Laboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan.
Biochem Biophys Res Commun. 2011 Apr 1;407(1):74-8. doi: 10.1016/j.bbrc.2011.02.110. Epub 2011 Mar 6.
Ebola virus (EBOV) infection is initiated by the interaction of the viral surface envelope glycoprotein (GP) with the binding sites on target cells. Differences in the mortality among different species of the Ebola viruses, i.e., Zaire ebolavirus (ZEBOV) and Reston ebolavirus (REBOV), correspond to the in vitro infectivity of the pseudo-typed virus constructed with the GPs in cells expressing macrophage galactose-type calcium-type lectin (MGL/CD301). Through mutagenesis of GP2, the transmembrane-anchored subunit of GP, we found that residues 502-527 of the GP2 sequence determined the different infectivity between VSV-ZEBOV GP and -REBOV GP in MGL/CD301-expressing cells and a histidine residue at position 516 of ZEBOV GP2 appeared essential in the differential infectivity. These findings may provide a clue to clarify a molecular basis of different pathogenicity among EBOV species.
埃博拉病毒（EBOV）感染是由病毒表面包膜糖蛋白（GP）与靶细胞结合位点的相互作用引发的。不同种属的埃博拉病毒（即扎伊尔埃博拉病毒[ZEBOV]和雷斯顿埃博拉病毒[REBOV]）之间的死亡率差异，与用在表达巨噬细胞半乳糖型钙型凝集素（MGL/CD301）的细胞中构建的假型病毒的 GP 所对应的体外感染性相对应。通过对 GP2（GP 的跨膜锚定亚单位）进行诱变，我们发现 GP2 序列的 502-527 位残基决定了 MGL/CD301 表达细胞中 VSV-ZEBOV GP 和 -REBOV GP 的不同感染性，而 ZEBOV GP2 中第 516 位组氨酸残基在差异感染性中似乎是必需的。这些发现可能为阐明 EBOV 种属之间不同致病性的分子基础提供线索。
