Liao Wei-Hao, Huang Kuo-Jung, Chang Yu-Fen, Wang Shiu-Mei, Tseng Ying-Tzu, Chiang Chien-Cheng, Wang Jaang-Jiun, Wang Chin-Tien
Department of Medical Research and Education, Taipei Veterans General Hospital, Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei 11217, Taiwan.
J Virol. 2007 May;81(10):5155-65. doi: 10.1128/JVI.01796-06. Epub 2007 Mar 7.
We demonstrate that a genetically engineered human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) composed mainly of p66 or p51 subunits can be incorporated into virus-like particles (VLPs) when coexpressed with HIV-1 Pr55(gag). VLP-associated RT exhibited a detergent-resistant association with immature cores during sucrose gradient equilibrium centrifugation, suggesting that RT is incorporated into VLPs. However, RT that retains downstream integrase (IN) is severely inhibited in terms of incorporation into VLPs. Results from immunofluorescence tests reveal that RT-IN is primarily localized at the perinuclear area and exhibits poor colocalization with Gag. IN removal leads to a redistribution of RT throughout the cytoplasm and improved RT incorporation into VLPs. Similar results were observed for RT-IN in which alanine was substituted for 186-Lys-Arg-Lys-188 residues of the IN putative nuclear localization signal, suggesting that IN karyophilic properties may partly account for the inhibitory effect of IN on RT incorporation. Although the membrane-binding capacity of RT was markedly reduced compared to that of wild-type Gag or Gag-Pol, the correlation of membrane-binding ability with particle incorporation efficiency was incomplete. Furthermore, we observed that membrane-binding-defective myristylation-minus RT can be packaged into VLPs at the same level as its normal myristylated counterpart. This suggests that the incorporation of RT into VLPs is independent of membrane affinity but very dependent on RT-Gag interaction. Results from a genetic analysis suggest that the Gag-interacting regions of RT mainly reside in the thumb subdomain and that the RT-binding domains of Gag are located in the matrix (MA) and p6 regions.
我们证明,当与HIV-1 Pr55(gag)共表达时,主要由p66或p51亚基组成的基因工程化人类免疫缺陷病毒1型(HIV-1)逆转录酶(RT)可被整合到病毒样颗粒(VLP)中。在蔗糖梯度平衡离心过程中,与VLP相关的RT与未成熟核心呈现出耐去污剂的结合,这表明RT被整合到了VLP中。然而,保留下游整合酶(IN)的RT在整合到VLP方面受到严重抑制。免疫荧光测试结果显示,RT-IN主要定位于核周区域,与Gag的共定位较差。去除IN会导致RT在整个细胞质中重新分布,并提高RT整合到VLP中的效率。对于将丙氨酸替代IN假定核定位信号的186-Lys-Arg-Lys-188残基的RT-IN也观察到了类似结果,这表明IN的亲核性质可能部分解释了IN对RT整合的抑制作用。尽管与野生型Gag或Gag-Pol相比,RT的膜结合能力明显降低,但膜结合能力与颗粒整合效率之间的相关性并不完全。此外,我们观察到膜结合缺陷的肉豆蔻酰化缺失RT可以与正常肉豆蔻酰化的对应物以相同水平包装到VLP中。这表明RT整合到VLP中与膜亲和力无关,但非常依赖于RT-Gag相互作用。遗传分析结果表明,RT的Gag相互作用区域主要位于拇指亚结构域,而Gag的RT结合结构域位于基质(MA)和p6区域。