Stewart W E, Gosser L B, Lockart R Z
J Virol. 1971 Jun;7(6):792-801. doi: 10.1128/JVI.7.6.792-801.1971.
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.
当L细胞感染MM病毒时，不会产生干扰素。然而，当用干扰素处理过的L细胞感染MM病毒时，会产生几千单位的干扰素。我们将细胞从非产生者转变为产生者的这种转变称为引发。细胞完全引发所需的时间取决于与之孵育的干扰素浓度。引发的细胞比受其他诱导剂刺激的正常细胞更早产生干扰素。在蛋白质合成抑制剂存在的情况下接触干扰素的细胞会完全引发，但不会产生病毒抗性。此外，引发的细胞会对低浓度的聚肌苷酸·聚胞苷酸产生干扰素，而这种物质在正常细胞中不会诱导产生干扰素。因此，引发似乎是干扰素的一种功能，与其抗病毒活性是可分离的。其他几种在L细胞、人胚肺细胞或猴肾细胞中未能诱导产生干扰素的小RNA病毒，当这些细胞被同源干扰素引发后，确实会诱导产生干扰素。
