literature

HIV mutation literature information.

HIV-1 Resistance Dynamics in Patients With Virologic Failure to Dolutegravir Maintenance Monotherapy.

PMID: 29617822 2018 The Journal of infectious diseases

Abstract: INSTI-RAMs (S230R, R263K, N155H, and E92Q+N155H) were detected in 4 patients, no INSTI-RAMs were detected in 4 patients, and sequencing of the integrase gene was unsuccessful in 2 patients.

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.

PMID: 30409215 2018 AIDS research and therapy

Result: As expected, the number and type of mutations with frequencies > 20% (those within Sanger sequencing-based detection level) matched the cART history of the patient, e.g., the virus from patient SG28 had mutations associated with resistance to ABC (L74I 97.6% frequency), 3TC (M184V 99.7%), and EFV (K103N 98.8%, P225H 99.5%) and had been exposed to RTV, DRV, ABC, 3TC, and EFV; while patient SG86 had a virus with resistance to FTC (M184V 98.9%) and RAL (L74M 97.9%, E92Q 86.1% and T97A 99.8%) after being treated over the years with RTV, LPV, DRV, FTC, TDF, and RAL (Additional file 1: Table S1).

Result: Most of these minority drug resistance mutations were detected in the 67 cART-experienced individuals, e.g., the

Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.

PMID: 30119633 2018 Retrovirology

Abstract: With EVG, T66I/A, E92G/V/Q, T97A or R263K (n = 16, 3, 2 and 1, respectively) arose by weeks 8-16, followed by 1-4 accessory mutations, conferring high-level resistance (> 100-fold) by week 36.

Introduction: Drug resistance is associated with the accumulation of primary resistance substitutions and relevant compensatory substitutions along several pathways including the (1) N155H and G140A/G148R/H/Q pathways conferring high level cross-resistance to RAL and EVG; (2) the T66I or E92Q/G pathways leading to resistance to EVG; or (3) the Y143R/H/C RAL-specific resistance pathway.

Result: Clinical isolates that failed to devel

Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.

PMID: 29137637 2017 Virology journal

Method: Major INSTI resistance mutations (T66I, E92Q, F121Y, Y143CHR, S147G, Q148HKR, N155H) that confer substantial phenotypic resistance to at least one of the currently approved INSTI as well as minor INSTI resistance mutations (T66AK, L74 M, E92G, T97A, E138AK, G140AS, R263K) that increase INSTI resistance and/or viral

Unravelling the dynamics of selection of multiresistant variants to integrase inhibitors in an HIV-1-infected child using ultra-deep sequencing.

PMID: 27999055 2017 The Journal of antimicrobial chemotherapy

Abstract: At the last timepoint under raltegravir (week 17), Y143R emerged, leading to different resistance mutation patterns: single mutants N155H (47%) and Y143R (24%) and double mutants E92Q + N155H (13%), Y143R + N155H (2%) and E92Q + Y143R (2%).

Abstract: The double mutant E92Q + N155H, conferring resistance to the entire integrase inhibitor class, including dolutegravir, emerged at week 8 (16%) and became rapidly dominant (57% by week 13).

Abstract: The polymorphic substitution M50I was preferentially selected on resistant va

Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.

PMID: 28212411 2017 PloS one

Result: In 6 of these 14 patients (EVG, n = 4; RAL, n = 2), the T97A (or T97T/A) integrase mutation emerged in the presence of primary INSTI RAM(s) (N155H, n = 5; E92Q, n = 1) and all had HIV-1 subtype B (Table 1 and Fig 2; S2 Table and S2 Fig).

Result: None of these pre-treatment integrase sequences contained primary integrase mutations most often associated with emergent EVG (T66I, E92Q, S147G, Q148R/H/K, and N155H) or RAL (Y143C/R/H,

PMID: 28472323 2017 The Journal of antimicrobial chemotherapy

Introduction: Resistance to elvitegravir and raltegravir occurs via several mutational pathways, including: (i) N155H or G140A/G148RHQ pathways conferring raltegravir and elvitegravir cross-resistance; (ii) T66I or E92Q/G elvitegravir-specific pathways; or (iii) the Y143R/H/C raltegravir-specific resistance pathway.

Antiviral Activity of Bictegravir and Cabotegravir against Integrase Inhibitor-Resistant SIVmac239 and HIV-1.

PMID: 28923862 2017 Antimicrobial agents and chemotherapy

Abstract: In single cycle SIV infections, none of the E92Q, T97A, Y143R, or N155H substitutions had a significant effect on susceptibility to BIC (<=4-fold increase in EC50), whereas G118R and R263K conferred ~14-fold and ~6-fold increases in EC50, respectively.

Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).

PMID: 28891788 2017 HIV clinical trials

Method: Primary INSTI-R substitutions assessed were T66A/I/K, E92G/Q, T97A, Y143C/H/R, S147G, Q148H/K/R, and N155H/S in IN.

Therapy-Emergent Drug Resistance to Integrase Strand Transfer Inhibitors in HIV-1 Patients: A Subgroup Meta-Analysis of Clinical Trials.

PMID: 27532886 2016 PloS one

Abstract: The resistance of DTG is mainly shown in 13 integrase mutations (including T97T/A, E138E/D, V151V/I, N155H, Q148, Y143C/H/R, T66A and E92Q).

Abstract: The ten major integrase mutations (including N155H, Y143C/R, Q148H/R, Y143Y/H, L74L/M, E92Q, E138E/A, Y143C, Q148Q and

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