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Component(s) of Sendai virus that can induce interferon in mouse spleen cells.

机译：仙台病毒的一种或多种成分，可以在小鼠脾细胞中诱导干扰素。

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To identify the active component of Sendai virus that induces interferon in mouse spleen cells, infectious and noninfectious viruses, envelope particles derived from them, and isolated hemagglutinin-neuraminidase (HN) glycoproteins were examined for interferon induction. The interaction between membranous structures containing Sendai virus HN glycoprotein and the receptors on the cell surface was shown to be sufficient for interferon induction in mouse spleen cells, suggesting that the actual inducer of interferon in mouse spleen cells is the HN glycoprotein of Sendai virus. When mouse spleen cells were stimulated in vitro with Sendai virus grown in eggs or LLC-MK2 cells or with membranous structures containing glycoproteins obtained from these viruses, interferon could be detected in the culture fluid. Furthermore, isolated HN glycoprotein per se could induce interferon in the cells. A linear correlation was found between the titer of interferon induced and the hemagglutinating activity of the membranous structure containing the HN glycoprotein. It was concluded from these findings that HN glycoprotein was the active component of Sendai virus responsible for interferon induction in mouse spleen cells and that viral RNA and F glycoprotein were not required. The results also showed that the interaction between HN glycoprotein and receptors on the cell surface triggered production of type I interferon (IFN-alpha and IFN-beta). Although when Sendai virus was incubated at 56 degrees C for 5 min it lost its hemolytic and hemagglutinating activities, it induced a considerable amount of interferon in the culture fluid of mouse spleen cells. The interferon-inducing ability of heat-inactivated virus could be absorbed with mouse spleen cells but not with sheep erythrocytes or mouse erythrocytes, indicating that the inactivated virus retained ability to bind to mouse lymphoid cells.
机译：为了鉴定在小鼠脾细胞中诱导干扰素的仙台病毒的活性成分，感染性和非感染性病毒，衍生自它们的包膜颗粒和分离的血凝素神经氨酸酶（HN）糖蛋白，检查干扰素的诱导作用。含有仙台病毒HN糖蛋白的膜结构与细胞表面受体之间的相互作用被证明足以诱导小鼠脾脏细胞中的干扰素，这表明小鼠脾脏细胞中干扰素的实际诱导物是仙台病毒的HN糖蛋白。当用鸡蛋或LLC-MK2细胞中生长的仙台病毒或含有从这些病毒获得的糖蛋白的膜状结构体外刺激小鼠脾细胞时，可以在培养液中检测到干扰素。此外，分离的HN糖蛋白本身可以在细胞中诱导干扰素。在诱导的干扰素效价与含有HN糖蛋白的膜结构的血凝活性之间发现线性相关。从这些发现可以得出结论，HN糖蛋白是仙台病毒的活性成分，负责在小鼠脾细胞中诱导干扰素，并且不需要病毒RNA和F糖蛋白。结果还表明，HN糖蛋白与细胞表面受体之间的相互作用触发了I型干扰素（IFN-α和IFN-β）的产生。尽管仙台病毒在56摄氏度下孵育5分钟后会失去溶血和血凝活性，但会在小鼠脾细胞的培养液中诱导大量干扰素。小鼠脾细胞可吸收热灭活病毒的干扰素诱导能力，而绵羊红细胞或小鼠红细胞则不能吸收，表明灭活病毒保留了与小鼠淋巴样细胞结合的能力。

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