Browne M J
Antimicrob Agents Chemother. 1981 May;19(5):712-5. doi: 10.1128/AAC.19.5.712.
Actinomycin D inhibited the yield of influenza virus hemagglutinin from MDCK cells infected at high multiplicity, but had little effect on the yield of parainfluenza virus hemagglutinin. In similar hemagglutinin yield experiments, ribavirin was only slightly more active (threefold) against influenza virus than against parainfluenza virus replication. In plaque inhibition experiments, ribavirin depressed influenza virus plaque formation by 50% at a concentration of approximately 3 micrograms/ml, whereas the corresponding figure for parainfluenza viruses was threefold higher. The concentration of ribavirin demonstrating anti-influenza activity was indistinguishable for that inhibiting host cell growth. It is concluded that, unlike actinomycin D, ribavirin is unlikely to have a major effect on the provision of host cell 5-germinal methylated cap structures and the subsequent priming of influenza messenger ribonucleic acid synthesis.
放线菌素D抑制了高感染复数感染的MDCK细胞中流感病毒血凝素的产量,但对副流感病毒血凝素的产量影响很小。在类似的血凝素产量实验中,利巴韦林对流感病毒的活性仅比对副流感病毒复制的活性略高(三倍)。在蚀斑抑制实验中,利巴韦林在浓度约为3微克/毫升时可使流感病毒蚀斑形成减少50%,而副流感病毒的相应数值则高三倍。显示抗流感活性的利巴韦林浓度与抑制宿主细胞生长的浓度无法区分。结论是,与放线菌素D不同,利巴韦林不太可能对宿主细胞5-甲基化帽结构的提供以及随后流感信使核糖核酸合成的引发产生重大影响。