Involvement of a small GTP binding protein in HIV-1 release
Involvement of a small GTP binding protein in HIV-1 release
复制标题
DOI：
10.1186/1742-4690-2-48
复制
发表时间：
2005-08-04
期刊：
影响因子：
3.3
通讯作者：
Gluschankof, P
中科院分区：
文献类型：
--
作者：
Audoly, G;Popoff, MR;Gluschankof, P
背景：有证据表明，肌动蛋白与HIV-1编码蛋白的结合，甚至肌动蛋白本身的动态变化，可能在病毒萌发和/或从感染细胞释放的过程中发挥关键作用。肌动蛋白细胞骨架重组的关键步骤是各种不同的GTP结合蛋白的结合。因此，我们研究了GTP结合蛋白在HIV-1病毒复制周期的最后步骤中的参与。结果：我们的结果表明，当参与肌动蛋白聚合的细胞GTP结合蛋白被特定毒素抑制时，病毒的产生被取消。结论：我们提出了一个新的HIV萌芽工作模型，需要GAG与先前存在的内体细胞轨迹以及与尚未确定的肌动蛋白聚合途径的元件相互作用，以便允许HIV-1从感染细胞中释放。
Background: There is evidence suggesting that actin binding to HIV-1 encoded proteins, or even actin dynamics themselves, might play a key role in virus budding and/or release from the infected cell. A crucial step in the reorganisation of the actin cytoskeleton is the engagement of various different GTP binding proteins. We have thus studied the involvement of GTP-binding proteins in the final steps of the HIV-1 viral replication cycle.Results: Our results demonstrate that virus production is abolished when cellular GTP binding proteins involved in actin polymerisation are inhibited with specific toxins.Conclusion: We propose a new HIV budding working model whereby Gag interactions with preexisting endosomal cellular tracks as well as with a yet non identified element of the actin polymerisation pathway are required in order to allow HIV-1 to be released from the infected cell.