Suomalainen M, Liljeström P, Garoff H
Department of Molecular Biology, Karolinska Institute, Huddinge, Sweden.
J Virol. 1992 Aug;66(8):4737-47. doi: 10.1128/JVI.66.8.4737-4747.1992.
Semliki Forest virus (SFV) particles are released from infected cells by budding of nucleocapsids through plasma membrane regions that are modified by virus spike proteins. The budding process was studied with recombinant SFV genomes which lacked the nucleocapsid protein gene or, alternatively, the spike genes. No subviral particles were released from cells which expressed only the nucleocapsid protein or the spike proteins. Virus release was found to be strictly dependent on the coexpression of the nucleocapsid and the spike proteins. These results provide direct proof for the hypothesis that the alphavirus budding is driven by nucleocapsid-spike interactions. The importance of the viral 42S RNA for virus assembly and budding was investigated by using the heterologous vaccinia virus-T7 expression system for the synthesis of the SFV structural proteins. The results demonstrate that the viral genome is not absolutely required for formation of budding competent nucleocapsids, since small amounts of viruslike particles were assembled in the absence of 42S RNA.
辛德毕斯病毒（SFV）粒子通过核衣壳在由病毒刺突蛋白修饰的质膜区域出芽，从受感染细胞中释放出来。利用缺乏核衣壳蛋白基因或刺突基因的重组SFV基因组研究了出芽过程。仅表达核衣壳蛋白或刺突蛋白的细胞未释放亚病毒粒子。发现病毒释放严格依赖于核衣壳蛋白和刺突蛋白的共表达。这些结果为甲病毒出芽由核衣壳-刺突相互作用驱动这一假说提供了直接证据。通过使用异源痘苗病毒-T7表达系统合成SFV结构蛋白，研究了病毒42S RNA对病毒组装和出芽的重要性。结果表明，形成具有出芽能力的核衣壳并非绝对需要病毒基因组，因为在没有42S RNA的情况下也组装了少量病毒样颗粒。
