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多克隆牛血清而非病毒中和单克隆抗体可阻断牛白血病病毒(BLV)糖蛋白51(gp51)与重组牛白血病病毒受体BLVRcp1的结合。

Polyclonal bovine sera but not virus-neutralizing monoclonal antibodies block bovine leukemia virus (BLV) gp51 binding to recombinant BLV receptor BLVRcp1.

作者信息

Orlik O, Ban J, Hlavaty J, Altaner C, Kettmann R, Portetelle D, Splitter G A

机构信息

Department of Animal Health and Biomedical Sciences, University of Wisconsin-Madison, 53706, USA.

出版信息

J Virol. 1997 Apr;71(4):3263-7. doi: 10.1128/JVI.71.4.3263-3267.1997.

Abstract

Bovine leukemia virus (BLV), a transactivating lymphotropic retrovirus, is the etiologic agent of enzootic lymphosarcoma or leukemia in cattle. Sera from BLV-infected animals possess high BLV-neutralizing antibody titres. The availability of the recombinant BLV receptor candidate, BLVRcp1, allowed us to determine a mechanism of virus neutralization by polyclonal sera and monoclonal antibodies (MAbs). Bovine sera from animals naturally infected with BLV blocked gp51 binding to recombinant BLVRcp1. In contrast, virus-neutralizing MAbs specific for gp51 F, G, and H epitopes did not prevent gp51-receptor attachment. Furthermore, gp51 neutralization epitopes F, G, and H were accessible to antibodies following gp51 attachment to BLVRcp1. This finding implies that virus neutralization by MAbs to defined BLV gp51 epitopes can occur subsequent to virus engagement of the receptor while polyclonal sera can specifically block virus attachment to the receptor. In conclusion, these data suggest that cell infection by BLV is a multistep process requiring receptor binding (inhibited by polyclonal sera) followed by a second, postbinding event(s) at the cell membrane (inhibited by anti-gp51 MAbs).

摘要

牛白血病病毒(BLV)是一种具有反式激活作用的嗜淋巴细胞性逆转录病毒,是牛群中地方流行性淋巴肉瘤或白血病的病原体。感染BLV的动物血清具有较高的BLV中和抗体效价。重组BLV受体候选物BLVRcp1的可得性,使我们能够确定多克隆血清和单克隆抗体(MAb)中和病毒的机制。来自自然感染BLV动物的牛血清可阻断gp51与重组BLVRcp1的结合。相比之下,针对gp51 F、G和H表位的病毒中和单克隆抗体并不能阻止gp51与受体的结合。此外,在gp51与BLVRcp1结合后,抗体可接触到gp51中和表位F、G和H。这一发现表明,针对特定BLV gp51表位的单克隆抗体在病毒与受体结合后可中和病毒,而多克隆血清可特异性阻断病毒与受体的结合。总之,这些数据表明,BLV感染细胞是一个多步骤过程,需要受体结合(多克隆血清可抑制),随后在细胞膜上发生第二次结合后事件(抗gp51单克隆抗体可抑制)。

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