literature

HIV mutation literature information.

Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.

PMID: 23840622 2013 PloS one

Table: I50L

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: Only 6 (1.9%) index patients experiencing virological failure had a major atazanavir-associated mutation, all in isolation: I50L (n = 3), I84V (n = 2) and N88S (n = 1) (Table 2).

Result: Specifically, none of the patients who were observed to have I15S, K43T, I50L, V82T, I84V, N88S or L89V mutations at virological failure had a baseline resistance test.

Discussion: Our findings show that very few patients failing a therapy containing atazanavir are likely to have developed one of the major protease resistance mutations (I50L, I84V

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.

PMID: 23469241 2013 PloS one

Table: I50L/V

Significantly improved HIV inhibitor efficacy prediction employing proteochemometric models generated from antivirogram data.

PMID: 23436985 2013 PLoS computational biology

Result: For the PIs mutations that are accurately reproduced include D30N, I50L, V82S, and I84, while the I64L and I93M mutations are assigned less importance than in previous work.

Structural and thermodynamic basis of amprenavir/darunavir and atazanavir resistance in HIV-1 protease with mutations at residue 50.

PMID: 23365446 2013 Journal of virology

Abstract: Analysis of the crystal structures showed that the substitutions at residue 50 affect how APV, DRV, and ATV bind the protease with altered van der Waals interactions and that the selection of I50V versus I50L is greatly influenced by the chemical moieties at the P1 position for APV/DRV and the P2 position for ATV.

Abstract: Reduced affinity to both I50V/A71V and I50L/A71V double mutants is largely due to decreased binding entropy, which is compensated for by enhanced enthalpy for ATV binding to I50V variants and APV binding to I50L variants, leading to hypersusceptibility in these two cases.

Abstract: The I50V substitution is often

"Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."

PMID: 23349869 2013 PloS one

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.

Mutations selected in HIV-2-infected patients failing a regimen including atazanavir.

PMID: 22977160 2013 The Journal of antimicrobial chemotherapy

Abstract: Besides I50L, four PR mutations previously associated with protease inhibitor resistance (I54L, I64V, V71I and I82F) and six PR mutations of unknown impact (V10I, E37D, S43T, K45R, I75V and F85L) in HIV-2 were also identified in this small group of patients.

Abstract: CONCLUSIONS: Several mutations were associated with virological failure of a regimen including atazanavir/ritonavir in HIV-2-infected patients, including I50L for the first time.

Abstract: RESUL

Transmitted drug resistance and phylogenetic relationships among acute and early HIV-1-infected individuals in New York City.

PMID: 22592583 2012 Journal of acquired immune deficiency syndromes (1999)

4Method: ARV resistance was defined by mutations at the following positions: M41L, A62V, K65R, D67N, T69ins, K70R, L74VI, Y115F, F116Y, Q151M, M184VI, T210W, T215YF and K219QE for Nucleoside Reverse Transcriptase Inhibitors (NRTI), L100I, K101EP, K103NS, V106AM

Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.

PMID: 22448246 2012 PloS one

Method: The following resistance mutations were scored: to nucleoside reverse transcriptase inhibitors (NRTIs): M41L, K65R, D67N/G/E, T69D/insertion, K70R/E, L74V/I, V75M/T/A/S, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215Y/F/I/S/C/D/V/E, K219Q/EN/R; to non-nucleoside revers

Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.

PMID: 22239286 2012 The journal of physical chemistry. B

Introduction: Mutation I50L is a signature mutation for atazanavir (ATV) resistance, and has increased susceptibility to other inhibitors with the presence of other primary and secondary resistance mutations.

Result: For the mutation from Ile50 to Leu50, the binding enhancement can be mainly attributed to the electrostatic by -1.05kcal/mol and van der Waals by -0.38 kcal/mol, yet considerably being compromised by the increase of the polarization energy of 0.58 kcal/mol; whereas from Ile50' to Leu50' the contribution from the electrostatic is only -0.24 kcal/mol and the van der waals term is significant by -0.48kcal/mol.

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