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黏附增加作为抗体依赖和抗体非依赖补体介导的人类免疫缺陷病毒感染增强机制。

Increased adhesion as a mechanism of antibody-dependent and antibody-independent complement-mediated enhancement of human immunodeficiency virus infection.

作者信息

Lund O, Hansen J, Søorensen A M, Mosekilde E, Nielsen J O, Hansen J E

机构信息

Physics Department, Technical University of Denmark, Lyngby.

出版信息

J Virol. 1995 Apr;69(4):2393-400. doi: 10.1128/JVI.69.4.2393-2400.1995.

Abstract

Enhancement of human immunodeficiency virus (HIV) infection by complement alone or in conjunction with antibodies was studied experimentally and theoretically. Experimental studies showed that while HIV-positive sera neutralize HIV infection, the addition of fresh complement abrogated neutralization and could even cause enhancement. Enhancement was blocked by anti-complement receptor 2 antibodies, and infection under enhancing conditions could be blocked by soluble CD4. Antibody-dependent complement-mediated enhancement (C'ADE) was dependent on the alternative complement activation pathway, as factor B-deficient serum could enhance only after the addition of factor B. The observed enhancement was also antibody dependent, since the addition of antibodies increased the level of enhancement. Under C'ADE conditions, infection reached a plateau within 5 min and was not caused by activation of cells by factors in the human serum. On the contrary, preincubation of cells with complement decreased the level of enhancement. A theoretical model of HIV infection in vitro which exhibited similar enhancement in an antibody- and complement concentration-dependent way was developed. Model studies indicated that the enhanced infection process could be explained by the fact that virions, because of complement deposition on the surface, bind more efficiently to cells. The model also indicated that the saturation of the enhanced infection process seen after a few minutes could be caused by saturation of the complement receptors. The effect of neutralizing antibodies can thus be overcome by the enhancing effect of complement that facilitates the contact between gp120 and CD4. These studies demonstrate that the main features of the complement-dependent enhancement phenomenon can be understood in terms of a simple mathematical model.

摘要

对单独补体或补体与抗体联合作用增强人类免疫缺陷病毒(HIV)感染进行了实验和理论研究。实验研究表明,虽然HIV阳性血清可中和HIV感染,但加入新鲜补体可消除中和作用,甚至可导致增强作用。抗补体受体2抗体可阻断增强作用,在增强条件下的感染可被可溶性CD4阻断。抗体依赖性补体介导的增强作用(C'ADE)依赖于替代补体激活途径,因为缺乏B因子的血清只有在加入B因子后才能增强。观察到的增强作用也依赖于抗体,因为加入抗体可提高增强水平。在C'ADE条件下,感染在5分钟内达到平台期,并非由人血清中的因子激活细胞所致。相反,细胞与补体预孵育可降低增强水平。建立了体外HIV感染的理论模型,该模型在抗体和补体浓度依赖性方面表现出类似的增强作用。模型研究表明,增强的感染过程可以用以下事实来解释:由于补体沉积在病毒粒子表面,病毒粒子与细胞的结合更有效。该模型还表明,几分钟后观察到的增强感染过程的饱和可能是由补体受体的饱和引起的。因此,中和抗体的作用可被补体的增强作用克服,补体的增强作用促进了gp120与CD4之间的接触。这些研究表明,补体依赖性增强现象的主要特征可以用一个简单的数学模型来理解。

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