Arnheiter H, Haller O
J Virol. 1983 Sep;47(3):626-30. doi: 10.1128/JVI.47.3.626-630.1983.
The allele Mx regulates the extent to which interferon alpha/beta inhibits the growth of influenza viruses in mouse cells such as peritoneal macrophages. The time course of induction of the antiviral state against an influenza A virus is comparable in macrophages with and without Mx and is similar to that found with vesicular stomatitis virus. In contrast, the decay of the antiviral state against influenza virus is markedly slower in Mx-positive cells and slower than that against vesicular stomatitis virus observed in either Mx-positive or Mx-negative cells. Thus, after removal of interferon alpha/beta, Mx-positive cells remain protected against influenza virus at times when they have lost protection against vesicular stomatitis virus. These results suggest that interferon alpha/beta treatment activates different antiviral mechanisms, each acting against distinct groups of viruses and each independently controlled by host genes.
等位基因Mx调节干扰素α/β抑制流感病毒在小鼠细胞(如腹膜巨噬细胞)中生长的程度。在有和没有Mx的巨噬细胞中,针对甲型流感病毒诱导抗病毒状态的时间进程是相当的,并且与水泡性口炎病毒的情况相似。相比之下,在Mx阳性细胞中,针对流感病毒的抗病毒状态的衰减明显较慢,并且比在Mx阳性或Mx阴性细胞中观察到的针对水泡性口炎病毒的抗病毒状态的衰减要慢。因此,在去除干扰素α/β后,Mx阳性细胞在失去对水泡性口炎病毒的保护时,仍对流感病毒具有保护作用。这些结果表明,干扰素α/β处理激活了不同的抗病毒机制,每种机制作用于不同的病毒组,并且每种机制都由宿主基因独立控制。