Priming: a Nonantiviral Function of Interferon
Priming: a Nonantiviral Function of Interferon
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引发：干扰素的非抗病毒功能
作者：
W. Stewart;L. Gosser;R. Lockart
当L细胞感染MM病毒时，它们不产生干扰素。然而，当干扰素处理的L细胞感染MM病毒时，产生数千单位的干扰素。我们把细胞从非生产者到生产者的转变称为启动。细胞完全致敏所需的时间取决于与它们孵育的干扰素浓度。致敏细胞产生干扰素的时间早于其他诱导剂刺激的正常细胞。在蛋白质合成抑制剂存在的情况下暴露于干扰素的细胞变得完全致敏，但没有产生病毒抗性。此外，致敏细胞产生干扰素，以响应低浓度的聚核糖肌苷酸·聚核糖胞苷酸，而在正常细胞中不诱导干扰素。因此，引发似乎是干扰素的功能，与其抗病毒活性分离。其他几种不能在L细胞、人胚肺细胞或猴肾细胞中诱导干扰素的小核糖核酸病毒，在这些细胞被同源干扰素引发后确实诱导了干扰素。
No interferon is made by L cells when they are infected with MM virus. However, several thousand units of interferon are produced when interferon-treated L cells are infected with MM virus. We call the conversion of cells, from nonproducers to producers, priming. The time required for cells to become fully primed is dependent on the interferon concentration with which they are incubated. Primed cells produced interferon earlier than normal cells stimulated by other inducers. Cells which were exposed to interferon in the presence of inhibitors of protein synthesis became fully primed yet developed no virus resistance. Also, primed cells produced interferon in response to low concentrations of polyriboinosinic acid · polyribocytidylic acid that did not induce interferon in normal cells. Therefore, priming appears to be a function of interferon separable from its antiviral activity. Several other picornaviruses that failed to induce interferon in L cells, human embryonic lung cells, or monkey kidney cells did induce interferon when these cells had been primed by homologous interferons.