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腺病毒感染的人细胞系中胸苷激酶的起源

Origin of thymidine kinase in adenovirus-infected human cell lines.

作者信息

Kit S, Nakajima K, Dubbs D R

出版信息

J Virol. 1970 Apr;5(4):446-50. doi: 10.1128/JVI.5.4.446-450.1970.

Abstract

Human adenovirus type 5 enhances the thymidine kinase activity of KB cells but does not induce the enzyme in kinase-deficient HeLa (BU25) cells. Vaccinia induces thymidine kinase activity in both KB and HeLa (BU25) cells. Human adenovirus types 2, 4, 7, and 12 also fail to induce the enzyme in HeLa (BU25) cells. Vaccinia replicates equally well in the presence or absence of HATG (hypoxanthine-aminopterin-thymidine-glycine) in KB and HeLa (BU25) cells. Adenovirus type 5 replicates in KB and in HeLa (BU25) cells in the absence of HATG, and adenovirus type 5 replicates in kinase-positive KB cells in the presence of HATG. However, replication of adenovirus type 5 is grossly inhibited in HeLa (BU25) cells in the presence of HATG. These results suggest that human adenoviruses do not code for a new virus-specific thymidine kinase.

摘要

人5型腺病毒可增强KB细胞的胸苷激酶活性,但在缺乏激酶的HeLa(BU25)细胞中不诱导该酶的产生。痘苗病毒可在KB细胞和HeLa(BU25)细胞中诱导胸苷激酶活性。人2型、4型、7型和12型腺病毒也不能在HeLa(BU25)细胞中诱导该酶的产生。在KB细胞和HeLa(BU25)细胞中,无论有无HATG(次黄嘌呤-氨基蝶呤-胸腺嘧啶-甘氨酸),痘苗病毒的复制情况均良好。5型腺病毒在无HATG的情况下可在KB细胞和HeLa(BU25)细胞中复制,在有HATG的情况下可在激酶阳性的KB细胞中复制。然而,在有HATG的情况下,5型腺病毒在HeLa(BU25)细胞中的复制受到严重抑制。这些结果表明,人腺病毒不编码新的病毒特异性胸苷激酶。

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