Rabies virus inactivates cofilin to facilitate viral budding and release

狂犬病毒使肌动蛋白丝切蛋白失活,以促进病毒出芽和释放

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作者:Jie Zan, Shu-Ting An, Kai-Kun Mo, Jian-Wei Zhou, Juan Liu, Hai-Long Wang, Yan Yan, Min Liao, Ji-Yong Zhou

Abstract

Cytoplasmic actin and actin-associated proteins have been identified in RABV particles. Although actin is involved in RABV entry into cells, the specific role of actin in RABV budding and release remains unknown. Our study found that RABV M protein-mediated virion budding depends on intact actin filaments. Confocal microscopy demonstrated a block to virions budding, with a number of M protein-mediated budding vesicles detained in the cell cytoplasm. Furthermore, RABV infection resulted in inactivation of cofilin and upregulation of phosphorylated cofilin. Knockdown of cofilin reduced RABV release. These results for the first time indicate that RABV infection resulted in upregulation of phosphorylated cofilin to facililtate actin polymerization for virus budding.

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