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.

中文翻译：

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IP6 在未成熟和成熟逆转录病毒组装中作用的结构视角

大约 20 年来，已知小细胞分子肌醇六磷酸 (IP6) 可促进 HIV-1 在体外组装成未成熟的病毒样颗粒。然而，这种效应背后的分子细节直到最近才确定，在未成熟的 Gag 晶格中发现了 IP6 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 还增强了慢病毒和 Alpharetrovirus 属的其他逆转录病毒的组装。这些发现表明 IP6 在整个逆转录病毒科中可能具有保守的功能。在这里，我们讨论受 IP6 影响的病毒生命周期中的不同步骤，