Combined action of mouse alpha and beta interferons in influenza virus-infected macrophages carrying the resistance gene Mx
Combined action of mouse alpha and beta interferons in influenza virus-infected macrophages carrying the resistance gene Mx
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小鼠α和β干扰素对携带抗性基因Mx的流感病毒感染的巨噬细胞的联合作用
DOI：
10.1128/jvi.49.3.709-716.1984
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发表时间：
1984
影响因子：
5.4
通讯作者：
M. Horisberger
中科院分区：
文献类型：
--
作者：
T. Meyer;M. Horisberger
在小鼠中，α 和 β 干扰素 (IFN) 对抗流感病毒的联合作用受到宿主基因 Mx 的调节。高浓度的IFN不能有效阻止甲型流感病毒在缺乏Mx基因的培养巨噬细胞中的复制，而携带Mx的培养巨噬细胞即使在低浓度的IFN下也能产生很强的抗病毒活性。在用 IFN-α + β 处理的 Mx/Mx 和 +/+ 小鼠巨噬细胞中比较了流感病毒复制周期的几个步骤。脱漆不受影响。无论宿主细胞的遗传构成如何，在最高浓度的 IFN 下，在 IFN 处理的巨噬细胞中观察到初级转录物积累的两倍减少。没有获得证据表明当用 IFN-α + β 处理时，缺乏 Mx 的巨噬细胞中流感病毒翻译受到抑制。相比之下，尽管初级转录物在无细胞系统中指导病毒多肽的合成方面具有活性，但在用这些 IFN 处理的携带 Mx 的巨噬细胞中发生了流感病毒多肽合成的显着停止。我们得出结论，流感病毒翻译的特定抑制机制是由携带抗性基因 Mx 的巨噬细胞中的 IFN-α + β 诱导的。
In mice, the combined action of alpha and beta interferons (IFNs) against influenza viruses is modulated by the host gene Mx. High concentrations of IFN fail to prevent efficiently the replication of influenza A virus in cultured macrophages lacking the gene Mx, whereas cultured macrophages carrying Mx develop strong antiviral activity even at low concentrations of IFN. Several steps in the replication cycle of influenza virus were compared in Mx/Mx and +/+ mouse macrophages treated with IFN-alpha + beta. Uncoating was not affected. A twofold reduction in the accumulation of primary transcripts was observed in IFN-treated macrophages at the highest concentration of IFN regardless of the genetic constitution of the host cell. No evidence was obtained for inhibition of influenza virus translation in macrophages which lacked Mx when treated with IFN-alpha + beta. In contrast, a marked shut-off of influenza virus polypeptide synthesis occurred in Mx-bearing macrophages treated with these IFNs, although the primary transcripts were active in directing the synthesis of viral polypeptides in a cell-free system. We concluded that a specific inhibitory mechanism for influenza virus translation was induced by IFN-alpha + beta in macrophages bearing the resistance gene Mx.