HOST GENE INFLUENCES SENSITIVITY TO INTERFERON ACTION SELECTIVITY FOR INFLUENZA-VIRUS
HOST GENE INFLUENCES SENSITIVITY TO INTERFERON ACTION SELECTIVITY FOR INFLUENZA-VIRUS
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DOI：
10.1038/283660a0
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发表时间：
1980-01-01
期刊：
影响因子：
64.8
通讯作者：
GRESSER, I
中科院分区：
文献类型：
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作者：
HALLER, O;ARNHEITER, H;GRESSER, I
已经在小鼠中研究了几个由基因决定的对不同病毒的抗性的例子1。由等位基因Mxin A2 G小鼠引起的先天性抗性可表征如下：抗性对正粘病毒家族（流感病毒）成员具有特异性2;它在不同器官和细胞中表达2 -6;并且它不依赖于功能性免疫系统3，4，7。使抗性小鼠对流感病毒完全易感的唯一方法是用有效的抗干扰素血清治疗8，这表明干扰素在抗性中是重要的。干扰素一般被认为相对无差别地抑制所有动物病毒的增殖。因此，干扰素似乎不太可能参与这种抗性，因为A2 G小鼠对流感病毒具有选择性抗性，尽管与对照小鼠对几种其他病毒一样敏感4。然而，也有这样的例子，即干扰素产生的遗传控制或对干扰素作用的敏感性对于给定的病毒是选择性地表达的。因此，De Maeyer及其同事已经证明，四个不同的If基因座控制了小鼠注射纽卡斯尔病病毒（NDV）9、小鼠乳腺肿瘤病毒10或仙台病毒后产生的循环干扰素的量（个人交流）。Hansonet al.11发现，当用Arbo B病毒检测时，来自C3 H RV小鼠的细胞培养物（对Arbo B病毒感染具有抗性）比来自易感C3 H小鼠的培养物更易受干扰素抑制作用的影响。我们在这里提出的结果，显示抗正粘病毒（Mx阳性）的小鼠的巨噬细胞的文化可以保护的干扰素的量少得多的是必要的，以保护文化从易感小鼠当这些文化感染流感病毒，而没有差异的敏感性干扰素时，观察文化感染水泡性口炎病毒（VSV）或脑心肌炎病毒（EMC）。我们认为，这些结果显示了对特定病毒的干扰素作用敏感性的遗传控制与A2 G小鼠对流感病毒的体内抗性有关。如果适用于人，这些结果也可能是重要的，在了解个体差异的敏感性病毒感染。
Several examples of genetically determined resistance to different viruses have been studied in mice1. Inborn resistance due to the alleleMxin A2G mice may be characterised as follows: resistance is specific for members of the orthomyxo family (influenza virus)2; it is expressed in different organs and cells2–6; and it is independent of a functioning immune system3,4,7. The only means of rendering resistant mice fully susceptible to influenza virus has been treatment with potent anti-interf eron serum8, indicating that interf eron is important in resistance. Interf eron is generally thought to inhibit the multiplication of all animal viruses relatively indiscriminately. Therefore, it had seemed unlikely that interferon was involved in this resistance, as A2G mice were selectively resistant to influenza virus albeit as sensitive as control mice to several other viruses4. There are, however, examples in which the genetic control of the production of interferon or the sensitivity to interferon action is expressed selectively for a given virus. Thus, De Maeyer and coworkers have shown that four differentIfloci control the amount of circulating interferon produced after injection of mice with Newcastle disease virus (NDV)9, mouse mammary tumour virus10, or Sendai virus (personal communication). Hansonet al.11found that cultures of cells from C3H RV mice, resistant to Arbo B virus infection, were much more susceptible to the inhibitory effect of interferon when tested with Arbo B viruses than cultures taken from susceptible C3H mice. We present here results, showing that cultures of macrophages from mice resistant to orthomyxoviruses (Mxpositive) can be protected by much smaller amounts of interferon than are necessary to protect cultures from susceptible mice when these cultures are infected with influenza virus; whereas no difference in sensitivity to interferon is observed when cultures are infected with vesicular stomatitis virus (VSV) or encephalomyocarditis virus (EMC). We believe that these results showing a genetic control of sensitivity to interferon action specific for a given virus are related to thein vivoresistance of A2G mice to influenza virus. If applicable to man, these results may also be of importance in understanding individual variations in sensitivity to viral infections.