Ayata Minoru, Shingai Masashi, Ning Xiaojun, Matsumoto Misako, Seya Tsukasa, Otani Sanae, Seto Toshiyuki, Ohgimoto Shinji, Ogura Hisashi
Department of Virology, Osaka City University Medical School, Asahimachi, Abeno-ku, Osaka 545-8585, Japan.
Virus Res. 2007 Dec;130(1-2):260-8. doi: 10.1016/j.virusres.2007.07.017. Epub 2007 Sep 7.
Measles virus (MV) is the causative agent of subacute sclerosing panencephalitis (SSPE) and viruses isolated from brains of the patients contain numerous mutations. We have previously demonstrated that the hemagglutinin (H) protein of MV SSPE strains can interact with the signaling lymphocyte activation molecule (SLAM) and an unidentified molecule on Vero cells, but not with CD46, as a receptor. The mechanism by which MV SSPE strains can induce cell-cell fusion in SLAM-negative Vero cells is not understood. We report here on the effect of mutations in the fusion (F) proteins of three MV SSPE strains on syncytium formation. The F proteins of the three SSPE strains were functional and co-expression with H protein from the MV wild-type or SSPE strains in this study induced formation of large syncytia in Vero cells as well as in cell lines expressing SLAM or CD46. Expression of chimeric F proteins of SSPE strains showed that amino acid substitutions in the F protein extracellular as well as cytoplasmic domain contributed to enhanced cell-cell fusion in Vero cells. These findings suggest a common molecular mechanism and a key role of the F protein for syncytium formation in cells expressing an unidentified third receptor for MV.
麻疹病毒(MV)是亚急性硬化性全脑炎(SSPE)的病原体,从患者大脑中分离出的病毒含有大量突变。我们之前已经证明,MV SSPE毒株的血凝素(H)蛋白可以与信号淋巴细胞激活分子(SLAM)以及Vero细胞上一种未鉴定的分子相互作用,但不与作为受体的CD46相互作用。MV SSPE毒株在SLAM阴性的Vero细胞中诱导细胞间融合的机制尚不清楚。我们在此报告三种MV SSPE毒株的融合(F)蛋白中的突变对多核巨细胞形成的影响。在本研究中,三种SSPE毒株的F蛋白具有功能,与MV野生型或SSPE毒株的H蛋白共表达可在Vero细胞以及表达SLAM或CD46的细胞系中诱导形成大型多核巨细胞。SSPE毒株嵌合F蛋白的表达表明,F蛋白胞外结构域和胞质结构域中的氨基酸取代有助于增强Vero细胞中的细胞间融合。这些发现提示了一种共同的分子机制以及F蛋白在表达MV未鉴定的第三种受体的细胞中多核巨细胞形成中的关键作用。