细胞因子在促进 HIV 出芽中的作用。
The role of cellular factors in promoting HIV budding.
机构信息
Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA 01605, USA.
出版信息
J Mol Biol. 2011 Jul 22;410(4):525-33. doi: 10.1016/j.jmb.2011.04.055.
Abstract
Human immunodeficiency virus type 1 (HIV-1) becomes enveloped while budding through the plasma membrane, and the release of nascent virions requires a membrane fission event that separates the viral envelope from the cell surface. To facilitate this crucial step in its life cycle, HIV-1 exploits a complex cellular membrane remodeling and fission machinery known as the endosomal sorting complex required for transport (ESCRT) pathway. HIV-1 Gag directly interacts with early-acting components of this pathway, which ultimately triggers the assembly of the ESCRT-III membrane fission complex at viral budding sites. Surprisingly, HIV-1 requires only a subset of ESCRT-III components, indicating that the membrane fission reaction that occurs during HIV-1 budding differs in crucial aspects from topologically related cellular abscission events.
摘要
人类免疫缺陷病毒 1 型（HIV-1）在通过质膜出芽时被包裹，新生病毒粒子的释放需要一个膜分裂事件，将病毒包膜与细胞表面分离。为了促进其生命周期中的这一关键步骤，HIV-1 利用了一种称为内体分选复合物必需的运输（ESCRT）途径的复杂细胞膜重塑和分裂机制。HIV-1 Gag 直接与该途径的早期作用成分相互作用，最终触发 ESCRT-III 膜分裂复合物在病毒出芽部位的组装。令人惊讶的是，HIV-1 只需要 ESCRT-III 成分的一部分，这表明 HIV-1 出芽过程中发生的膜分裂反应在关键方面与拓扑相关的细胞分离事件不同。
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