Influenza virus assembly and budding.
Influenza virus assembly and budding.
复制标题
DOI：
10.1016/j.virol.2010.12.003
复制
发表时间：
2011-03-15
期刊：
影响因子：
3.7
通讯作者：
Lamb RA
中科院分区：
文献类型：
--
作者：
Rossman JS;Lamb RA
甲型流感病毒引起季节性流行和散发大流行，是一个重大的全球卫生负担。流感病毒是一种包膜病毒，含有一个分段负链RNA基因组。流感病毒子代的组装和出芽是一个复杂的多步骤过程，发生在感染细胞顶膜的脂筏结构域。病毒蛋白血凝素（HA）和神经氨酸酶（NA）靶向脂筏，引起脂筏结构域的合并和扩大。这种HA和NA的聚集可能引起膜的变形和病毒出芽事件的开始。M1随后被认为与HA和NA的细胞质尾部结合，在那里它可以聚合并形成新出现的病毒粒子的内部结构。M1与HA和NA的细胞质尾部结合，还作为病毒RNPs募集的对接位点，并可能介导M2募集到病毒出芽位点。M2最初稳定出芽位置，可能使基质蛋白聚合和丝状病毒粒子的形成成为可能。随后，M2能够改变出芽病毒颈部的膜曲率，导致膜断裂并释放子代病毒粒子。本文综述了流感病毒出芽的最新研究，试图对流感病毒的组装和出芽过程进行一步一步的分析。
Influenza A virus causes seasonal epidemics, sporadic pandemics and is a significant global heath burden. Influenza virus is an enveloped virus that contains a segmented negative strand RNA genome. Assembly and budding of progeny influenza virions is a complex, multistep process that occurs in lipid raft domains on the apical membrane of infected cells. The viral proteins hemagglutinin (HA) and neuraminidase (NA) are targeted to lipid rafts, causing the coalescence and enlargement of the raft domains. This clustering of HA and NA may cause a deformation of the membrane and the initiation of the virus budding event. M1 is then thought to bind to the cytoplasmic tails of HA and NA where it can then polymerize and form the interior structure of the emerging virion. M1, bound to the cytoplasmic tails of HA and NA, additionally serves as a docking site for the recruitment of the viral RNPs and may mediate the recruitment of M2 to the site of virus budding. M2 initially stabilizes the site of budding, possibly enabling the polymerization of the matrix protein and the formation of filamentous virions. Subsequently, M2 is able to alter membrane curvature at the neck of the budding virus, causing membrane scission and the release of the progeny virion. This review investigates the latest research on influenza virus budding in an attempt to provide a step-by-step analysis of the assembly and budding processes for influenza viruses.