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关于腺病毒合成所需精氨酸的机制

On the mechanism of arginine requirement for adenovirus synthesis.

作者信息

Plaat D, Weber J

出版信息

Arch Virol. 1979;60(3-4):187-96. doi: 10.1007/BF01317490.

Abstract

The effects of arginine deprivation on the synthesis and processing of viral proteins and the assembly of incomplete and complete virions were studied during infection with human adenovirus type 2. Arginine deprivation greatly reduced the synthesis of all viral proteins, particularly the precursor to core protein VII. The inhibition was completely reversible by the addition of arginine to the medium. Arginine deprivation between 7 and 20 hours post-infection inhibited the processing of PVII to VII, suggesting that PVII is not cleaved autocatalytically. The assembly of incomplete virions was sensitive to arginine deprivation only prior to 20 hours, while the assembly of complete virions was dependent on the continuous presence of arginine. This observation supports the hypothesis that incomplete virions are precursors of complete virions. The experiments on the PVII-specific endoprotease activity showed that arginine deprivation caused only slight reduction in the in vitro activity, although no activity was observed in vivo. The present results lead to the hypothesis that arginine deficiency inhibits the synthesis of a functional protein essential for virion maturation, other than the synthesis or processing of PVII.

摘要

在人2型腺病毒感染期间,研究了精氨酸剥夺对病毒蛋白合成与加工以及不完全和完整病毒粒子组装的影响。精氨酸剥夺极大地降低了所有病毒蛋白的合成,尤其是核心蛋白VII的前体。通过向培养基中添加精氨酸,这种抑制作用完全可逆。感染后7至20小时之间的精氨酸剥夺抑制了PVII向VII的加工,这表明PVII不是自动催化裂解的。不完全病毒粒子的组装仅在20小时之前对精氨酸剥夺敏感,而完整病毒粒子的组装则依赖于精氨酸的持续存在。这一观察结果支持了不完全病毒粒子是完整病毒粒子前体的假说。关于PVII特异性内切蛋白酶活性的实验表明,精氨酸剥夺仅使体外活性略有降低,尽管在体内未观察到活性。目前的结果提出了这样一个假说,即精氨酸缺乏抑制了病毒粒子成熟所必需的功能性蛋白质的合成,而不是PVII的合成或加工。

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