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首页> 外文期刊>Journal of Virology >Viral protein synthesis in mouse hepatitis virus strain A59-infected cells: effect of tunicamycin.
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Viral protein synthesis in mouse hepatitis virus strain A59-infected cells: effect of tunicamycin.

机译：小鼠肝炎病毒株中的病毒蛋白合成A59感染细胞：唐氏霉素的作用。

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We identified eight protein species in virions of mouse hepatitis virus strain A59. Based on their sizes, prosthetic groups, and locations in virions, these proteins were designated gp180/E2, gp90/E2, pp54/N, gp26.5/E1, gp25.5/E1, p24/E1, p22/X, and p14.5/Y. The positions of the last two proteins in virions are not known. Host protein synthesis in Sac(-) cells infected with mouse hepatitis virus strain A59 was inhibited, and the following novel proteins appeared: gp150, gp90, p54, gp26.5, gp25.5, p24, p22, and p14.5. Except for gp150, these polypeptides all co-electrophoresed with mouse hepatitis virus strain A59 structural proteins. In addition, all of these proteins could be immunoprecipitated with a convalescent mouse serum or a rabbit antiserum raised against purified disrupted virus. After a 15-min pulse of infected cells with radioactive amino acids at 7h postinfection, gp90 was not detected, whereas gp26.5 and gp25.5 were only labeled to a small extent. During a subsequent chase period gp150 was processed to gp90, whereas the radioactivity in gp26.5 and gp25.5 increased concomitantly with a reduction of label in p24. Tunicamycin, an antibiotic which inhibits the synthesis of glycopeptides bearing N glycosidically linked oligosaccharides, prevented the appearance of gp150 in mouse hepatitis virus strain A59-infected cells. Instead, a 110,000-dalton protein accumulated. In contrast, the syntheses of the smaller viral glycoproteins gp26.5 and gp25.5 were resistant to this drug, indicating that these glycosylations were of the O glycosidical type. Although the production of infectious virus in tunicamycin-treated cells was inhibited by more than 99%, release of noninfectious viral particles continued. An analysis of these particles revealed that they lacked the peplomeric glycoproteins gp90/E2 and gp180/E2. Obviously, although the surface projections were not essential for budding of virus particles from the cells, they were required for infectivity.
机译：我们确定了小鼠肝炎病毒菌株A59中的八种蛋白质。基于它们的尺寸，假体组和病毒粒子的位置，这些蛋白质被指定为GP180 / E2，GP90 / E2，PP54 / N，GP26.5 / E1，GP25.5 / E1，P24 / E1，P22 / X和p14.5 / y。在病毒粒中的最后两种蛋白质的位置是未知的。抑制了感染小鼠肝炎病毒菌株A59的囊（ - ）细胞中的宿主蛋白质合成，并出现以下新蛋白质：GP150，GP90，P54，GP26.5，GP25.5，P24，P22和P14.5。除GP150外，这些多肽均与小鼠肝炎病毒菌株A59结构蛋白共同电泳。此外，所有这些蛋白质都可以用康复小鼠血清或兔子抗血清免疫沉淀到纯化破坏的病毒。在7小时发射氨基酸的15分钟脉冲具有放射性氨基酸的感染细胞之后，未检测到GP90，而GP26.5和GP25.5仅在很小程度上标记。在随后的呼应期间，将GP150加工至GP90，而GP26.5和GP25.5中的放射性伴随着P24中的标签的减少增加。 Tunicamycin，一种抑制含有n糖苷连接的低聚糖的合成糖肽的抗生素，防止了GP150在小鼠肝炎病毒菌株A59感染细胞中的出现。相反，积累了110,000-dalton蛋白质。相反，较小的病毒糖蛋白GP26.5和GP25.5的合成对该药物抵抗力，表明这些糖基化是糖基类型的。虽然在唐尼霉素处理的细胞中产生的传染性病毒抑制了99％以上，但释放无排血病毒颗粒仍在继续。对这些颗粒的分析显示它们缺乏Peplomeric糖蛋白GP90 / E2和GP180 / E2。显然，尽管表面突起对来自细胞的病毒颗粒萌芽不是必需的，但是感染性需要它们。

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