Method: In our study, samples with at least one of the major PI RAM of the IAS-USA list as follows: D30N, V32I, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, L90M were considered as PI-resistant issued from PI-experienced patients.
Cooperative effects of drug-resistance mutations in the flap region of HIV-1 protease.
Abstract: A particular drug resistant variant (L10I/G48V/I54V/V82A) displays extreme entropy-enthalpy compensation relative to wild-type enzyme but a similar variant (L10I/G48V/I54A/V82A) does not.
Introduction: Besides G48V or I54V, Flap+(I54V) has an additional active site mutation V82A, as does Flap+(I54A).
Introduction: Binding thermodynamics of the two Flap+ variants and three single mutants (I54V, I54A, G48V) were measured by isoth
Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
Restriction fragment mass polymorphism (RFMP) analysis based on MALDI-TOF mass spectrometry for detecting antiretroviral resistance in HIV-1 infected patients.
PMID: 23480551
2013
Clinical microbiology and infection
Abstract: The concordance rates between the RFMP and direct sequencing assays for the examined codons were 97% (K65R), 97% (T69Ins/D), 97% (L74VI), 97% (K103N), 96% (V106AM), 97% (Q151M), 97% (Y181C), 97% (M184VI) and 94% (T215YF) in the reverse transcriptase coding region, and 100% (D30N), 100% (M46I), 100% (G48V), 100% (I50V), 100% (I54LS), 99% (V82A), 99% (I84V) and 100% (L90M) in th
Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.
PMID: 23711895
2013
The Journal of antimicrobial chemotherapy
Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and I93M) or were not significantly associated with atazanavir exposure (L10I/F/V, G16E, K20R/M/I/T, L24I, V32I, L33I/F/V, M36L/V, M46L, G48V, I54V
Revealing the drug resistance mechanism of saquinavir due to G48V and V82F mutations in subtype CRF01_AE HIV-1 protease: molecular dynamics simulation and binding free energy calculations.
PMID: 26587633
2013
Journal of chemical theory and computation
Abstract: In this work, we examine L10I, G48V, L63P, A71V, G73S, V82A, and I84V single mutant HIV-1 PR strains in complexes with saquinavir to elucidate drug-protease interactions and dynamics.
Abstract: It was shown that mutations conferring major resistance (G48V, L63P, I84V) did not present these interactions.
Abstract: It was shown that mutations, which increase the flexibility of the flaps (G48V, L63P, L10I) diminish binding.
Abstract: Mutants lacking this
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and K219QENR; (ii) the
Persistence of HIV-1 transmitted drug resistance mutations.
PMID: 23904291
2013
The Journal of infectious diseases
Table: G48 V
Increasing trends in primary NNRTI resistance among newly HIV-1-diagnosed individuals in Buenos Aires, Argentina.
PMID: 24093951
2013
Journal of the International AIDS Society
Method: Sequences were analyzed to identify mutations associated with reduced susceptibility to protease and RT inhibitors, as reported by the International AIDS Society-USA in 2010: RT-M41L, A62V, K65R, D67N, 69 insert, K70R, L74V,V75I, F77L, L100I, K101P, K103N, V106A, V106M, V108I, Y115F, F116Y,
HIV mutation literature information.
PMID: 
2014
Journal of the International AIDS Society
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