literature

HIV mutation literature information.

Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.

PMID: 26147742 2016 Journal of medical virology

Result: The PR RAMs for this sample were V32I, I47V, I54L, V82A and L90M.

Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.

PMID: 26107265 2015 PloS one

Result: Three subjects harboured major protease mutations (V32I, M46I, I47V, L90M), selected in prior failures.

Table: V32I

Exploring the drug resistance of V32I and M46L mutant HIV-1 protease to inhibitor TMC114: flap dynamics and binding mechanism.

PMID: 25562662 2015 Journal of molecular graphics & modelling

Abstract: Although the second binding of TMC114 with flap does increase binding energy for the mutants (V32I-2T and M46L-2T), the considerable entropy loss results in the lower binding Gibbs free energies.

Abstract: For the single binding (1T) the less binding affinity can be attributed to the entropic loss for both V32I-1T and M46L-1T.

Abstract: However, for some mutants such as V32I and M46L the TMC114 can bind not only to the active cavity but also to the groove of the flexible flaps.

A Comparative Insight into Amprenavir Resistance of Mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 Protease Based on Thermodynamic Integration and MM-PBSA Methods.

PMID: 26317593 2015 Journal of chemical information and modeling

Abstract: Drug resistance of mutations V32I, G48V, I50V, I54V, and I84V in HIV-1 protease (PR) was found in clinical treatment of HIV patients with the drug amprenavir (APV).

Conformational variation of an extreme drug resistant mutant of HIV protease.

PMID: 26397743 2015 Journal of molecular graphics & modelling

Introduction: Recently; for example; the effects of single mutations V32I and M46L were studied by molecular dynamics in.

Method: Plasmid DNA encoding PR (subtype B of group M) with 20 mutations Q7K; L10F; I13V; I15V; D30N; V32I; L33F; E35D; M36I; S37N; I47V; I54L; Q58E; I62V; L63P; A71V; I84V;

PMID: 29124158 2015 Biochemistry and biophysics reports

Introduction: L33F was initially identified as an accessory mutation to I54L/M, V32I+I47V, and I84V/I but is now recognized as a nonpolymorphic major drug resistance mutation.

Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.

PMID: 26695135 2015 BMC bioinformatics

Introduction: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I, I47V, V82AS, D30N, G48V; and accompanied by minor mutations like- L10I, I13V, L63P, A71V, L89M, I93L, E35DN, I15V, D60E, L24I etc.

HIV-1 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.

PMID: 26717411 2015 PloS one

Result: The remaining 8% of viruses with predicted intermediate or high-level LPV resistance had a combination of two or more PI DRMs with lower mutation scores, including V32I, M46I, I54M/L/V, I47V, V82S/T/M and L90M.

Table: V32I

HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.

PMID: 26558396 2015 PloS one

Table: V32I

Dimerization of HIV-1 protease occurs through two steps relating to the mechanism of protease dimerization inhibition by darunavir.

PMID: 25092296 2014 Proc Natl Acad Sci U S A

Abstract: Notably, DRV failed to bind to mutant PR containing four amino acid substitutions (V32I, L33F, I54M, and I84V) that confer resistance to DRV on HIV-1.

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