A temperature-sensitive mutant of herpes simplex virus type 1 defective in the synthesis of the major capsid polypeptide.

A temperature-sensitive mutant of herpes simplex virus type 1 defective in the synthesis of the major capsid polypeptide.
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1 型单纯疱疹病毒的温度敏感突变体,其主要衣壳多肽的合成存在缺陷。

DOI:
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发表时间:
1974
影响因子:
3.8
通讯作者:
R. Courtney
R. Courtney
中科院分区:
医学3区
文献类型:
--
作者:
D. R. Bone;R. Courtney

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总结 用SDS-聚丙烯酰胺凝胶电泳在允许温度(34 °C)和非允许温度(39 °C)下检测了感染单纯疱疹病毒I型的DNA阴性温度敏感突变体ts 4的人胚肺细胞中合成的病毒诱导多肽。在34 °C下感染ts 4的细胞合成病毒特异性多肽的比例与34和39 °C下野生型感染的细胞相同。在39 °C下用ts 4感染的细胞表现出多种多肽缺陷,其中最突出的是抑制主要病毒衣壳多肽VP 154的合成。与VP 154相关的温度敏感性缺陷的表达仅发生在感染后4小时之前,如移位研究所示。与VP 154相关的温度敏感性缺陷在39 °C下的表达可以通过将感染的细胞下移至34 °C来逆转,即使在非允许温度下12小时后也是如此。这种逆转在阿糖胞苷存在下发生,但在放线菌素D存在下不发生。
Summary The virus-induced polypeptides synthesized in human embryonic lung cells infected with ts4, a DNA negative temperature-sensitive mutant of herpes simplex virus type I, were examined at the permissive (34 °C) and non-permissive (39 °C) temperatures using SDS-polyacrylamide gel electrophoresis. Cells infected with ts4 at 34 °C synthesized virus-specific polypeptides in the same proportion as did wild-type-infected cells at 34 and 39 °C. Cells infected with ts4 at 39 °C exhibited multiple polypeptide defects, the most prominent of which was the inhibition of the synthesis of the major virus capsid polypeptide, VP154. The expression of the temperature-sensitive defect relating to VP154 only occurred prior to 4 h after infection, as shown by shift-up studies. The expression of the temperature-sensitive defect at 39 °C relating to VP154 could be reversed by shifting down infected cells to 34 °C, even after 12 h at the non-permissive temperature. This reversal occurred in the presence of cytosine arabinoside but not in the presence of actinomycin D.