Abstract

BackgroundImmunity plays an important role in controlling human papillomavirus (HPV) infection and associated lesions. Unlike infections caused by other viruses, natural HPV infection does not always result in a protective antibody response. Therefore, HPV antibodies are also considered markers of cumulative exposure. The aim of this study was to identify determinants of HPV16 seroreactivity at enrollment among women from the Ludwig-McGill cohort, a natural history study of HPV infection and risk of cervical neoplasia.MethodsHPV16 serology was assessed by ELISA for L1 and L2 capsid antigens, while HPV typing and viral load measurements were performed by PCR-based methods. The associations were analyzed by unconditional logistic regression.ResultsOf 2049 subjects, 425 (20.7%) were strongly seropositive for HPV16. In multivariate analysis, seroreactivity was positively correlated with age, lifetime number of sexual partners, frequency of sex, and HPV16 viral load, and negatively associated with duration of smoking.ConclusionsHPV16 seroreactivity is determined by factors that reflect viral exposure.

Highlights

  • Immunity plays an important role in controlling human papillomavirus (HPV) infection and associated lesions

  • In a previous report we described the reproducibility of the assay and calculation of seroreactivity and demonstrated that this method is suitable to minimize measurement error in Enzyme linked immuno sorbent assay (ELISA) assays [14]

  • Seroreactivity increased significantly with age, and decreased with higher levels of education and income, albeit non-significantly. These associations were not attenuated upon adjustment for cervical HPV16 DNA positivity

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Summary

Introduction

Immunity plays an important role in controlling human papillomavirus (HPV) infection and associated lesions. Unlike infections caused by other viruses, natural HPV infection does not always result in a protective antibody response. Persistent infection by human papillomavirus (HPV) is a necessary cause of cervical cancer, but only a small proportion of HPV positive women develop cervical lesions. Most infections seem to clear spontaneously within 12 to 24 months [2,3] as a result of either humoral immune response or cell mediated mechanisms [4,5]. The high frequency of HPV-related diseases in immunocompromised individuals underscores the important role of immune response to control HPV infection [6]. Since there is no viremia and no cell lysis upon viral shedding, the low availability of antigens and the absence of danger signals contribute to keep HPV infection unknown to the host’s immune system

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