Dawson K M, Stewart A, Stebbing N
J Gen Virol. 1979 Oct;45(1):237-40. doi: 10.1099/0022-1317-45-1-237.
The protein synthesis inhibitor beta-gamma-methylene guanosine triphosphate (Gpp-CH2p) is shown here to be ineffective as a 'leaky membrane' antiviral agent against encephalomyocarditis virus infection of L cells and mice. Studies with GppCH2p in encephalomyocarditis virus-infected L cells indicate that the cells only become permeable to the inhibitor late in infection because the compound significantly inhibits protein synthesis only when added at 4 h p.i. At this time 50 to 70% of the new infectious virus particles have already been synthesized, and this is reflected in maximum inhibition of virus yields of only about 40%. Moreover, comparison of inhibition of protein synthesis by GppCH2p in vitro and in cell cultures indicates that the intracellular concentration attained is only 0.25% of that in the medium. The lack of antiviral activity of GppCH2p in encephalomyocarditis virus-infected mice is probably due to leakiness of infected cells occurring too late for sufficient inhibition of virus synthesis to be obtained.
本文显示，蛋白质合成抑制剂β-γ-亚甲基鸟苷三磷酸（Gpp-CH2p）作为一种“渗漏膜”抗病毒剂，对L细胞和小鼠的脑心肌炎病毒感染无效。对感染脑心肌炎病毒的L细胞进行的GppCH2p研究表明，细胞仅在感染后期才对该抑制剂通透，因为该化合物仅在感染后4小时添加时才会显著抑制蛋白质合成。此时，50%至70%的新感染病毒颗粒已经合成，这反映在病毒产量的最大抑制率仅约为40%。此外，比较GppCH2p在体外和细胞培养中对蛋白质合成的抑制作用表明，细胞内达到的浓度仅为培养基中的0.25%。GppCH2p在感染脑心肌炎病毒的小鼠中缺乏抗病毒活性，可能是由于感染细胞的渗漏发生得太晚，无法充分抑制病毒合成。
