Thymidine kinase (TK) induction after infection of TK-deficient rabbit cell mutants with bovine herpesvirus type 1 (BHV-1): isolation of TK- BHV-1 mutants.
Thymidine kinase (TK) induction after infection of TK-deficient rabbit cell mutants with bovine herpesvirus type 1 (BHV-1): isolation of TK- BHV-1 mutants.
复制标题
用牛疱疹病毒 1 型 (BHV-1) 感染 TK 缺陷型兔细胞突变体后胸苷激酶 (TK) 诱导：TK-BHV-1 突变体的分离。
DOI：
10.1016/0042-6822(83)90092-2
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发表时间：
1983
期刊：
影响因子：
3.7
通讯作者：
Qavi,H
中科院分区：
文献类型：
--
作者：
Kit,S;Qavi,H
牛疱疹病毒1型（BHV-1）洛杉矶株和库珀株感染牛胚胎气管（EBTr）和兔皮肤成纤维细胞（RAB-9）细胞6小时后，细胞质胸苷激酶（TK）活性增强。为了了解这种增强是否源于病毒特异性TK活性的诱导，进行了生化和遗传研究。生化实验表明：(1)bhv -1诱导的TK活性具有其他疱疹病毒编码TK的相对圆盘PAGE迁移率（Rm）特征，与宿主细胞胞浆TK的Rm值明显不同；bhv -1诱导的TK对arabinosylthymine （araT）竞争性抑制的敏感性明显高于EBTr和rabb -9细胞的细胞质TK。遗传实验包括分离出缺乏胞浆TK活性的BrdUrd （BrdUrd）抗性家兔细胞系[RAB(BU)]以及BrdUrd和arat抗性BHV-1突变体。RAB（BU）细胞在被野生型TK+BHV-1感染后获得TK活性，但不具有耐药BHV-1突变体。实验强烈提示野生型BHV-1诱导病毒特异性TK活性。
Cytosol thymidine kinase (TK) activity is enhanced at 6 hr after bovine embryo tracheal (EBTr) and rabbit skin fibroblast (RAB-9) cells are infected with the Los Angeles and Cooper strains of bovine herpesvirus type 1 (BHV-1). To learn whether this enhancement resulted from the induction of a virus-specific TK activity, biochemical and genetic studies were carried out. The biochemical experiments demonstrated that: (i) the BHV-1-induced TK activity had a relative disc PAGE mobility (Rm) characteristic of other herpesvirus-encoded TKs and distinctly different from the Rm value of the cytosol TK of host cells; and (ii) the BHV-1-induced TK was significantly more sensitive to competitive inhibition by arabinosylthymine (araT) than the cytosol TKs of EBTr and RAB-9 cells. The genetic experiments entailed the isolation of a bromodeoxyuridine (BrdUrd)-resistant rabbit cell line [RAB(BU)] deficient in cytosol TK activity and of BrdUrd- and araT-resistant BHV-1 mutants. RAB(BU) cells acquired TK activity after they were infected by wild-type, TK+BHV-1, but not drug-resistant BHV-1 mutants. The experiments strongly suggest that wild-type BHV-1 induces a virus-specific TK activity.