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针对呼肠孤病毒σ1和μ1蛋白的单克隆抗体可抑制铬从小鼠L细胞中释放。

Monoclonal antibodies to reovirus sigma 1 and mu 1 proteins inhibit chromium release from mouse L cells.

作者信息

Hooper J W, Fields B N

机构信息

Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

J Virol. 1996 Jan;70(1):672-7. doi: 10.1128/JVI.70.1.672-677.1996.

Abstract

Reovirus intermediate subviral particles (ISVPs) but not intact virions or cores have been shown to possess the capacity to permeabilize mouse L cells as determined by a 51Cr release assay. We used monoclonal antibodies (MAbs) directed against proteins exposed on the ISVP surface (sigma 1, mu 1, and lambda 2) to probe the role(s) of these proteins in membrane interaction and penetration. One sigma 1-specific MAb (MAb-G5) and two mu 1-specific MAbs (MAb-10H2 and MAb-8H6) inhibited reovirus-induced 51Cr release when added pre- or post-ISVP attachment to L cells. MAb-G5 inhibits 51Cr release by interfering with ISVP attachment (via sigma 1) to L-cell receptor sites. The mu 1-specific MAbs (MAb-10H2 and MAb-8H6) inhibit 51Cr release by interfering with an undefined post-L-cell-attachment event that involves bivalent binding of the mu 1-specific MAbs to an epitope located in a central region of the mu 1 protein.

摘要

呼肠孤病毒中间亚病毒颗粒(ISVPs)而非完整病毒粒子或核心,已被证明具有使小鼠L细胞通透化的能力,这是通过51Cr释放试验确定的。我们使用针对暴露于ISVP表面的蛋白质(σ1、μ1和λ2)的单克隆抗体(MAbs)来探究这些蛋白质在膜相互作用和穿透中的作用。一种σ1特异性单克隆抗体(MAb-G5)和两种μ1特异性单克隆抗体(MAb-10H2和MAb-8H6)在ISVP附着于L细胞之前或之后添加时,抑制呼肠孤病毒诱导的51Cr释放。MAb-G5通过干扰ISVP(通过σ1)与L细胞受体位点的附着来抑制51Cr释放。μ1特异性单克隆抗体(MAb-10H2和MAb-8H6)通过干扰未定义的L细胞附着后事件来抑制51Cr释放,该事件涉及μ1特异性单克隆抗体与位于μ1蛋白中心区域的表位的二价结合。

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