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传染性法氏囊病病毒VP2蛋白抗原性的遗传基础。

The genetic basis for the antigenicity of the VP2 protein of the infectious bursal disease virus.

作者信息

Schnitzler D, Bernstein F, Müller H, Becht H

机构信息

Institut für Virologie, Justus-Liebig-Universität Giessen, Germany.

出版信息

J Gen Virol. 1993 Aug;74 ( Pt 8):1563-71. doi: 10.1099/0022-1317-74-8-1563.

Abstract

The genomic region coding for the antigenic structure responsible for the induction of neutralizing antibodies was localized in the central variable region of the VP2 gene by comparing the nucleotide sequence of five escape mutants derived from the standard infectious bursal disease virus strain Cu-1. Exchange of a single amino acid at one of the prominent hydrophilic parts of this region proved to be sufficient for altering the neutralizing properties. The reactivity of neutralizing antibodies with peptides expressed in vitro encompassing both hydrophilic areas suggests that the entire variable region is engaged in the formation of this conformation-dependent antigenic site. VP2-specific, non-neutralizing monoclonal antibodies directed against the sequence-dependent epitope of the serotype I strain Cu-1 and the serotype II strain 23/82 cross-reacted with peptides located towards the carboxy terminus of VP2; no reaction occurred with peptides derived from the amino-terminal side adjacent to the variable region.

摘要

通过比较源自标准传染性法氏囊病病毒株Cu-1的五个逃逸突变体的核苷酸序列,编码负责诱导中和抗体的抗原结构的基因组区域定位在VP2基因的中央可变区。在该区域一个突出的亲水区之一处单个氨基酸的交换被证明足以改变中和特性。中和抗体与体外表达的包含两个亲水区的肽的反应性表明,整个可变区参与了这种构象依赖性抗原位点的形成。针对I型菌株Cu-1和II型菌株23/82的序列依赖性表位的VP2特异性、非中和单克隆抗体与位于VP2羧基末端的肽发生交叉反应;与源自可变区相邻氨基末端侧的肽没有反应。

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