For example, our estimate of HPV 16/18 prevalence among the total population of 16–24 year olds was around 26% lower, at 13%. However, the available variables do not fully describe risk of infection and therefore our population estimates, even weighted by these variables, are still likely to overestimate the true population prevalence. Sexually active females under 16 years are probably less representative of the general population at this age than older NCSP participants as they are sexually active relatively young (the median age of first sexual intercourse for females in the UK is ∼16 years [23]). We also had only a small number of samples from this age group. The data

BLU9931 mw for these girls are nevertheless of particular interest as they provide some information about the prevalence of HPV in girls at the ages being targeted with HPV immunisation and PFI-2 ic50 who are rarely assessable or included in epidemiological studies of HPV. The clustering of sample collection from just five NHS sites contributes to uncertainty around estimates extrapolated to the wider population: the 95% confidence intervals around our HPV 16/18 prevalence amongst NSCP participants aged 16–24 years, of 16.0–19.3% widens to 13.3–22.8% when allowing for clustered collection from five sites. VVS samples were used for this study, which, although not validated as a sample type for either hc2 or LA by the test

manufacturers, have been shown to be suitable for HPV DNA detection and to have greater sensitivity for HPV than urine [24]. Prevalence estimates from VVS samples are not directly comparable to findings from cervical samples as they are likely to include viruses which have not infected the host’s cervical cells, and may not do so [25]. In cross-sectional prevalence studies such as ours, it is not possible to distinguish transient infections

from those that will persist. The poorer sample quality, either due to degradation of the DNA after longer storage (some NCSP samples), freeze–thaw cycles (POPI samples) or inhibition of tests by sample media, Farnesyltransferase and the reduced sensitivity of hc2 with our sample type (with lower cellular content), may have resulted in HPV prevalence being underestimated in our study, and more so for single infections (and so overestimating the proportion of infections with multiple HPV types). The lower prevalence of HPV (HR, 16/18 and multiple HR) in samples from POPI participants compared to women of the same age-range participating in the NCSP, probably reflects real differences in the prevalence of infection between these two populations. While some of the differences seen may be due to other factors, the lower prevalence is consistent with data from the NCSP where chlamydia positivity of screens conducted in educational settings is less than half that identified in screens conducted at GP and family planning and youth clinics [26]. Previously, Kitchener et al.