Antibody-dependent enhancement of coxsackievirus b4 infectivity of human peripheral blood mononuclear cells results in increased interferon-α synthesis
Antibody-dependent enhancement of coxsackievirus b4 infectivity of human peripheral blood mononuclear cells results in increased interferon-α synthesis
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DOI：
10.1086/323801
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发表时间：
2001-11-01
影响因子：
6.4
通讯作者：
Wattré, P
中科院分区：
文献类型：
--
作者：
Hober, D;Chehadeh, W;Wattré, P
IgG缺乏中和活性，并通过色谱法从供体血浆中分离，与柯萨奇病毒B4（CVB 4）形成免疫复合物，并显着增加外周血单个核细胞与CVB 4的感染。IgG增强的CVB 4感染的主要宿主细胞是单核细胞CD 14（+）细胞。CVB和腺病毒受体以及Fc受体II和III的作用已经显示。当感染细胞产生的干扰素（IFN）-α首先被抗体中和时，证明了病毒复制增加和感染性颗粒的释放。CVB 4 IgG诱导的单核细胞IFN-α的合成反映了CVB 4的进入和脱壳，但不是病毒复制，并且需要细胞内存在CVB 4 RNA。因此，CVB 4可以通过抗体依赖性机制感染单核细胞，通过病毒，抗病毒抗体和特异性受体之间的相互作用，导致IFN-α的产生。
IgG devoid of neutralizing activity and isolated from donor plasma by chromatography formed immune complexes with coxsackievirus B4 (CVB4) and significantly increased the infection of peripheral blood mononuclear cells with CVB4. The major host cells for CVB4 infection enhanced with IgG are monocytic CD14(+) cells. The roles of CVB and adenovirus receptor and Fc receptor II and III have been shown. Increased viral replication and the release of infectious particles were demonstrated when interferon (IFN)-alpha produced by infected cells was first neutralized by use of antibodies. The CVB4 IgG-induced synthesis of IFN-alpha by monocytes reflected entry and uncoating of CVB4 but not of viral replication and required the presence of CVB4 RNA inside the cells. Thus, CVB4 can infect monocytes by an antibody-dependent mechanism through interactions between the virus, antiviral antibodies, and specific receptors that result in IFN-alpha production.