Gauntt C J, Lockart R Z
J Virol. 1968 Jun;2(6):567-75. doi: 10.1128/JVI.2.6.567-575.1968.
Interferon, when added to L cells, inhibited the synthesis of infectious Mengo viral ribonucleic acid, hemagglutinins, and infectious virus by 85 to 95%. Serum-blocking antigens were also reduced by the action of interferon, but threefold excess amounts of these antigens accumulated in interferon-treated cultures above the amounts expected for the quantity of infectious virus that was produced in these cultures. Radioautographic analysis showed that 28 to 36% of the cells of an interferon-treated population synthesized viral ribonucleic acid and 36 to 47% produced viral antigens as determined by an immunofluorescence technique. Despite the reductions in synthesis of viral components, all cells in an interferon-treated culture underwent cytopathic effects at the same time as cells in infected cultures which had not been treated with interferon. The results are compatible with the hypothesis that the cell destruction which results from the infection of L cells with Mengo virus is due to a protein which is coded for by the virus but is not a component of the mature virion.
将干扰素添加到L细胞中时，可使感染性门戈病毒核糖核酸、血凝素和感染性病毒的合成受到85%至95%的抑制。干扰素的作用还可使血清封闭抗原减少，但在经干扰素处理的培养物中，这些抗原的量比这些培养物中产生的感染性病毒量预期的多三倍。放射自显影分析表明，经干扰素处理的细胞群体中有28%至36%的细胞合成病毒核糖核酸，通过免疫荧光技术测定，有36%至47%的细胞产生病毒抗原。尽管病毒成分的合成有所减少，但经干扰素处理的培养物中的所有细胞与未用干扰素处理的感染培养物中的细胞同时出现细胞病变效应。这些结果与以下假设相符，即L细胞感染门戈病毒后导致的细胞破坏是由一种由病毒编码但不是成熟病毒粒子组成部分的蛋白质引起的。
