Université de Paris, BFA, UMR 8251, CNRS, ERL U1133, Inserm, F-75013 Paris, France.
Molecules. 2021 Jan 25;26(3):611. doi: 10.3390/molecules26030611.
The use of antiretroviral drugs is accompanied by the emergence of HIV-2 resistances. Thus, it is important to elucidate the mechanisms of resistance to antiretroviral drugs. Here, we propose a structural analysis of 31 drug-resistant mutants of HIV-2 protease (PR2) that is an important target against HIV-2 infection. First, we modeled the structures of each mutant. We then located structural shifts putatively induced by mutations. Finally, we compared wild-type and mutant inhibitor-binding pockets and interfaces to explore the impacts of these induced structural deformations on these two regions. Our results showed that one mutation could induce large structural rearrangements in side-chain and backbone atoms of mutated residue, in its vicinity or further. Structural deformations observed in side-chain atoms are frequent and of greater magnitude, that confirms that to fight drug resistance, interactions with backbone atoms should be favored. We showed that these observed structural deformations modify the conformation, volume, and hydrophobicity of the binding pocket and the composition and size of the PR2 interface. These results suggest that resistance mutations could alter ligand binding by modifying pocket properties and PR2 stability by impacting its interface. Our results reinforce the understanding of the effects of mutations that occurred in PR2 and the different mechanisms of PR2 resistance.
抗逆转录病毒药物的使用伴随着 HIV-2 耐药性的出现。因此,阐明抗逆转录病毒药物耐药的机制非常重要。在这里,我们提出了对 HIV-2 蛋白酶 (PR2) 的 31 种耐药突变体进行结构分析,PR2 是对抗 HIV-2 感染的重要靶点。首先,我们对每个突变体进行建模。然后,我们定位了推测由突变引起的结构位移。最后,我们比较了野生型和突变型抑制剂结合口袋和界面,以探索这些诱导的结构变形对这两个区域的影响。我们的结果表明,一个突变可以诱导突变残基及其附近或更远的侧链和骨架原子发生大的结构重排。观察到的侧链原子的结构变形很频繁,幅度也更大,这证实了为了对抗耐药性,应该优先考虑与骨架原子的相互作用。我们表明,这些观察到的结构变形改变了结合口袋的构象、体积和疏水性,以及 PR2 界面的组成和大小。这些结果表明,耐药突变可能通过改变口袋特性和影响 PR2 稳定性来改变配体结合,从而影响其接口。我们的研究结果加深了对 PR2 中发生的突变的影响以及 PR2 耐药性的不同机制的理解。