Institute of Virology, University of Bonn Medical Centre, Sigmund-Freud-Str. 25, 53105, Bonn, Germany.
Med Microbiol Immunol. 2011 May;200(2):85-97. doi: 10.1007/s00430-010-0174-x. Epub 2010 Oct 8.
Monoclonal antibody (MAb) 2c, specific for glycoprotein B of herpes simplex virus (HSV), had been shown to mediate clearance of infection from the mucous membranes of mice, thereby completely inhibiting mucocutaneous inflammation and lethality, even in mice depleted of both CD4(+) and CD8(+) cells. Additionally, ganglionic infection was highly restricted. In vitro, MAb 2c exhibits a potent complement-independent neutralising activity against HSV type 1 and 2, completely inhibits the viral cell-to-cell spread as well as the syncytium formation induced by syncytial HSV strains (Eis-Hübinger et al. in Intervirology 32:351-360, 1991; Eis-Hübinger et al. in J Gen Virol 74:379-385, 1993). Here, we describe the mapping of the epitope for MAb 2c. The antibody was found to recognise a discontinuous epitope comprised of the HSV type 1 glycoprotein B residues 299 to 305 and one or more additional discontinuous regions that can be mimicked by the sequence FEDF. Identification of the epitope was confirmed by loss of antibody binding to mutated glycoprotein B with replacement of the epitopic key residues, expressed in COS-1 cells. Similarly, MAb 2c was not able to neutralise HSV mutants with altered key residues, and MAb 2c was ineffective in mice inoculated with such mutants. Interestingly, identification and fine-mapping of the discontinuous epitope was not achieved by binding studies with truncated glycoprotein B variants expressed in COS cells but by peptide scanning with synthetic overlapping peptides and peptide key motif analysis. Reactivity of MAb 2c was immensely increased towards a peptide composed of the glycoprotein B residues 299 to 305, a glycine linker, and a C-terminal FEDF motif. If it could be demonstrated that antibodies of the specificity and bioactivity of MAb 2c can be induced by the epitope or a peptide mimicking the epitope, strategies for active immunisation might be conceivable.
单克隆抗体(MAb)2c 特异性针对单纯疱疹病毒(HSV)的糖蛋白 B,已被证明可介导清除小鼠粘膜中的感染,从而完全抑制粘膜炎症和致死性,即使在耗尽 CD4(+)和 CD8(+)细胞的小鼠中也是如此。此外,神经节感染受到高度限制。在体外,MAb 2c 对 HSV 1 型和 2 型表现出强大的补体非依赖性中和活性,完全抑制病毒细胞间传播以及合胞体 HSV 株诱导的合胞体形成(Eis-Hübinger 等人,Intervirology 32:351-360, 1991;Eis-Hübinger 等人,J Gen Virol 74:379-385, 1993)。在这里,我们描述了 MAb 2c 表位的作图。该抗体被发现识别一个不连续的表位,由 HSV 1 型糖蛋白 B 的残基 299 至 305 和一个或多个额外的不连续区域组成,这些区域可以被序列 FEDF 模拟。通过用突变的糖蛋白 B 替换表位关键残基在 COS-1 细胞中表达,证实了抗体结合的丧失,从而确认了表位的识别。同样,MAb 2c 不能中和具有改变的关键残基的 HSV 突变体,并且 MAb 2c 在接种此类突变体的小鼠中无效。有趣的是,通过与在 COS 细胞中表达的截短糖蛋白 B 变体的结合研究而不是通过用合成重叠肽和肽关键模体分析进行肽扫描,未能鉴定和精细绘制不连续表位。MAb 2c 对由糖蛋白 B 的残基 299 至 305、甘氨酸接头和 C 末端 FEDF 基序组成的肽的反应性大大增加。如果能够证明具有 MAb 2c 的特异性和生物活性的抗体可以由表位或模拟表位的肽诱导,则可以设想主动免疫的策略。