Sulfated homologues of heparin inhibit hepatitis C virus entry into mammalian cells
Sulfated homologues of heparin inhibit hepatitis C virus entry into mammalian cells
复制标题
DOI：
10.1128/jvi.02622-06
复制
发表时间：
2007-04-01
影响因子：
5.4
通讯作者：
Ray, Ranjit
中科院分区：
文献类型：
--
作者：
Basu, Arnab;Kanda, Tatsuo;Ray, Ranjit
丙型肝炎病毒（HCV）通过包膜糖蛋白和特异性细胞表面受体之间的相互作用进入的机制目前仍不清楚。我们先前已经用水泡性口炎病毒（VSV）/HCV假型模型表明，HCV E2包膜糖蛋白的高变区I有助于与细胞表面上存在的糖胺聚糖结合。在这项研究中，我们研究了丙型肝炎病毒包膜糖蛋白与化学修饰的肝素衍生物的结合。此外，我们已经确定了肝素衍生物与HCV包膜糖蛋白的相互作用的感染性的功能相关性，通过使用人类免疫缺陷病毒（HIV）/HCV假型，VSV/HCV假型，和细胞培养生长的HCV基因型1a。两者合计，我们的研究结果表明，HCV包膜糖蛋白依赖于O-硫酸酯的肝素同系物，以促进进入哺乳动物细胞。
The mechanism of entry of hepatitis C virus (HCV) through interactions between the envelope glycoproteins and specific cell surface receptors remains unclear at this time. We have previously shown with the vesicular stomatitis virus (VSV)/HCV pseudotype model that the hypervariable region I of the HCV E2 envelope glycoprotein helps in binding with glycosaminoglycans present on the cell surface. In this study, we have examined the binding of HCV envelope glycoproteins with chemically modified derivatives of heparin. Furthermore, we have determined the functional relevance of the interaction of heparin derivatives with HCV envelope glycoproteins for infectivity by using a human immunodeficiency virus (HIV)/HCV pseudotype, a VSV/HCV pseudotype, and cell culture-grown HCV genotype 1a. Taken together, our results suggest that the HCV envelope glycoproteins rely upon O-sulfated esters of a heparin homologue to facilitate entry into mammalian cells.