Fukami Y, Hosaka Y, Yasuda Y, Bonilla J A
Infect Immun. 1979 Dec;26(3):815-21. doi: 10.1128/iai.26.3.815-821.1979.
Studies were made on the abilities of Sendai virus envelope components to induce primary and secondary generations of virus-specific cytotoxic mouse T lymphocytes (CTL). The primary CTL response in BALB/c mice was induced by reassembled envelope particles that had fusion activity but not by envelope glycoproteins without fusion activity, although both preparations induced a humoral immune response. Reconstitution of membrane-bound envelope proteins from envelope glycoproteins with lipids restored the fusion activity and the capacity to induce CTL. Target cells susceptible to virus-specific CTL could be induced by reassembled envelope particles, but not by envelope glycoproteins or LLC-MK2 cell-grown Sendai virus, neither of which had fusion activity. On the other hand, all the viruses and envelope components tested were found to stimulate a virus-specific CTL response in the in vitro secondary generation of CTL from virus-primed spleen cells. These results suggest that Senaei virus fusion activity is involved in primary induction of the CTL response as well as in target cell formation, but that it is not essential for secondary stimulation of the CTL response.
对仙台病毒包膜成分诱导初代和次代病毒特异性细胞毒性小鼠T淋巴细胞(CTL)的能力进行了研究。在BALB/c小鼠中,初代CTL反应是由具有融合活性的重组包膜颗粒诱导的,而不是由没有融合活性的包膜糖蛋白诱导的,尽管这两种制剂都能诱导体液免疫反应。用脂质将包膜糖蛋白重构为膜结合包膜蛋白可恢复融合活性和诱导CTL的能力。重组包膜颗粒可诱导对病毒特异性CTL敏感的靶细胞,但包膜糖蛋白或LLC-MK2细胞培养的仙台病毒则不能,这两者均无融合活性。另一方面,发现所有测试的病毒和包膜成分在由病毒致敏的脾细胞体外次代生成CTL的过程中均能刺激病毒特异性CTL反应。这些结果表明,仙台病毒融合活性参与CTL反应的初代诱导以及靶细胞形成,但对CTL反应的次代刺激并非必需。