Levinson W, Oppermann H, Jackson J
J Gen Virol. 1977 Oct;37(1):183-90. doi: 10.1099/0022-1317-37-1-183.
Kethoxal bis (thiosemicarbazone) (KTS) inhibited replication of, and plaque formation by, vesicular stomatitis virus (VSV) in chick embryo cells. No other thiosemicarbazones tested were effective. Virus-specific m-RNA and protein synthesis were inhibited by KTS. However, virion RNA-dependent RNA synthesis was not inhibited by the drug. Treatment of VSV virions directly with KTS produced enhancement, rather than inactivation, of plaque formation. KTS inhibited cellular DNA and RNA synthesis by 67 and 25% respectively. Since cellular DNA and RNA synthesis are not required for VSV replication, the inhibition of these processes is probably unrelated to the antivirial activity of KTS. Cellular protein synthesis was inhibited 24% by KTS. Unexpectedly, synthesis of four proteins was induced in KTS-treated uninfected cells.
乙二醛双(硫代半卡巴腙)(KTS)抑制了水泡性口炎病毒(VSV)在鸡胚细胞中的复制和蚀斑形成。所测试的其他硫代半卡巴腙均无效。KTS抑制了病毒特异性mRNA和蛋白质的合成。然而,该药物并未抑制病毒粒子RNA依赖性RNA合成。用KTS直接处理VSV病毒粒子反而增强了蚀斑形成,而非使其失活。KTS分别抑制细胞DNA和RNA合成67%和25%。由于VSV复制并不需要细胞DNA和RNA合成,因此这些过程的抑制可能与KTS的抗病毒活性无关。KTS抑制细胞蛋白质合成24%。出乎意料的是,在经KTS处理的未感染细胞中诱导了四种蛋白质的合成。