A CONFORMATIONAL CHANGE IN SINDBIS VIRUS GLYCOPROTEIN-E1 AND GLYCOPROTEIN-E2 IS DETECTED AT THE PLASMA-MEMBRANE AS A CONSEQUENCE OF EARLY VIRUS-CELL INTERACTION
A CONFORMATIONAL CHANGE IN SINDBIS VIRUS GLYCOPROTEIN-E1 AND GLYCOPROTEIN-E2 IS DETECTED AT THE PLASMA-MEMBRANE AS A CONSEQUENCE OF EARLY VIRUS-CELL INTERACTION
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DOI：
10.1128/jvi.64.8.3643-3653.1990
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发表时间：
1990-08-01
影响因子：
5.4
通讯作者：
JOHNSTON, RE
中科院分区：
文献类型：
--
作者：
FLYNN, DC;MEYER, WJ;JOHNSTON, RE
辛德毕斯（SB）病毒的结构中的构象变化后，病毒粒子附着到婴儿仓鼠肾细胞，但在内化检测。这种改变表现为识别过渡表位的某些糖蛋白E1和E2单克隆抗体（Mab）的病毒体结合增加。这些表位是天然病毒体上的单克隆抗体无法接近的，但在感染的早期阶段，它们的同源单克隆抗体可以接近这些表位。通过低pH区室的病毒体的过境显然是不需要的构象变化。过渡表位的暴露不受NH 4Cl处理BHK细胞的影响，并且在对内体酸化温度敏感的中国仓鼠卵巢细胞中正常发生。然而，重排与SB病毒穿透的时间过程和温度依赖性相关，并且重排发生在具有加速穿透表型的SB病毒突变体的早期。此外，针对过渡表位的单克隆抗体，一种对重排颗粒具有特异性的探针，延缓了感染性病毒粒子的渗透。这些结果表明，SB病毒E1/E2糖蛋白刺突经历了结构重排的病毒体与细胞表面的相互作用的结果，这种改变的病毒体形式可能是一个重要的早期中间体的进入途径，导致生产性感染。
A conformational change in the structure of Sindbis (SB) virus was detected after virion attachment to baby hamster kidney cells but before internalization. The alteration was manifested as increased virion binding of certain glycoprotein E1 and E2 monoclonal antibodies (Mabs) that recognized transitional epitopes. These epitopes were inaccessible to Mab on native virions but became accessible to their cognate Mabs in the early stages of infection. Transit of virions through a low-pH compartment apparently was not required for the conformational change. Exposure of transitional epitopes was unaffected by treatment of BHK cells with NH4Cl and occurred normally in Chinese hamster ovary cells temperature sensitive for endosomal acidification. However, the rearrangement was correlated with both the time course and temperature dependence of SB virus penetration, and the rearangement occurred earlier with an SB virus mutant having an accelarated penetration phenotype. In addition, Mab to a transitional epitope, a probe specific for rearanged particles, retarded penetration of infectious virions. These results suggested that the SB virus E1/E2 glycoprotein spike undergoes a structural rearrangement as a consequence of virion interaction with the cell surface and that this altered virion form may be an important early intermediate in an entry pathway leading to productive infection.