Migus D O, Dobos P
J Gen Virol. 1980 Mar;47(1):47-57. doi: 10.1099/0022-1317-47-1-47.
Ribavirin (1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide) at concentrations of 10 microgram/ml or more, inhibited the replication of infectious pancreatic necrosis virus (IPNV) in both Chinook salmon embryo (CHSE-214) and rainbow trout gonad (RTG-2) cells. The drug was most effective when added just before or within 8 h p.i. Incorporation studies with radioactive precursors demonstrated that ribavirin suppressed cellular DNA and RNA synthesis within 2 to 3 h after addition of the drug. The inhibition of nucleic acid synthesis and the antiviral activity was gradually reversed within 3 to 5 days after removal of the drug from the infected cells. Polyacrylamide slab-gel electrophoresis combined with fluorography revealed that: (i) 0.5 microgram/ml actinomycin D sufficiently inhibited host cell RNA synthesis thereby enabling the study of virus-specific RNA synthesis in infected cells and (ii) ribavirin inhibited the synthesis of all three virus RNA forms: the transcription intermediate, virus mRNA and progeny dsRNA.
利巴韦林（1-β-D-呋喃核糖基-1,2,4-三唑-3-羧酰胺）浓度在10微克/毫升及以上时，可抑制传染性胰腺坏死病毒（IPNV）在奇努克鲑胚胎（CHSE-214）细胞和虹鳟性腺（RTG-2）细胞中的复制。该药物在感染前或感染后8小时内添加时效果最佳。用放射性前体进行的掺入研究表明，利巴韦林在添加药物后2至3小时内可抑制细胞DNA和RNA合成。从感染细胞中去除药物后，核酸合成的抑制作用和抗病毒活性在3至5天内逐渐逆转。聚丙烯酰胺平板凝胶电泳结合荧光自显影显示：（i）0.5微克/毫升放线菌素D足以抑制宿主细胞RNA合成，从而能够研究感染细胞中病毒特异性RNA合成；（ii）利巴韦林抑制所有三种病毒RNA形式的合成：转录中间体、病毒mRNA和子代双链RNA。
