Abstract

BackgroundPersistent infection of human papillomavirus (HPV) types 16 and 18 causes cervical cancer. To better understand immune responses to the prophylactic vaccine, HPV 16/18 L1 virus-like particles (HPV-VLPs), we investigated B cell epitopes of HPV16 L1-derived peptides.MethodsSera from mice immunized with HPV-16/18 L1 VLPs were analyzed for their IgG titers against 10 different HPV16 L1-derived peptides (20-mer) that contain human leukocyte antigen (HLA)-class I A-2, A-24 and class II DR.ResultsOne 20-mer peptide at positions 300 to 319 was identified as a common B cell epitope in both Balb/c (H-2d) and C57BL/6 (H-2b) mice. Mapping analysis showed that the 10-amino-acid sequence at positions 304to 313 was an immunogenic portion. It is of note that the binding capability of this 10-mer peptide to the HLA-A2 and HLA-A24 molecules was confirmed by the HLA class I stabilization assay. In addition, one unique 20-mer was determined as a B cell epitope in each strain.ConclusionsThese results might provide new information for better understanding of immune responses to HPV 16 L1.

Highlights

  • Persistent infection of human papillomavirus (HPV) types 16 and 18 causes cervical cancer

  • A 100-fold dilution of samples was used to determine the levels of IgG reactive to each of 10 different HPV16 L1-derived peptides (20-mer), and the results were given in fluorescent intensity units (FIU) (Figure 1)

  • Epitope mapping of peptide These results indicated that peptide 6 is the major common B cell epitope shared by the two strains

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Summary

Introduction

Persistent infection of human papillomavirus (HPV) types 16 and 18 causes cervical cancer. To better understand immune responses to the prophylactic vaccine, HPV 16/18 L1 virus-like particles (HPV-VLPs), we investigated B cell epitopes of HPV16 L1-derived peptides. HPV 16 is the most common type associated with cervical cancer [1]. The preventive effect of the HPV-VLPs vaccine has been reported to last up to 7.3 years [4], the durability is unclear at the present time, either for the entire vaccinated population or for individuals. This hurdle could be in part overcome if predictable biomarkers were identified. Little information is presently available with regard to humoral responses against the HPV-VLPs, primarily

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