Comparison of the immunogenicity of the human papillomavirus (HPV)-16/18 vaccine and the HPV-6/11/16/18 vaccine for oncogenic non-vaccine types HPV-31 and HPV-45 in healthy women aged 18-45 years

Comparison of the immunogenicity of the human papillomavirus (HPV)-16/18 vaccine and the HPV-6/11/16/18 vaccine for oncogenic non-vaccine types HPV-31 and HPV-45 in healthy women aged 18-45 years
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DOI:
10.4161/hv.7.12.18282
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发表时间:
2011-12-01
期刊:
HUMAN VACCINES
影响因子:
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通讯作者:
Descamps, Dominique
Descamps, Dominique
中科院分区:
其他
文献类型:
--
作者:
Einstein, Mark H.;Baron, Mira;Descamps, Dominique

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人乳头瘤病毒(HPV)疫苗提供的对致癌非疫苗类型的保护(交叉保护)可能提供显着的医疗益处。现有的临床疗效数据表明,两种许可的疫苗[HPV-16/18疫苗,葛兰素史克生物制品(GSK)和HPV-6/11/16/18疫苗,默克公司,Inc.,]不同的是对致癌的非疫苗HPV类型-31/45的保护。在一项长达24个月(接种后18个月)的双盲研究中,比较了两种疫苗诱导的针对这两种非疫苗HPV类型的免疫应答(交叉反应性),研究对象为HPV DNA阴性和血清学阴性的女性,在接种分析的HPV类型之前[HPV-010(NCT 00423046)]。HPV-31/45疫苗之间通过基于假病毒体的中和试验(PBNA)和酶联免疫吸附试验(ELISA)测量的几何平均抗体滴度(GMT)相似。两种疫苗之间HPV-31的血清阳性率也相似;然而,HPV-16/18疫苗(13.0-16.7%)与HPV-6/11/16/18疫苗(0.0-5.0%)相比,HPV-45的PBNA血清阳性率更高,但ELISA没有。HPV-31/45交叉反应性记忆B细胞应答在疫苗之间相当。HPV-16/18疫苗的循环抗原特异性CD 4(+)T细胞频率高于HPV-6/11/16/18疫苗{HPV-31 [几何平均比率(GMR)= 2.0; p = 0.0002]和HPV-45 [GMR = 2.6; P = 0.0092]},T细胞应答者的比例也是如此(HPV-31,p = 0.0009; HPV-45,p = 0.0793)。总之,两种疫苗对致癌非疫苗HPV-31/45型的免疫应答基本相似,但HPV-16/18疫苗的T细胞应答更高。考虑到两种疫苗之间交叉保护效力的差异,结果可能会提供对潜在保护机制的见解。
Protection against oncogenic non-vaccine types (cross-protection) offered by human papillomavirus (HPV) vaccines may provide a significant medical benefit. Available clinical efficacy data suggest the two licensed vaccines [HPV-16/18 vaccine, GlaxoSmithKline Biologicals (GSK), and HPV-6/11/16/18 vaccine, Merck and Co., Inc.,] differ in terms of protection against oncogenic non-vaccine HPV types -31/45. The immune responses induced by the two vaccines against these two non-vaccine HPV types (cross-reactivity) was compared in an observer-blind study up to Month 24 (18 mo post-vaccination), in women HPV DNA-negative and seronegative prior to vaccination for the HPV type analyzed [HPV-010 (NCT00423046)]. Geometric mean antibody titers (GMTs) measured by pseudovirion-based neutralization assay (PBNA) and enzyme-linked immunosorbent assay (ELISA) were similar between vaccines for HPV-31/45. Seropositivity rates for HPV-31 were also similar between vaccines; however, there was a trend for higher seropositivity with the HPV-16/18 vaccine (13.0-16.7%) vs. the HPV-6/11/16/18 vaccine (0.0-5.0%) for HPV-45 with PBNA, but not ELISA. HPV-31/45 cross-reactive memory B-cell responses were comparable between vaccines. Circulating antigen-specific CD4(+) T-cell frequencies were higher for the HPV-16/18 vaccine than the HPV-6/11/16/18 vaccine {HPV-31 [geometric mean ratio (GMR) = 2.0; p = 0.0002] and HPV-45 [GMR = 2.6; p = 0.0092]}, as were the proportion of T-cell responders (HPV-31, p = 0.0009; HPV-45, p = 0.0793). In conclusion, immune response to oncogenic non-vaccine HPV types -31/45 was generally similar for both vaccines with the exception of T-cell response which was higher with the HPV-16/18 vaccine. Considering the differences in cross-protective efficacy between the two vaccines, the results might provide insights into the underlying mechanism(s) of protection.