Heminway B R, Yu Y, Tanaka Y, Perrine K G, Gustafson E, Bernstein J M, Galinski M S
Department of Molecular Biology, Cleveland Clinic Foundation, Ohio 44195.
Virology. 1994 May 1;200(2):801-5. doi: 10.1006/viro.1994.1245.
Recombinant expression of the human respiratory syncytial virus (RSV) fusion (F) glycoprotein, receptor-binding glycoprotein (G), and small hydrophobic (SH) protein was performed to determine the role(s) of these proteins in syncytia formation. These studies used a vaccinia virus expressing the bacteriophage (T7) RNA polymerase gene and plasmid vectors containing the RSV genes under the control of a T7 promoter. Within the context of this expression system, expression of any individual RSV gene, or coexpression of F+G genes, did not elicit the formation of syncytia. However, at plasmid input levels which were 10-fold higher than those normally used, coexpression of F+G induced low but detectable levels of cell fusion. In contrast, coexpression of F, G, and SH together elicited extensive cell fusion resembling that of an authentically infected cell monolayer. In addition, coexpression of F and SH elicited significant cell fusion, although to a lesser extent than was observed when G was included. Cell fusion induced by coexpression of F+SH was found to be specific to the RSV proteins, since coexpression of SH with the analogous F proteins from human parainfluenza virus type 3, human parainfluenza virus type 2, Sendai virus, or simian virus type 5 (SV5) did not elicit cell fusion. Finally, coexpression of the SV5 SH protein with the RSV or SV5 glycoproteins also failed to induce syncytia, suggesting type-specific restrictions between the two sets of viral proteins.
进行了人类呼吸道合胞病毒（RSV）融合（F）糖蛋白、受体结合糖蛋白（G）和小疏水（SH）蛋白的重组表达，以确定这些蛋白在多核细胞形成中的作用。这些研究使用了一种表达噬菌体（T7）RNA聚合酶基因的痘苗病毒和在T7启动子控制下含有RSV基因的质粒载体。在这个表达系统中，任何单个RSV基因的表达，或F+G基因的共表达，都不会引发多核细胞的形成。然而，在比正常使用水平高10倍的质粒输入水平下，F+G的共表达诱导了低但可检测水平的细胞融合。相比之下，F、G和SH一起共表达引发了广泛的细胞融合，类似于真正感染的细胞单层。此外，F和SH的共表达引发了显著的细胞融合，尽管程度比包含G时观察到的要小。发现F+SH共表达诱导的细胞融合对RSV蛋白具有特异性，因为SH与人副流感病毒3型、人副流感病毒2型、仙台病毒或猴病毒5型（SV5）的类似F蛋白共表达不会引发细胞融合。最后，SV5 SH蛋白与RSV或SV5糖蛋白的共表达也未能诱导多核细胞形成，表明两组病毒蛋白之间存在型特异性限制。
