N-1 inked glycan in tick-borne encephalitis virus envelope protein affects viral secretion in mammalian cells, but not in tick cells.
N-1 inked glycan in tick-borne encephalitis virus envelope protein affects viral secretion in mammalian cells, but not in tick cells.
复制标题
蜱传脑炎病毒包膜蛋白中的 N-1 墨迹聚糖影响哺乳动物细胞中的病毒分泌，但不影响蜱细胞中的病毒分泌。
DOI：
10.1099/vir.0.055269-0
复制
发表时间：
2013
影响因子：
3.8
通讯作者：
Hiroaki Kariwa
中科院分区：
文献类型：
--
作者：
Kentaro Yoshii;Natsumi Yanagihara;Mariko Ishizuka;Mizuki Sakai;Hiroaki Kariwa
蜱传脑炎病毒 (TBEV) 是一种人畜共患疾病病原体，可导致人类严重脑炎。 TBEV的包膜蛋白E具有一个N联糖基化共有序列，但人们对N联聚糖的生物学功能知之甚少。在本研究中，使用带有或不带有蛋白质 EN 连接聚糖的重组 TBEV 研究了蛋白质 E 糖基化的功能。使用N-糖苷酶F去除N-连接聚糖后，病毒粒子的感染性不受影响。在哺乳动物细胞中，糖基化的丧失影响了分泌过程中蛋白E的构象，从而降低了分泌的病毒粒子的感染性。皮下感染缺乏蛋白E糖基化的TBEV的小鼠没有表现出疾病迹象，并且与亲代病毒相比，外周器官中的病毒增殖有所减少。相反，糖基化的丧失并不影响蜱细胞中感染性病毒粒子的分泌过程。此外，抑制向高尔基体的运输会影响哺乳动物细胞中的 TBEV 分泌，但不会影响蜱细胞中的分泌，表明 TBEV 在蜱细胞内质网中合成后通过未知途径分泌。这些结果增加了我们对 TBEV 成熟分子机制的理解。
Tick-borne encephalitis virus (TBEV) is a zoonotic disease agent that causes severe encephalitis in humans. The envelope protein E of TBEV has oneN-linked glycosylation consensus sequence, but little is known about the biological function of theN-linked glycan. In this study, the function of protein E glycosylation was investigated using recombinant TBEV with or without the protein EN-linked glycan. Virion infectivity was not affected after removing theN-linked glycans usingN-glycosidase F. In mammalian cells, loss of glycosylation affected the conformation of protein E during secretion, reducing the infectivity of secreted virions. Mice subcutaneously infected with TBEV lacking protein E glycosylation showed no signs of disease, and viral multiplication in peripheral organs was reduced relative to that with the parental virus. In contrast, loss of glycosylation did not affect the secretory process of infectious virions in tick cells. Furthermore, inhibition of transport to the Golgi apparatus affected TBEV secretion in mammalian cells, but not in tick cells, indicating that TBEV was secreted through an unidentified pathway after synthesis in endoplasmic reticulum in tick cells. These results increase our understanding of the molecular mechanisms of TBEV maturation.