Jacquemont B, Huppert J
J Virol. 1977 Apr;22(1):160-7. doi: 10.1128/JVI.22.1.160-167.1977.
5' S-isobutyl-adenosine (SIBA), a structural analogue of S-adenosylhomocysteine, reversibly blocks the multiplication of herpes simplex type 1 virus. In the presence of SIBA, viral protein synthesis is inhibited. After removing SIBA the synthesis of proteins starts rapidly again. The new polypeptides are mainly alpha proteins (Honess and Roizman, J. Virol. 14:8-19, 1974,), normally the first to be synthesized after infection. The rapid synthesis of proteins after release of inhibition seems to be directed by mRNA formed in the presence of SIBA as indicated by experiments using actinomycin D but which was undermethylated as shown by analysis of methyl groups on RNA. SIBA inhibits the methylation of mRNA and especially that of the 5' cap. Capping of mRNA thus seems to be essential for efficient translation. The analogue affected various methylations to different extents.
5'-S-异丁基腺苷（SIBA）是S-腺苷同型半胱氨酸的结构类似物，可可逆地阻断单纯疱疹病毒1型的增殖。在SIBA存在的情况下，病毒蛋白质合成受到抑制。去除SIBA后，蛋白质合成又迅速重新开始。新的多肽主要是α蛋白（霍尼斯和罗伊兹曼，《病毒学杂志》14:8-19，1974年），通常是感染后最先合成的。如使用放线菌素D的实验所示，抑制解除后蛋白质的快速合成似乎是由在SIBA存在下形成的mRNA指导的，但通过对RNA上甲基的分析表明，该mRNA甲基化不足。SIBA抑制mRNA的甲基化，尤其是5'帽的甲基化。因此，mRNA的加帽似乎是有效翻译所必需的。该类似物对各种甲基化的影响程度不同。
