Rentier B, Hooghe-Peters E L, Dubois-Dalcq M
J Virol. 1978 Nov;28(2):567-77. doi: 10.1128/JVI.28.2.567-577.1978.
Virus-induced cell fusion has been studied after infection of Vero cells with measles virus. Scanning and transmission electron microscopy were combined with immunoperoxidase labeling of measles antigens to correlate viral production and distribution of virus-induced erythrocyte binding sites with progress of fusion. Release of infectious virus started before syncytia were detected and decreased while the number and size of syncytia were increasing. Most virions were seen budding from mononucleated cells or from the periphery of syncytia where cells were being recruited. Moving inward, the surfaces of syncytia where cells were being recruited. Moving inward, the surfaces of syncytia were covered with numerous ridges containing viral antigen, but few viral buds were seen, suggesting that syncytia might be sites of defective viral formation. Hemadsorption occurred predominantly within the confines of syncytia. Erythrocytes were scattered sparsely over immature syncytia but were densely packed in the center of mature syncytia. Active binding sites for erythrocytes were located on cell villi and ridges covered with measles antigens. Hemadsorption was completely inhibited in measles virus-infected cultures pretreated with virus-specific immunoglobulin G for 1 h at 4 degrees C. However, when these cultures were shifted to 37 degrees C, hemadsorbing sites were recovered at the periphery of enlarging syncytia. Virus-induced sites for erythrocyte adsorption were found to move centripetally on syncytium membranes as fusion progressed.
在用麻疹病毒感染Vero细胞后，对病毒诱导的细胞融合进行了研究。扫描电子显微镜和透射电子显微镜与麻疹抗原的免疫过氧化物酶标记相结合，以将病毒产生以及病毒诱导的红细胞结合位点的分布与融合进程相关联。在检测到多核巨细胞之前，感染性病毒就开始释放，并且在多核巨细胞的数量和大小增加时减少。大多数病毒粒子可见于从单核细胞或正在被募集细胞的多核巨细胞周边出芽。向内移动时，正在被募集细胞的多核巨细胞表面。向内移动时，多核巨细胞表面覆盖着许多含有病毒抗原的嵴，但可见到的病毒芽很少，这表明多核巨细胞可能是有缺陷病毒形成的部位。血细胞吸附主要发生在多核巨细胞范围内。红细胞稀疏地散布在未成熟的多核巨细胞上，但在成熟多核巨细胞的中心密集堆积。红细胞的活性结合位点位于覆盖有麻疹抗原的细胞绒毛和嵴上。在用病毒特异性免疫球蛋白G在4℃预处理1小时的麻疹病毒感染培养物中，血细胞吸附被完全抑制。然而，当将这些培养物转移到37℃时，在扩大的多核巨细胞周边恢复了血细胞吸附位点。随着融合的进展，发现病毒诱导的红细胞吸附位点在多核巨细胞膜上向心移动。
