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感染新城疫病毒和人副流感病毒2型的K562细胞中多核巨细胞形成失败。

Failure of multinucleated giant cell formation in k562 cells infected with newcastle disease virus and human parainfluenza type 2 virus.

作者信息

Yamakawa Izumi, Tsurudome Masato, Kawano Mitsuo, Nishio Machiko, Komada Hiroshi, Ito Morihiro, Uji Yukitaka, Ito Yasuhiko

机构信息

Department of Microbiology, Mie University Graduate School of Medicine, Japan.

出版信息

Microbiol Immunol. 2007;51(6):601-8. doi: 10.1111/j.1348-0421.2007.tb03946.x.

Abstract

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.

摘要

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。

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