Sergiescu D
Int J Cancer. 1982 Apr 15;29(4):459-64. doi: 10.1002/ijc.2910290416.
Infection of Kirsten sarcoma virus-transformed non-producer BALB-3T3 mouse cells with UV-irradiated mouse cytomegalovirus (MCMV) resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat or mink cells. The levels of type C virus activated by MCMV were related to the UV dose applied. Under optimal conditions the frequencies of activation varied from 3.0 to 8.0 x 10(-4). The capacity of MCMV to activate type C virus was abolished by heat inactivation and by neutralization with specific antiserum against MCMV. Virus induction decreased under conditions of cell exposure to hydroxyurea or actinomycin D, inhibitors of DNA and RNA synthesis, respectively, with actinomycin D having a greater inhibitory effect. This suggests that both DNA and RNA synthesis are required for UV-MCMV induction of murine xenotropic virus.
用紫外线照射过的小鼠巨细胞病毒（MCMV）感染 Kirsten 肉瘤病毒转化的非产生性 BALB - 3T3 小鼠细胞，导致在允许性大鼠或貂细胞中通过感染中心形成检测到一种嗜异性 C 型病毒被激活。MCMV 激活的 C 型病毒水平与所施加的紫外线剂量有关。在最佳条件下，激活频率在 3.0 至 8.0×10⁻⁴ 之间变化。MCMV 激活 C 型病毒的能力通过热灭活以及用抗 MCMV 的特异性抗血清中和而被消除。在细胞分别暴露于羟基脲或放线菌素 D（DNA 和 RNA 合成抑制剂）的条件下，病毒诱导减少，其中放线菌素 D 具有更大的抑制作用。这表明 DNA 和 RNA 合成对于紫外线 - MCMV 诱导鼠嗜异性病毒都是必需的。
