Lothrop D, Nicholson B L
J Virol. 1974 Sep;14(3):485-92. doi: 10.1128/JVI.14.3.485-492.1974.
In asynchronous RTG-2 cell cultures infected with infectious pancreatic necrosis (IPN) virus, inhibition of cellular DNA synthesis, but not protein synthesis, was detected 5 to 6 h postinfection and was 80 to 90% complete by 7 to 8 h. Inhibition of DNA synthesis was largely abolished by UV irradiation of the virus. Sedimentation analyses of phenol-extracted DNA indicated that native cellular DNA was not degraded during infection. Sedimentation on alkaline sucrose gradients of DNA from cells pulsed with radioactive thymidine for varying periods indicated that elongation of nascent DNA chains proceeded normally in infected cells. These and previous results suggest that IPN virus infection results in a reduction of the number of chromosomal sites active in DNA synthesis but does not affect the rate of polymerization at active sites. Cells synchronized with excess thymidine and hydroxyurea and infected with virus at the time of release from the block demonstrated an inhibition of DNA synthesis 3 h postinfection. Cells infected 4 h prior to release continued to synthesize normal amounts of DNA for 1 to 2 h after release. These results indicated that DNA synthesis in early synthetic phase is relatively insensitive to inhibition by IPN virus.
在感染传染性胰腺坏死（IPN）病毒的异步RTG - 2细胞培养物中，感染后5至6小时检测到细胞DNA合成受到抑制，但蛋白质合成未受影响，到7至8小时时抑制程度达到80%至90%。病毒经紫外线照射后，DNA合成抑制作用基本消除。对酚抽提DNA的沉降分析表明，感染期间天然细胞DNA未被降解。对用放射性胸苷脉冲不同时间的细胞的DNA在碱性蔗糖梯度上进行沉降分析表明，在受感染细胞中新生DNA链的延伸正常进行。这些以及先前的结果表明，IPN病毒感染导致DNA合成中活跃的染色体位点数量减少，但不影响活跃位点处的聚合速率。用过量胸苷和羟基脲同步化并在解除阻断时感染病毒的细胞，在感染后3小时显示出DNA合成受到抑制。在解除阻断前4小时感染的细胞在解除阻断后1至2小时继续合成正常量的DNA。这些结果表明，早期合成阶段的DNA合成对IPN病毒的抑制相对不敏感。
