Institute of Science and Technology (IST) Austria, 3400 Klosterneuburg, Austria.
Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Viruses. 2021 Sep 17;13(9):1853. doi: 10.3390/v13091853.
The small cellular molecule inositol hexakisphosphate (IP6) has been known for ~20 years to promote the in vitro assembly of HIV-1 into immature virus-like particles. However, the molecular details underlying this effect have been determined only recently, with the identification of the IP6 binding site in the immature Gag lattice. IP6 also promotes formation of the mature capsid protein (CA) lattice via a second IP6 binding site, and enhances core stability, creating a favorable environment for reverse transcription. IP6 also enhances assembly of other retroviruses, from both the Lentivirus and the Alpharetrovirus genera. These findings suggest that IP6 may have a conserved function throughout the family Retroviridae. Here, we discuss the different steps in the viral life cycle that are influenced by IP6, and describe in detail how IP6 interacts with the immature and mature lattices of different retroviruses.
已经有大约 20 年的时间了，人们一直都知道小分子细胞六磷酸肌醇（IP6）可以促进 HIV-1 在体外组装成不成熟的病毒样颗粒。然而，最近才确定了这种效应的分子细节，发现了不成熟 Gag 晶格中 IP6 的结合位点。IP6 还通过第二个 IP6 结合位点促进成熟衣壳蛋白（CA）晶格的形成，并增强核心稳定性，为逆转录创造有利环境。IP6 还增强了来自慢病毒属和α逆转录病毒属的其他逆转录病毒的组装。这些发现表明，IP6 在逆转录病毒科中可能具有保守功能。在这里，我们讨论了 IP6 影响的病毒生命周期的不同步骤，并详细描述了 IP6 如何与不同逆转录病毒的不成熟和成熟晶格相互作用。
