Corver J, Moesby L, Erukulla R K, Reddy K C, Bittman R, Wilschut J
Department of Physiological Chemistry, Groningen Institute for Drug Studies, University of Groningen, The Netherlands.
J Virol. 1995 May;69(5):3220-3. doi: 10.1128/JVI.69.5.3220-3223.1995.
Low-pH-induced membrane fusion of Semliki Forest virus (SFV) in a model system is mediated by sphingolipids in the target membrane; ceramide is the sphingolipid minimally required (J. L. Nieva, R. Bron, J. Corver, and J. Wilschut, EMBO J. 13:2797-2804, 1994). Here, using various ceramide analogs, we demonstrate that sphingolipid-dependent fusion of SFV with cholesterol-containing liposomes exhibits remarkable molecular specificity, the 3-hydroxyl group and the 4,5-trans carbon-carbon double bond of the sphingosine backbone being critical for the sphingolipid to mediate the process. This observation supports the notion that sphingolipids act as a cofactor in SFV fusion, interacting directly with the viral fusion protein to induce its ultimate fusion-active conformation.
在模型系统中，低pH诱导的塞姆利基森林病毒（SFV）膜融合由靶膜中的鞘脂介导；神经酰胺是最低限度所需的鞘脂（J.L.涅瓦、R.布龙、J.科弗和J.威尔舒特，《欧洲分子生物学组织杂志》13:2797 - 2804，1994年）。在此，我们使用各种神经酰胺类似物证明，SFV与含胆固醇脂质体的鞘脂依赖性融合表现出显著的分子特异性，鞘氨醇主链的3 - 羟基和4,5 - 反式碳 - 碳双键对于鞘脂介导该过程至关重要。这一观察结果支持了鞘脂作为SFV融合中的辅助因子，直接与病毒融合蛋白相互作用以诱导其最终融合活性构象的观点。
