AIP1/Alix Is a Binding Partner of Sendai Virus C Protein and Facilitates Virus Budding

AIP1/Alix Is a Binding Partner of Sendai Virus C Protein and Facilitates Virus Budding
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DOI:
10.1128/jvi.79.14.8933-8941.2005
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发表时间:
2005-07
影响因子:
5.4
通讯作者:
T. Sakaguchi;A. Kato;Fumihiro Sugahara;Y. Shimazu;M. Inoue;K. Kiyotani;Y. Nagai;Tetsuya Yoshida
T. Sakaguchi;A. Kato;Fumihiro Sugahara;Y. Shimazu;M. Inoue;K. Kiyotani;Y. Nagai;Tetsuya Yoshida
中科院分区:
医学2区
文献类型:
--
作者:
T. Sakaguchi;A. Kato;Fumihiro Sugahara;Y. Shimazu;M. Inoue;K. Kiyotani;Y. Nagai;Tetsuya Yoshida

文献摘要

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仙台病毒C蛋白是仙台病毒的辅助蛋白,具有抗干扰素和抑制病毒RNA合成的作用。此外,认为C蛋白参与病毒出芽,因为从C-敲除病毒感染的细胞释放子代病毒体的效率低,并且因为需要C蛋白来有效释放病毒样颗粒。在这里,我们确定了AIP 1/阿利克斯,一个主机蛋白参与细胞凋亡和内体膜运输,作为一个相互作用的合作伙伴的C蛋白使用酵母双杂交系统。AIP 1/阿利克斯的氨基末端和C蛋白的羧基末端对于哺乳动物细胞中的相互作用是重要的。不能结合AIP 1/阿利克斯的突变C蛋白不能加速病毒样颗粒从细胞中释放。此外,AIP 1/阿利克斯的过表达以C蛋白依赖的方式增强了感染细胞中的SeV出芽,同时也增强了无核衣壳的空病毒体的释放。最后,AIP 1/阿利克斯消耗小干扰RNA导致抑制SeV出芽。本研究的结果表明,AIP 1/阿利克斯在有效的SeV出芽中起作用,并且SeV C蛋白通过与AIP 1/阿利克斯的相互作用促进病毒出芽。
ABSTRACT The C protein, an accessory protein of Sendai virus (SeV), has anti-interferon capacity and suppresses viral RNA synthesis. In addition, it is thought that the C protein is involved in virus budding because of the low efficiency of release of progeny virions from C-knockout virus-infected cells and because of the requirement of the C protein for efficient release of virus-like particles. Here, we identified AIP1/Alix, a host protein involved in apoptosis and endosomal membrane trafficking, as an interacting partner of the C protein using a yeast two-hybrid system. The amino terminus of AIP1/Alix and the carboxyl terminus of the C protein are important for the interaction in mammalian cells. Mutant C proteins unable to bind AIP1/Alix failed to accelerate the release of virus-like particles from cells. Furthermore, overexpression of AIP1/Alix enhanced SeV budding from infected cells in a C-protein-dependent manner, while the release of nucleocapsid-free empty virions was also enhanced. Finally, AIP1/Alix depletion by small interfering RNA resulted in suppression of SeV budding. The results of this study suggest that AIP1/Alix plays a role in efficient SeV budding and that the SeV C protein facilitates virus budding through interaction with AIP1/Alix.