Herpesvirus glycoprotein synthesis and insertion into plasma membranes.

Herpesvirus glycoprotein synthesis and insertion into plasma membranes.
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疱疹病毒糖蛋白合成并插入质膜。

DOI:
10.1128/jvi.42.2.678-690.1982
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发表时间:
1982
影响因子:
5.4
通讯作者:
Pizer,LI
Pizer,LI
中科院分区:
医学2区
文献类型:
--
作者:
Peake,ML;Nystrom,P;Pizer,LI

文献摘要

相似文献

在抗生素衣霉素(TM)的存在下,单纯疱疹病毒糖蛋白的糖基化被抑制,并且合成类似于糖蛋白的非糖基化多肽(Pizer等人,J. Virol. 34:142-153,1980)。病毒蛋白质和DNA的合成发生在TM处理的细胞中。电镜下可见核衣壳存在于细胞核和细胞质中,细胞表面可见少量有包膜的病毒粒子。在部分纯化的病毒中的蛋白质的分析很容易检测到病毒糖蛋白在对照细胞中,但既不是糖蛋白,也没有nonglycosylated多肽类似物中观察到的病毒从TM处理的细胞制备。通过用125 I标记感染细胞的表面,即使用放线菌酮抑制蛋白质合成并且用TM阻断糖基化,在感染后90分钟也能检测到病毒糖蛋白。用[35 S]甲硫氨酸标记感染细胞中合成的蛋白质表明,在放线菌酮和TM处理的细胞中检测到的表面糖蛋白在感染后没有从头合成,而是被感染病毒置于细胞表面。代谢抑制剂和温度敏感突变体的研究在感染周期的早期阻断表明,糖蛋白gA/gB和gD的合成感染后不久,但gC的合成被推迟。在感染条件下,其中gC及其前体pgC不产生,我们已经能够观察到对应于pgA/pgB的糖基化多肽和在TM存在下制备的非糖基化类似物之间的关系。
In the presence of the antibiotic tunicamycin (TM), glycosylation of herpes simplex virus glycoproteins is inhibited and non-glycosylated polypeptides analogous to the glycoproteins are synthesized (Pizer et al., J. Virol. 34:142-153, 1980). The synthesis of viral proteins and DNA occurs in TM-treated cells. By electron microscopy, nucleocapsids can be observed both in the nucleus and the cytoplasm of TM-treated cells; a small number of enveloped virions were observed on the cell surface. Analyses of the proteins in partially purified virus readily detects viral glycoproteins in the control cells, but neither glycoproteins nor nonglycosylated polypeptide analogs were observed in the virus prepared from TM-treated cells. By labeling the surface of infected cells with 125I, viral glycoproteins were detected as soon as 90 min after infection even when protein synthesis was inhibited with cycloheximide and glycosylation was blocked with TM. Labeling the proteins synthesized in infected cells with [35S]methionine showed that the surface glycoproteins detected in the cycloheximide- and TM-treated cells were not synthesized de novo after infection, but were placed on the cell surface by the infecting virus. Studies with metabolic inhibitors and a temperature-sensitive mutant blocked early in the infectious cycle showed that glycoproteins gA/gB and gD were synthesized soon after infection, but that the synthesis of gC was delayed. Under conditions of infection, in which gC and its precursor pgC are not produced, we have been able to observe the relationships between the glycosylated polypeptides that correspond to pgA/pgB and the nonglycosylated analog made in the presence of TM.