Oomens Antonius G P, Bevis Kevin P, Wertz Gail W
Department of Pathology, University of Virginia, MR5 Building, P.O. Box 800904, Charlottesville, VA 22908-0904, USA.
J Virol. 2006 Nov;80(21):10465-77. doi: 10.1128/JVI.01439-06. Epub 2006 Aug 23.
The importance of the F protein cytoplasmic tail (CT) for replication of human respiratory syncytial virus (HRSV) was examined by monitoring the behavior of viruses expressing F proteins with a modified COOH terminus. The F protein mutant viruses were recovered and amplified under conditions where F protein function was complemented by expression of a heterologous viral envelope protein. The effect of the F protein modifications was then examined in the context of a viral infection in standard cell types (Vero and HEp-2). The F protein modifications consisted of a deletion of the predicted CT or a replacement of the CT with the CT of the vesicular stomatitis virus (VSV) G protein. In addition, engineered HRSVs that lacked all homologous glycoprotein genes (SH, G, and F) and expressed instead either the authentic VSV G protein or a VSV G containing the HRSV F protein CT were examined. We found that deletion or replacement of the F protein CT seriously impaired the production of infectious progeny. Cells infected with viruses bearing CT modifications displayed increased F protein surface expression and increased syncytium formation. The distribution of F protein in the plasma membrane of infected cells was altered, resulting in an F protein that was evenly distributed rather than localized predominantly to virus-induced surface filaments. CT deletion or exchange also abrogated interaction of F protein with Triton-insoluble lipid rafts. Addition of the F protein CT to the VSV G protein, expressed as the only viral glycoprotein in an HRSV genome, had the opposite effects: the number of infectious progeny was higher, the surface distribution was changed from relatively even to localized, and the proportion of VSV G protein associated with lipid rafts was higher. Together, these results show that the HRSV F protein CT plays a critical role in F protein cellular localization and production of infectious virus and suggest that the function provided by the CT is independent of the F protein ectodomain and transmembrane domain and is mediated by F protein-lipid raft interaction.
通过监测表达具有修饰COOH末端的F蛋白的病毒行为,研究了F蛋白细胞质尾(CT)对人呼吸道合胞病毒(HRSV)复制的重要性。在F蛋白功能由异源病毒包膜蛋白表达互补的条件下,回收并扩增F蛋白突变病毒。然后在标准细胞类型(Vero和HEp-2)的病毒感染背景下检查F蛋白修饰的效果。F蛋白修饰包括预测的CT缺失或用水泡性口炎病毒(VSV)G蛋白的CT替换CT。此外,还检查了缺乏所有同源糖蛋白基因(SH、G和F)并取而代之表达真实VSV G蛋白或含有HRSV F蛋白CT的VSV G的工程化HRSV。我们发现F蛋白CT的缺失或替换严重损害了感染性子代的产生。感染带有CT修饰病毒的细胞显示F蛋白表面表达增加且合胞体形成增加。F蛋白在感染细胞质膜中的分布发生改变,导致F蛋白均匀分布,而不是主要定位于病毒诱导的表面细丝。CT缺失或交换也消除了F蛋白与Triton不溶性脂筏的相互作用。将F蛋白CT添加到作为HRSV基因组中唯一病毒糖蛋白表达的VSV G蛋白中,产生了相反的效果:感染性子代数量更高,表面分布从相对均匀变为局部化,并且与脂筏相关的VSV G蛋白比例更高。总之,这些结果表明HRSV F蛋白CT在F蛋白细胞定位和感染性病毒产生中起关键作用,并表明CT提供的功能独立于F蛋白胞外域和跨膜域,且由F蛋白-脂筏相互作用介导。