宿主 IQGAP1 与埃博拉病毒 VP40 相互作用促进病毒样颗粒出芽。
Host IQGAP1 and Ebola virus VP40 interactions facilitate virus-like particle egress.
机构信息
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
出版信息
J Virol. 2013 Jul;87(13):7777-80. doi: 10.1128/JVI.00470-13. Epub 2013 May 1.
Abstract
We have identified host IQGAP1 as an interacting partner for Ebola virus (EBOV) VP40, and its expression is required for EBOV VP40 virus-like particle (VLP) budding. IQGAP1 is involved in actin cytoskeletal remodeling during cell migration and formation of filopodia. The physical interaction and the functional requirement for IQGAP1 in EBOV VP40 VLP egress link virus budding to the cytoskeletal remodeling machinery. Consequently, this interaction represents a novel target for development of therapeutics to block budding and transmission of filoviruses.
摘要
我们已经确定宿主 IQGAP1 是埃博拉病毒（EBOV）VP40 的相互作用伙伴，其表达是 EBOV VP40 病毒样颗粒（VLP）出芽所必需的。IQGAP1 参与细胞迁移过程中的肌动蛋白细胞骨架重塑和丝状伪足的形成。VP40 与 IQGAP1 的物理相互作用及其在 EBOV VP40 VLP 出芽中的功能需求将病毒与细胞骨架重塑机制联系起来。因此，这种相互作用代表了开发治疗药物的新靶点，以阻止丝状病毒的出芽和传播。
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