Kuroda K, Maeda T, Ohnishi S
Proc Natl Acad Sci U S A. 1980 Feb;77(2):804-7. doi: 10.1073/pnas.77.2.804.
Transfer of phospholipid from the envelope of Sendai virus to erythrocyte membrane was measured by using spin-labeled phosphatidylcholine. The transfer was enhanced autocatalytically above a threshold dose (about five adsorbed viruses per cell). There was an inflection point in the time course of transfer, after which the transfer was greatly accelerated. The time to reach the inflection point became shorter with increased viral dose. The transfer reaction was markedly enhanced above 19 degrees C and the inflection point was observed above this temperature. There was negligible transfer from trypsin-treated virus to erythrocyte membrane, but the transfer was greatly enhanced by intact virus. The enhancement was larger with increased amount of intact virus, and the inflection point was observed in the transfer curves. All the kinetic data can be satisfactorily analyzed by a model which assumes that the virus modifies the cell membrane at the attachment site, the modification is propagated in the membrane, and transfer of phospholipid to the modified sites is greatly enhanced. The propagation rate is estimated as approximately equal to 10(-11) cm2s-1 and the activation energy as 13 kcal mol-1 (54 kJ mol-1). The viral F glycoproteins are suggested as a possible entity for the modification and its propagation: they are introduced into the target cell membrane by envelope fusion, diffuse laterally, and enhance both phospholipid exchange and envelope fusion with viruses attached to the membrane sites.
利用自旋标记的磷脂酰胆碱测定了仙台病毒包膜中的磷脂向红细胞膜的转移。在高于阈值剂量(约每个细胞吸附五个病毒)时,转移以自动催化方式增强。转移的时间进程中有一个拐点,在此之后转移大大加速。随着病毒剂量增加,到达拐点的时间变短。转移反应在19摄氏度以上明显增强,且在此温度以上观察到拐点。经胰蛋白酶处理的病毒向红细胞膜的转移可忽略不计,但完整病毒能大大增强转移。完整病毒数量增加时增强作用更大,且在转移曲线中观察到拐点。所有动力学数据都可以通过一个模型得到满意分析,该模型假定病毒在附着位点修饰细胞膜,修饰在膜中传播,且磷脂向修饰位点的转移大大增强。传播速率估计约为10^(-11)平方厘米每秒,活化能为13千卡每摩尔(54千焦每摩尔)。病毒F糖蛋白被认为是进行修饰及其传播的一个可能实体:它们通过包膜融合被引入靶细胞膜,横向扩散,并增强磷脂交换以及与附着在膜位点的病毒的包膜融合。