The dynamics of hepatitis C virus binding to platelets and 2 mononuclear cell lines
The dynamics of hepatitis C virus binding to platelets and 2 mononuclear cell lines
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DOI：
10.1182/blood.v98.8.2293
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发表时间：
2001-10-15
期刊：
影响因子：
20.3
通讯作者：
Allain, JP
中科院分区：
文献类型：
--
作者：
Hamaia, S;Li, CY;Allain, JP
丙型肝炎病毒 (HCV) 与慢性感染患者的血小板结合，其中游离的 HCV 仅占总循环病毒的 5% 左右。游离HCV优先与人单核细胞系结合，但游离和复合病毒同等地与血小板结合。游离 HCV 与人 Molt-4 T 细胞（表达 CD81）和人早单核 U937 细胞或血小板（不表达 CD81）的结合程度相似。游离HCV与细胞系的结合在每个细胞1IU HCV RNA的病毒剂量下饱和，但与血小板的结合不饱和。人抗 HCV IgG（而非抗 CD81）以剂量依赖性方式显着抑制 HCV 与靶细胞的结合。 E2 糖蛋白 HCV 高变区 1 的人类抗体部分抑制病毒与靶细胞的结合。重组E2还以剂量依赖的方式抑制病毒与靶细胞的结合，其功效在Molt-4细胞的排列顺序中下降得比U937细胞多于血小板。与HCV相反，重组E2与Molt-4细胞的结合程度明显高于与U937细胞或血小板的结合程度。这些结果表明，HCV 与血细胞的结合是由多个细胞表面受体介导的，并且重组 E2 结合可能不能代表完整病毒与靶细胞的相互作用。 (C) 2001 年，美国血液学会。
Hepatitis C virus (HCV) binds to platelets in chronically infected patients where free HCV constitutes only about 5% of total circulating virus. Free HCV preferentially binds to human mononuclear cell lines but free and complexed virus binds equally to platelets. The extent of free HCV binding to human Molt-4 T cells (which express CD81) and to human promonocytic U937 cells or to platelets (which do not express CD81) was similar. The binding of free HCV to the cell lines was saturated at a virus dose of 1 IU HCV RNA per cell but binding to platelets was not saturable. Human anti-HCV IgG, but not anti-CD81, markedly inhibited HCV binding to target cells in a dose-dependent manner. Human antibodies to HCV hypervariable region 1 of E2 glycoprotein partially inhibited viral binding to target cells. Recombinant E2 also inhibited viral binding to target cells in a dose-dependent manner, with the efficacy of this decreasing in the rank order of Molt-4 cells more than U937 cells more than platelets. In contrast to HCV, recombinant E2 bound to Molt-4 cells to an extent markedly greater than that apparent with U937 cells or platelets. These results suggest that the binding of HCV to blood cells is mediated by multiple cell surface receptors and that recombinant E2 binding may not be representative of the interaction of the intact virus with target cells. (C) 2001 by The American Society of Hematology.