Abstract
BackgroundHPV vaccination with the bivalent vaccine is efficacious against HPV16 and 18 infections and cross-protection against non-vaccine HPV types has been demonstrated. Here, we assessed (cross-) protective effects of the bivalent HPV16/18 vaccine on incident and persistent infections and viral load (VL) of fifteen HPV types in an observational cohort study monitoring HPV vaccine effects.MethodsVaginal samples were obtained annually. Type-specific VL assays were developed for HPV6,11,31 33,35,39,45,51,52,56,58,59 and 66 and used in addition to existing HPV16 and 18 assays. Rate differences of incident clearing and persistent infections were correlated with differences in VL and vaccination status.ResultsHPV16/18 vaccination resulted in significantly lower incidence of HPV16/18 infections and significantly lower VL in breakthrough HPV16 (p<0.01) and 18 infections (p<0.01). The effects of vaccination on non-vaccine type VL were ambiguous. Incidence and/or persistence rates of HPV31, 33, 35 and 45 were reduced in the vaccinated group. However, no significant type specific VL effects were found against HPV31, 33, 45, 52 in the vaccinated group. For HPV 6, 59 and 66 no significant reductions in numbers of incident and persistent infections were found, however borderline) VL reductions following vaccination were observed for HPV6 (p = 0.01), 59 (p = 0.10) and 66 (p = 0.03), suggesting a minor effect of the vaccine on the VL level of these HPV types. Overall, vaccination resulted in infections with slightly lower VL, irrespective of HPV type.ConclusionsIn conclusion, vaccination with the bivalent HPV16/18 vaccine results in significantly reduced numbers of HPV16 and 18 incidence rates and reduced VL in breakthrough infections. Significant reductions in incident and/or persistent HPV31, 33, 35 and 45 infections were found, but no significant effect was observed on the VL for infections with these types. For the other non-vaccine HPV types no reduction in incident and/or persistent infections were found, but overall the VL tended to be somewhat lower in vaccinated women.
Highlights
Cervical intraepithelial lesions (CIN) and cervical cancer are caused by persistent high-risk human papillomavirus infections [1]
HPV16/18 vaccination resulted in significantly lower incidence of HPV16/18 infections and significantly lower viral load (VL) in breakthrough HPV16 (p
No significant type specific VL effects were found against HPV31, 33, 45, 52 in the vaccinated group
Summary
Cervical intraepithelial lesions (CIN) and cervical cancer are caused by persistent high-risk human papillomavirus (hrHPV) infections [1]. CIN2 and CIN3 are the most advanced precursor lesions for cervical cancer and are accepted by the WHO as surrogate cervical cancer endpoint markers for vaccine efficacy. Persistent HPV infections (>6 months) were accepted as adequate surrogate endpoint markers [4]. Among hrHPV types, HPV16 and 18 cause approximately 70% of all cervical cancers worldwide. HPV vaccination with the bivalent vaccine is efficacious against HPV16 and 18 infections and cross-protection against non-vaccine HPV types has been demonstrated. We assessed (cross-) protective effects of the bivalent HPV16/18 vaccine on incident and persistent infections and viral load (VL) of fifteen HPV types in an observational cohort study monitoring HPV vaccine effects
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