Yamakawa Izumi, Tsurudome Masato, Kawano Mitsuo, Nishio Machiko, Komada Hiroshi, Ito Morihiro, Uji Yukitaka, Ito Yasuhiko
Department of Microbiology, Mie University Graduate School of Medicine, Japan.
Microbiol Immunol. 2007;51(6):601-8. doi: 10.1111/j.1348-0421.2007.tb03946.x.
When K562 cells were infected with Newcastle disease virus (NDV) or human parainfluenza type 2 virus (hPIV-2), polykaryocyte formation could not be detected. Failure of multinucleated giant cell formation in K562 cells infected with either NDV or hPIV-2 is due to disturbance of the viral envelope-cell fusion step or to defect in the cell-cell fusion step, respectively. Especially, NDV completely replicated in K562 cells, and the hemagglutinin-neuraminidase and fusion proteins expressed on the cell surface of NDV-infected K562 cell were fully functional for fusion inducing activity. Therefore, the cell membranes of K562 cells are considered to be resistant to virus-induced cell fusion. Membrane fusion is regulated by many host factors including membrane fluidity, cytoskeletal systems, and fusion regulatory proteins system. An unknown regulatory mechanism of virus-induced cell fusion may function on the cell surface of K562 cells.
当K562细胞感染新城疫病毒(NDV)或人副流感病毒2型(hPIV - 2)时,未检测到多核巨细胞形成。感染NDV或hPIV - 2的K562细胞未能形成多核巨细胞,分别是由于病毒包膜 - 细胞融合步骤受到干扰或细胞 - 细胞融合步骤存在缺陷。特别是,NDV在K562细胞中完全复制,并且在感染NDV的K562细胞表面表达的血凝素 - 神经氨酸酶和融合蛋白具有完全的融合诱导活性。因此,K562细胞的细胞膜被认为对病毒诱导的细胞融合具有抗性。膜融合受许多宿主因素调节,包括膜流动性、细胞骨架系统和融合调节蛋白系统。一种未知的病毒诱导细胞融合调节机制可能在K562细胞的细胞表面发挥作用。