Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, United States.
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, United States.
Elife. 2023 Mar 15;12:e80328. doi: 10.7554/eLife.80328.
Darunavir (DRV) is exceptional among potent HIV-1 protease inhibitors (PIs) in high drug concentrations that are achieved in vivo. Little is known about the de novo resistance pathway for DRV. We selected for resistance to high drug concentrations against 10 PIs and their structural precursor DRV. Mutations accumulated through two pathways (anchored by protease mutations I50V or I84V). Small changes in the inhibitor P1'-equivalent position led to preferential use of one pathway over the other. Changes in the inhibitor P2'-equivalent position determined differences in potency that were retained in the resistant viruses and that impacted the selected mutations. Viral variants from the two pathways showed differential selection of compensatory mutations in Gag cleavage sites. These results reveal the high level of selective pressure that is attainable with fifth-generation PIs and how features of the inhibitor affect both the resistance pathway and the residual potency in the face of resistance.
达芦那韦(DRV)是一种高效的 HIV-1 蛋白酶抑制剂(PI),在体内能达到很高的药物浓度。但对于达芦那韦的耐药新途径知之甚少。我们选择了对 10 种 PI 及其结构前体达芦那韦进行高药物浓度耐药性。通过两种途径(由蛋白酶突变 I50V 或 I84V 锚定)积累突变。抑制剂 P1'-等价位置的微小变化导致一种途径优先于另一种途径。抑制剂 P2'-等价位置的变化决定了药物效力的差异,这种差异在耐药病毒中得以保留,并影响了所选的突变。来自两条途径的病毒变体在 Gag 切割位点的补偿性突变中表现出不同的选择。这些结果揭示了第五代 PI 所能达到的高度选择性压力,以及抑制剂的特征如何影响耐药途径和耐药性下的剩余效力。