Nagai Y, Maeno K, Iinuma M, Yoshida T, Matsumoto T
J Virol. 1972 Feb;9(2):234-43. doi: 10.1128/JVI.9.2.234-243.1972.
The effect of ouabain (g-strophanthin), a cardiac glycoside, on the growth of several enveloped viruses was examined. It was found that the growth of HVJ (Sendai virus) in chick embryo cells was markedly inhibited by the drug at a concentration as low as 5 x 10(-5)m. A virus-inhibitory concentration of ouabain did not cause morphological changes in uninfected cells, nor did it have the capacity to inactivate virus infectivity. Ouabain interfered with the intracellular synthesis of viral macromolecules. Although viral ribonucleic acid and viral antigens were synthesized by the ouabain-treated cells, the rate of synthesis was slower, and the total amounts of these macromolecules were smaller than those in the untreated control cells. It is suggested that ouabain inhibits the function of membrane-bound Na, K-adenosine triphosphatase of the chick embryo cells and thus prevents accumulation of K ion in them. Accumulation of intracellular K ion to a certain level would be needed for events of exponential growth of virus to proceed, and ouabain might inhibit this step by preventing such accumulation of K ion. This view was supported by the finding that the concentration of K ion in the HVJ-infected cells was rapidly reduced by the treatment with ouabain, and that, when the ouabain-treated culture was shifted to a medium containing a higher concentration of K ion than normal medium, virus production started in parallel with the increase of intracellular K ion. The fact that the concentration of K ion in BHK-21 cells, which support virus growth in the presence of ouabain, is not reduced by the treatment with the drug also suggested this possibility.
研究了强心苷哇巴因(毒毛花苷)对几种包膜病毒生长的影响。发现低至5×10⁻⁵m浓度的该药物能显著抑制鸡胚细胞中HVJ(仙台病毒)的生长。哇巴因的病毒抑制浓度不会引起未感染细胞的形态变化,也没有使病毒感染性失活的能力。哇巴因干扰病毒大分子的细胞内合成。虽然经哇巴因处理的细胞能合成病毒核糖核酸和病毒抗原,但合成速率较慢,且这些大分子的总量比未处理的对照细胞中的少。提示哇巴因抑制鸡胚细胞膜结合的钠钾 - 三磷酸腺苷酶的功能,从而阻止钾离子在细胞内积累。病毒指数生长的过程需要细胞内钾离子积累到一定水平,而哇巴因可能通过阻止钾离子的这种积累来抑制这一步骤。这一观点得到以下发现的支持:用哇巴因处理后,HVJ感染细胞中的钾离子浓度迅速降低;并且,当将经哇巴因处理的培养物转移到含有比正常培养基更高浓度钾离子的培养基中时,病毒产生与细胞内钾离子的增加同时开始。在哇巴因存在下支持病毒生长的BHK - 21细胞中,药物处理后钾离子浓度未降低这一事实也表明了这种可能性。