McKimm-Breschkin J L, Holmes I H
Infect Immun. 1982 Jun;36(3):857-63. doi: 10.1128/iai.36.3.857-863.1982.
Our investigations of interferon induction by rotaviruses showed that only when cells were pretreated with interferon, i.e., primed, could infectious rotaviruses induce significant quantities of interferon. As little as 0.5 U of interferon provided sufficient priming for this induction. UV-irradiated rotaviruses induced significant levels of interferon, and priming only marginally enhanced the yields. Neither heat-inactivated virus nor serum-neutralized virus was able to induce interferon, even when cells were primed. When cells were treated with purified virus double-stranded RNA in the presence of DEAE-dextran to facilitate uptake, interferon was induced, although priming did not enhance yields. These results strongly implicate the viral double-stranded RNA as the effector for interferon induction. The insensitivity of rotaviruses to interferon in vitro was also studied. Results suggested that this lack of sensitivity was not due to any inherent resistance of the virus to the antiviral proteins, but rather to lack of activation of cellular enzymes exhibiting antiviral activity.
我们对轮状病毒诱导干扰素的研究表明，只有当细胞用干扰素预处理（即启动）后，感染性轮状病毒才能诱导产生大量干扰素。低至0.5单位的干扰素就能为这种诱导提供足够的启动作用。紫外线照射的轮状病毒能诱导产生显著水平的干扰素，启动作用仅略微提高产量。热灭活病毒和血清中和病毒都不能诱导干扰素，即使细胞已启动。当在存在DEAE-葡聚糖以促进摄取的情况下，用纯化的病毒双链RNA处理细胞时，能诱导产生干扰素，尽管启动作用并未提高产量。这些结果强烈表明病毒双链RNA是干扰素诱导的效应物。还研究了轮状病毒在体外对干扰素的不敏感性。结果表明，这种不敏感性并非由于病毒对抗病毒蛋白有任何内在抗性，而是由于缺乏表现出抗病毒活性的细胞酶的激活。
