Result: In Class III, only the Gag mutation P453L positively correlated with some major mutations as follows: L33F (phi = 0.28, p = 0.004), M46I (phi = 0.30, p = 0.001), I54L (phi = 0.27, p = 0.022), I54V (phi = 0.38, p < 0.001), V82A (phi = 0.20, p = 0.031), V82T (phi = 0.27, p = 0.021), and I84V (phi = 0.38, p < 0.001), (Table 3).
Discussion: More precisely, Gag mutation P453L positively correlated with seven major protease resistance mutations (L33F, M46I, I54L,
Hybrid QM/MM Free-Energy Evaluation of Drug-Resistant Mutational Effect on the Binding of an Inhibitor Indinavir to HIV-1 Protease.
PMID: 35212226
2022
Journal of chemical information and modeling
Abstract: Here, we present a molecular simulation study on the ligand binding of indinavir, a potent transition state analogue inhibitor, to the wild-type protein and a V82T/I84V drug-resistant mutant of the HIV-1 protease.
Prevalence and factors associated with HIV-1 drug resistance mutations in treatment-experienced patients in Nairobi, Kenya: A cross-sectional study.
Result: Lopinavir was the only PI class that demonstrated significant HIVDRM with mutations at V32I (2 patients), I47 V/A (2 patients), and V82A/F/T/S (3 patients).
Acquired HIV-1 Protease Conformational Flexibility Associated with Lopinavir Failure May Shape the Outcome of Darunavir Therapy after Antiretroviral Therapy Switch.
Introduction: The major HIV-1 PI resistance mutations that affect the efficacy of boosted LPV regimen are V32I, L33F, M46I/L, I47V/A, I50V, I54V/T/A/L/M, L76V, V82A/F/T/S, I84V.
Multidrug-resistant HIV viral rebound during early syphilis: a case report.
Conclusion: A genotype resistance test (GRT) in June 2002 (Trugene HIV-1 Genotyping Assay, Siemens Healthcare Diagnostics GmbH, Eschborn, Germany) showed extensive resistance in the RT region (M41L, E44D, D67N, V118L, M184V, L210W, and T215Y) and the PR region (L10I, M46L, L63P, V82T, and L90M), and a tropism test in 2013 (envelope glycoprotein (gp)120 V3 loop sequencing) revealed a C-C chemokine receptor type 5 (CCR5) tropic virus with a false positive rate of 91.3% (geno2pheno c
HIV-1 acquired drug resistance to integrase inhibitors in a cohort of antiretroviral therapy multi-experienced Mexican patients failing to raltegravir: a cross-sectional study.
An in silico pharmacological approach toward the discovery of potent inhibitors to combat drug resistance HIV-1 protease variants.
PMID: 30506751
2019
Journal of cellular biochemistry
Abstract: Herein, we strive for compounds that can stifle the function of wild-type (WT) HIV-1 PR along with four major single mutants (I54M, V82T, I84V, and L90M) instigating resistance to the PIs using in silico approach.
Trends in the Molecular Epidemiology and Genetic Mechanisms of Transmitted Human Immunodeficiency Virus Type 1 Drug Resistance in a Large US Clinic Population.
Discussion: The side chains of mutations vary in size from the smaller V82A to bulkier V82F in addition to V82S, V82T, V82L, and V82I that are in between.
Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.
Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance
HIV mutation literature information.
PMID: 
2022
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