Characterization of minority HIV-1 drug resistant variants in the United Kingdom following the verification of a deep sequencing-based HIV-1 genotyping and tropism assay.
Result: Most of the minority mutations in viruses from both groups of naive patients were observed in the RT, e.g., M41L, E44D, A62V, K65R, D67N, D67G, V75I, L100I, K103N, K103R, V188I, M184I, L210W, K219Q, Y318F, etc., although a number of minority mutations associated with resistance to PI (L10F, V11I, M46I/
Prevalence of HIV-1 pre-treatment drug resistance in a southern province of Iran, 2016-2017.
Abstract: Although no major protease inhibitor (PI) resistance mutations were detected, the minor mutations L10F and L33F (2.5% each) as well as several highly frequent polymorphic mutations were identified.
Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.
Result: 1) contained the V32I substitution, although other substitutions such as L10F, L33F, M46I, A71V, and I84V had been acquired in a subset of the six clones.
Discussion: In contrast, a set of data compiled for NDA21-976/S003 and NDA21-976/S004 clearly indicates that 10 amino acid substitutions including L10F, V32I, L33F, S37N, M46I, I47V, I50V, L63P, A71V, and I84V are the most prevalent (https://www.accessdata.fda.gov/drugsatfda_docs/label/
Drug Resistance Mechanism of L10F, L10F/N88S and L90M mutations in CRF01_AE HIV-1 protease: Molecular dynamics simulations and binding free energy calculations.
PMID: 28645089
2017
Journal of molecular graphics & modelling
Abstract: In this work, we examined the effect of non active site mutations L10F, L10F/N88S and L90M with nelfinavir using molecular dynamics simulation and binding free energy calculations.
Abstract: Our present study shed light on the resistance mechanism of the strongly linked mutation L10F/N88S observed experimentally in AE subtype.
Abstract: The benzamide moiety of nelfinavir shows large positional deviation in L10F and L10F/N88S complexes and the L10F/N88S mutation changes the hydrogen bond between the side chain atoms of 30th residue and the 88th residue.
Abstract: The simulations suggested th
Antiviral Activity of Bictegravir (GS-9883), a Novel Potent HIV-1 Integrase Strand Transfer Inhibitor with an Improved Resistance Profile.
PMID: 27645238
2016
Antimicrobial agents and chemotherapy
Method: The protease inhibitor (PI)-resistant mutant viruses encoding mutations in the HIV-1 protease-coding sequence, L10F/M46I/I50V, I84V/L90M, G48V/I54V/V82S, and G48V/V82A/L90M, were produced in electroporated SupT1 cells via homologous recombination.
Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
Result: Outside of the clusters, mutations L10F in PR20 and possibly L10I in PRS17 could disrupt the ion pair between R8 and D29' of the opposite subunit, resulting in altered conformation of the binding cavity.
From antiretroviral therapy access to provision of third line regimens: evidence of HIV Drug resistance mutations to first and second line regimens among Ugandan adults.
Abstract: Also common were the accessory PI mutations L10I-27%, L10V-12.0% and L10F-5.0% that either reduce PI susceptibility or increase the replication of viruses containing PI-resistance mutations.
Result: The identified accessory PI resistance mutations that either reduce PI susceptibility or increase the replication of viruses containing PI-resistance mutations included: L10I:27.0%, L10V:12.0% and L10F:5.0% (Table 2).
Table: L10F
Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.
Abstract: Unlike the L10F mutation in PR20, L10I in PRS17 does not break the inter-subunit ion pair or diminish the dimer stability, consistent with a very low dimer dissociation constant comparable to that of wild type PR.
Result: In PR20, L10F mutation acts to break the inter-subunit ion pair between conserved Arg8 and Asp29' by shifting the side chain of Arg8 into a new conformation that makes van der Waals contacts with Phe10 (Fig 2B).
Result: Thus, L10I mutation in PRS17 does not break the inter-subunit ion pair, unlike the L10F mutation in PR20, and hence does
Single Genome Analysis for the Detection of Linked Multiclass Drug Resistance Mutations in HIV-1-Infected Children After Failure of Protease Inhibitor-Based First-Line Therapy.
PMID: 25923117
2015
Journal of acquired immune deficiency syndromes (1999)
Abstract: In one child, the majority species contained M184V in reverse transcriptase linked to L10F, M46I/L, I54V, and V82A in PR and a triple-class drug-resistant variant with these mutations linked to the NNRTI mutation V108I.
Discussion: Age adjusted full-dose RTV can select M46I, I54V, and V82A in children, as well as L10F, M46L, and Q58E in adults.
The use of dried blood spot specimens for HIV-1 drug resistance genotyping in young children initiating antiretroviral therapy.
PMID: 26192603
2015
Journal of virological methods
Introduction: Only one specimen was predicted to be resistant to protease inhibitors (PI) due to the presence of major and minor PI mutations (L10F, M46I, I54V, L76V and V82A) while 8 specimens had minor PI mutations (A71T (n=3), L10I/V (n=3) and M46L/T (n=2)).
HIV mutation literature information.
PMID: 
2018
AIDS research and therapy
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