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猴免疫缺陷病毒MneCL8的病毒感染性及无细胞衣壳组装特性

Characterization of virus infectivity and cell-free capsid assembly of SIVMneCL8.

作者信息

Dooher Julia E, Pineda Mario Javier, Overbaugh Julie, Lingappa Jaisri R

机构信息

Department of Pathobiology, University of Washington, Seattle, WA, USA.

出版信息

J Med Primatol. 2004 Oct;33(5-6):262-71. doi: 10.1111/j.1600-0684.2004.00074.x.

Abstract

We have previously described a cell-free system that reconstitutes immature capsid assembly of Gag polypeptides from viruses belonging to three major primate lentiviral lineages, including HIV-1, HIV-2 and SIVagm. Studies described here examine a member of the SIVmac/Mne lineage, SIVMneCL8, using assays for virus production and infectivity as well as cellular events in capsid formation. We report that SIVMneCL8, a molecular clone with properties typical of transmitted viral variants, is less infectious per unit p27 Gag than another member of the SIVmac/Mne lineage, SIVmac239. SIVMneCL8 Gag polypeptides are arrested at an early stage of capsid assembly in the cell-free system. Additionally, SIVMneCL8 Gag polypeptides associate minimally with the host factor human HP68. This is the first report of a primate lentivirus that does not complete capsid assembly in the cell-free system.

摘要

我们之前描述过一种无细胞系统,该系统可重构来自三种主要灵长类慢病毒谱系(包括HIV-1、HIV-2和SIVagm)病毒的Gag多肽的未成熟衣壳组装。本文所述研究使用病毒产生和感染性检测以及衣壳形成中的细胞事件,对SIVmac/Mne谱系的一个成员SIVMneCL8进行了研究。我们报告称,SIVMneCL8是一种具有典型传播病毒变体特性的分子克隆,每单位p27 Gag的感染性低于SIVmac/Mne谱系的另一个成员SIVmac239。SIVMneCL8 Gag多肽在无细胞系统中衣壳组装的早期阶段就停滞不前。此外,SIVMneCL8 Gag多肽与宿主因子人HP68的结合极少。这是关于一种在无细胞系统中不能完成衣壳组装的灵长类慢病毒的首次报道。

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