 18 at the time of infection will presumably be lower Megestrol Acetate than that estimated for 14 year olds. The association between young age at first sexual intercourse and cervical cancer suggests that although these girls represent an extremely small proportion of the target-population, they might be at increased future risk of cervical cancer due to early onset of sexual activity [30] and exposure prior to HPV vaccination. The proportion of vaccinated girls who are unlikely to gain full benefit from HPV immunisation will be higher

in the catch-up cohorts (up to 18 years), where for example (by the same logic and assumptions) up to 11% of 17 year olds have existing HPV 16/18 infections (assuming 60% have had sexual intercourse, and HPV 16/18 prevalence in these women to be 19%). At a population level, effectiveness will of course be reduced much more by non-uptake of vaccine. Girls vaccinated as part of the routine cohorts (aged 12–13 years) will turn 16 years and begin to enter the target group for chlamydia screening (16–24 years) from 2012. We shall repeat the collection and testing of samples from 16 to 24 year old NCSP participants over the coming years to measure the effectiveness of HPV immunisation against vaccine and non-vaccine types, and to estimate the herd-immunity effects in unvaccinated women.