The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc. Rockville, MD 20850, USA.
Virology. 2011 Dec 20;421(2):245-52. doi: 10.1016/j.virol.2011.08.026. Epub 2011 Oct 26.
Human monocytes are susceptible to dengue virus (DV) infection through an FcR-dependent pathway known as antibody-dependent enhancement (ADE). In this study, infection enhancement was observed when purified monocytes were infected with DV serotypes in the presence of serially diluted immune serum antibodies. Analyzing binding of the DV-antibody immune complexes to monocytes by quantifying the amount of viruses attached to monocytes, we found that binding did not correlate with the input amount of antibodies; rather, it peaked at suboptimal antibody concentrations, correlating with the observed infection enhancement. These results suggested that immune complexes are involved in hindering DV from binding to FcR-bearing cells; when such a protective feature is weakened, enhancement of viral attachment and ADE are observed. Further, increased cytokine production (TNF-alpha and IFN-alpha), and costimulatory marker expression (CD86 and CD40), were found to be associated with infection enhancement, suggesting a pathological role of ADE-affected monocytes in dengue hemorrhagic diseases.
人类单核细胞易受登革热病毒（DV）感染，这是一种通过 FcR 依赖途径实现的，称为抗体依赖性增强（ADE）。在这项研究中，当纯化的单核细胞在系列稀释的免疫血清抗体存在下感染 DV 血清型时，观察到感染增强。通过定量附着在单核细胞上的病毒量来分析 DV-抗体免疫复合物与单核细胞的结合，我们发现结合与输入的抗体量无关；相反，它在亚最佳抗体浓度下达到峰值，与观察到的感染增强相关。这些结果表明，免疫复合物参与阻止 DV 与 FcR 结合；当这种保护特征减弱时，观察到病毒附着和 ADE 的增强。此外，还发现细胞因子（TNF-α和IFN-α）的产生增加和共刺激标记物（CD86 和 CD40）的表达与感染增强相关，这表明 ADE 影响的单核细胞在登革出血热疾病中具有病理作用。
