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Antibody-dependent enhancement of viral infection: molecular mechanisms and in vivo implications.

机译:病毒感染的抗体依赖性增强作用:分子机制和体内意义。

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摘要

Besides the common receptor/coreceptor-dependent mechanism of cellular attachment, some viruses rely on antiviral antibodies for their efficient entry into target cells. This mechanism, known as antibody-dependent enhancement (ADE) of viral infection, depends on the cross-linking of complexes of virus-antibody or virus-activated complement components through interaction with cellular molecules such as Fc receptors or complement receptors, leading to enhanced infection of susceptible cells. Recent studies have suggested that additional mechanisms underlie ADE: involvement of complement component C1q and its receptor (Ebola virus), antibody-mediated modulation of the interaction between viral protein and its coreceptor (human immunodeficiency virus) and suppression of cellular antiviral genes by the replication of viruses entering cells via ADE (Ross River virus). Since ADE is exploited by a variety of viruses and has been associated with disease exacerbation, it may have broad relevance to the pathogenesis of viral infection and antiviral strategies.
机译:除了常见的依赖受体/共受体的细胞附着机制外,某些病毒还依赖抗病毒抗体有效进入靶细胞。这种机制被称为病毒感染的抗体依赖性增强(ADE),取决于病毒抗体或病毒激活的补体组分与细胞分子(例如Fc受体或补体受体)相互作用而交联,从而导致增强感染易感细胞。最近的研究表明,ADE构成了其他机制:补体成分C1q及其受体(埃博拉病毒)的参与,病毒介导的病毒蛋白与其共受体(人免疫缺陷病毒)之间相互作用的抗体介导调节和复制对细胞抗病毒基因的抑制病毒通过ADE(罗斯河病毒)进入细胞。由于ADE被多种病毒利用并与疾病恶化相关,因此它可能与病毒感染的发病机理和抗病毒策略有着广泛的联系。

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