Mechanism of inhibitory effect of dextran sulfate and heparin on human T-cell lymphotropic virus type I (HTLV-I)-induced syncytium formation in vitro: role of cell-to-cell contact.
Mechanism of inhibitory effect of dextran sulfate and heparin on human T-cell lymphotropic virus type I (HTLV-I)-induced syncytium formation in vitro: role of cell-to-cell contact.
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DOI：
10.1016/0166-3542(94)90041-8
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发表时间：
1994-02
影响因子：
7.6
通讯作者：
H. Ida;A. Kurata;K. Eguchi;Izumi Yamashita;M. Nakashima;M. Sakai;Y. Kawabe;Tatsufumi Nakamura;S. Nagataki
中科院分区：
文献类型：
--
作者：
H. Ida;A. Kurata;K. Eguchi;Izumi Yamashita;M. Nakashima;M. Sakai;Y. Kawabe;Tatsufumi Nakamura;S. Nagataki
细胞间接触通常对于 HTLV-I 感染细胞系的合胞体形成至关重要。本研究旨在确定聚阴离子化合物、硫酸葡聚糖和肝素对 HTLV-I 诱导的合胞体形成的抑制作用，如 HTLV-I 感染细胞与靶细胞的融合所证明的。这两种化合物在125 μg/ml的浓度下几乎完全阻断了反应早期的合胞体形成，但作为对照的葡聚糖在浓度高达625 μg/ml时并没有抑制它。在浓度为 2 μg/ml 硫酸葡聚糖 5000、3 μg/ml 硫酸葡聚糖 8000 和 8 μg/ml 肝素时检测到对合胞体形成的 50% 抑制。添加硫酸葡聚糖和肝素可抑制放射性标记的HTLV-I感染细胞（HCT-1）与靶细胞的结合，且抑制效果具有浓度依赖性。在将病毒感染的细胞暴露于聚阴离子化合物后，在病毒感染的细胞和靶细胞上的粘附分子的表达以及在病毒感染的细胞上的包膜蛋白的表达中没有检测到明显的变化。这些结果表明，聚阴离子化合物对细胞间接触的阻断（可能与表面粘附分子无关）对于它们对 HTLV-I 诱导的合胞体形成的抑制作用很重要。
Cell-to-cell contact is usually essential for syncytium formation by HTLV-I-infected cell lines. The present study was undertaken to determine the inhibitory effect of polyanionic compounds, dextran sulfate and heparin, on HTLV-I-induced syncytium formation, as demonstrated by the fusion of HTLV-I-infected cells with target cells. These two compounds almost completely blocked syncytium formation in the early phase of the reaction at a concentration of 125 μg/ml, but dextran, as a control, did not inhibit it at concentrations up to 625 μg/ml. 50% inhibition of syncytium formation was detected at a concentration of 2 μg/ml of dextran sulfate 5000, 3 μg/ml of dextran sulfate 8000 and 8 μg/ml of heparin. The binding of radiolabeled HTLV-I-infected cells (HCT-1) to the target cells was inhibited by addition of dextran sulfate and heparin, and the inhibitory effects were concentration-dependent. No marked changes were detected in the expression of adhesion molecules on the virus-infected cells and target cells, and in the expression of envelope proteins on the virus-infected cells after exposing them to the polyanionic compounds. These results suggest that the blocking of cell-to-cell contact by polyanionic compounds, probably independent of surface adhesion molecules, is important for their inhibitory effect on HTLV-I-induced syncytium formation.