Arboviral Diseases Branch, Division of Vector-Borne Disease, Centers for Disease Control and Prevention, Fort Collins, CO 80521, USA.
Department of Medicine, University of Rochester, Rochester, NY 14642, USA.
Virology. 2014 May;456-457:238-46. doi: 10.1016/j.virol.2014.03.031. Epub 2014 Apr 18.
Antibody-dependent enhancement (ADE) of infection may cause severe illness in patients suffering a secondary infection by a heterologous dengue virus (DENV) serotype. During ADE of infection, cross-reactive non- or poorly-neutralizing antibodies form infectious virus-Ab complexes with the newly infecting serotype and enhance virus infection by binding to the Fcγ receptors (FcγR) on FcγR-bearing cells. In this study, we determined that molecular determinants of DENV2 envelope protein critical for virus entry during non-ADE infection are also required for ADE infection mediated by FcγRIIA, and binding of virus-Ab complexes with FcγRIIA alone is not sufficient for ADE of infection. The FcγRIIA mainly plays an auxiliary role in concentrating the virus-Ab complex to the cell surface, and other primary cellular receptors are required for virus entry. Understanding the viral entry pathway in ADE of DENV infection will greatly facilitate rational designs of anti-viral therapeutics against severe dengue disease associated with ADE.
抗体依赖的增强(ADE)作用可能导致继发感染不同血清型登革病毒(DENV)的患者出现严重疾病。在感染的 ADE 过程中,交叉反应性非中和或低中和抗体与新感染的血清型形成感染性病毒-抗体复合物,并通过与 FcγR 受体(FcγR)结合来增强病毒感染。在这项研究中,我们确定了 DENV2 包膜蛋白的分子决定簇,这些决定簇对于非 ADE 感染期间的病毒进入至关重要,也对于 FcγRIIA 介导的 ADE 感染至关重要,并且病毒-抗体复合物与 FcγRIIA 的结合不足以引起感染的 ADE。FcγRIIA 主要在将病毒-抗体复合物集中到细胞表面方面发挥辅助作用,还需要其他主要的细胞受体来进行病毒进入。了解 DENV 感染的 ADE 中的病毒进入途径将极大地促进针对与 ADE 相关的严重登革热疾病的抗病毒治疗的合理设计。