猴病毒40最小功能的分析。3. 紫外线照射的猴病毒40致癌性和感染性“宿主细胞修复”的证据。
Analysis of minimal functions of simian virus 40. 3. Evidence for "host cell repair" of oncogenicity and infectivity of UV-irradiated simian virus 40.
作者信息
Seemayer N H, Defendi V
出版信息
J Virol. 1974 Jan;13(1):36-41. doi: 10.1128/JVI.13.1.36-41.1974.
Abstract
The in vitro transforming capacity of simian virus 40 (SV40) for Syrian hamster cells is highly resistant to inactivation by UV light in comparison to infectivity. In the same cell system, we demonstrated a "host cell repair mechanism" sensitive to caffeine which is, to a large extent, responsible for the high resistance to UV inactivation of the transforming capacity of SV40. The survival of infectivity of UV-irradiated SV40 in CV-1 cells was also sensitive to caffeine, again indicating host cell repair. On the other hand, depression of normal cell DNA synthesis by hydroxyurea during the first 24 h postinfection only modestly reduced, and to a similar extent, the transforming capacity of UV-irradiated and nonirradiated SV40.
摘要
与感染性相比，猿猴病毒40（SV40）对叙利亚仓鼠细胞的体外转化能力对紫外线灭活具有高度抗性。在同一细胞系统中，我们证明了一种对咖啡因敏感的“宿主细胞修复机制”，这种机制在很大程度上导致了SV40转化能力对紫外线灭活的高抗性。紫外线照射的SV40在CV-1细胞中的感染性存活也对咖啡因敏感，再次表明存在宿主细胞修复。另一方面，在感染后最初24小时内，羟基脲对正常细胞DNA合成的抑制仅适度降低了紫外线照射和未照射的SV40的转化能力，且降低程度相似。
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