literature

HIV mutation literature information.

Drug resistance in children at virological failure in a rural KwaZulu-Natal, South Africa, cohort.

PMID: 24444369 2014 AIDS research and therapy

Table: V82A

Natural polymorphisms and unusual mutations in HIV-1 protease with potential antiretroviral resistance: a bioinformatic analysis.

PMID: 24629078 2014 BMC bioinformatics

Result: We modelled the proteins with unusual mutations (L5F, D29V, L63G, L63R, P79L and T91V), natural polymorphisms (L63H andL63S), and drug-resistant mutant PRs with single mutations or patterns of mutations (D30N, V32I, M36I, M46I, I47V, G48V, I50V, I50L, I54M, Q58E, T74P,

Table: V82A

Effects of PRE and POST therapy drug-pressure selected mutations on HIV-1 protease conformational sampling.

PMID: 24983495 2014 FEBS letters

Result: The POST construct contains 8 additional drug-selected polymorphisms, including L10I, I15V, E34Q (negative to uncharged), M36I, T37N, I54A, R57E (positive to negative), and V82A.

Systematic molecular dynamics, MM-PBSA, and ab initio approaches to the saquinavir resistance mechanism in HIV-1 PR due to 11 double and multiple mutations.

PMID: 25036111 2014 The journal of physical chemistry. B

Abstract: Herein, we extend our analysis, which includes seven double (G48V-V82A, L10I-G48V, G48V-L90M, I84V-L90M, L10I-V82A, L10I-L63P, A71V-G73S) and four multiple (L10I-L63P-A71V, L10I-G48V-V82A, G73S-I84V-L90M,

Phenotypic characterization of virological failure following lopinavir/ritonavir monotherapy using full-length Gag-protease genes.

PMID: 25096075 2014 The Journal of antimicrobial chemotherapy

Result: Clonal sequence analysis revealed the presence of the V82A major PI resistance mutation in 1 of the 10 viral variants isolated from the time of treatment failure, as well as a number of protease polymorphisms at both screening and failure (Table S1, available as Supplementary data at JAC Online).

Result: Of note, the F5 variant containing the major PI resistance mutation V82A displayed significantly reduced susceptibility to lopinavir (17-fold).

Discussion: This degree of reduction in PI susceptibility was the same as observed for variant 1403 F6, which contained the V82A major PI resistance mutation, implying clinical relevance in the FCs observed for gag-associ

A multi-drug resistant HIV-1 protease is resistant to the dimerization inhibitory activity of TLF-PafF.

PMID: 25108107 2014 Journal of molecular graphics & modelling

Introduction: The multidrug-resistant (MDR)-769 HIV-1 protease consists of amino acid substitutions: L10I, M36V, M46L, I54V, I62V, L63P, A71V, V82A, I84V and L90M.

Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.

PMID: 25575025 2014 Retrovirology

Method: Baseline patient-derived viral protease genes harboring M46I, M46L, L90M or I54V + V82A + L90M or the N-terminus of RT containing M41L, M41L + T69S + L210E + T215S or K103N were introduced into HXB2 using the same vector system.

Result: In addition, two more complex transmitted viruses were studied: a protease-variant containing I54V + V82A +

Table: V82A

Use of dolutegravir in two INI-experienced patients with multiclass resistance resulted in excellent virological and immunological responses.

PMID: 25397500 2014 Journal of the International AIDS Society

Table: V82A

A uniquely prevalent nonnucleoside reverse transcriptase inhibitor resistance mutation in Russian subtype A HIV-1 viruses.

PMID: 25259833 2014 AIDS (London, England)

Result: Of the 243 patients who received one or more protease inhibitors, 32 (13%) had a study-defined protease inhibitor-resistance mutation most commonly L10F, K20T, V32I, L33F, M46I/L, I47V/A, I50L, F53L, I54V/L, Q58E, L76V, V82A/C, I84V, L89V, and L90M.

Drug Resistance Mutations Alter Dynamics of Inhibitor-Bound HIV-1 Protease.

PMID: 25136270 2014 Journal of chemical theory and computation

Abstract: Flap+ is a multidrug-resistant variant of HIV-1 protease with a combination of primary and secondary resistance mutations (L10I, G48V, I54V, V82A) and a strikingly altered thermodynamic profile for darunavir (DRV) binding relative to the wild-type protease.

Introduction: This variant Flap+ (L10I/G48V/I54V/V82A) was derived as a combination of mutations that simultaneously occur in patient sequences.

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