literature

HIV mutation literature information.

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

PMID: 30119633 2018 Retrovirology

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.

Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.

PMID: 29304821 2018 Retrovirology

Introduction: Resistance is commonly associated with selection of one of the signature raltegravir resistance mutations Y143C/R/H, Q148H/K/R or N155H.

Result: Before raltegravir therapy, mutation Y143H was detected at low frequency (0.2%) by NGS but did not appear in any of the later samples during raltegravir treatment.

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

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.

HIV-1 strains belonging to large phylogenetic clusters show accelerated escape from integrase inhibitors in cell culture compared with viral isolates from singleton/small clusters.

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.

Result: INSTI-associated mutations were present at really low frequency as determined by deep sequencing (R263K at 1.1% and Y143H at 1.6% in 14514 and 14380, respectively) (Figure5c and d).

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: 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, Q148H/K/R, and N155H) resistance.

Transmitted drug resistance of HIV-1 strains among individuals attending voluntary counselling and testing in Taiwan.

PMID: 26404079 2016 The Journal of antimicrobial chemotherapy

Abstract: Among the seven major integrase mutations (T66I, E92Q, G140S, Y143C/H/R, S147G, Q148H/K/R and N155H), only one strain harbouring the Q148R mutation was detected.

Prevalence of Integrase Strand Transfer Inhibitors (INSTI) Resistance Mutations in Taiwan.

PMID: 27779200 2016 Scientific reports

Method: The major INSTI mutations, which have been determined ha

Discussion: In patients experiencing virological failure to the first generation of INSTIs, raltegravir and elvitegravir, three genotypic mutation pathways have been defined: Q148H/R/K (+-G140S or E138A/K), N155H (+-E92Q), and Y143C/H/R (+-T97A).

Discussion: Of 30 subjects who failed INSTI-containing regimens in this study, 17 had Q148H/K/R mutations, 8 had N155H mutations, and 6 had Y143C/H/R mutations.

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

Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.

PMID: 26626277 2015 Journal of translational medicine

Abstract: Neither major resistance-associated IN mutations (T66I/A/K, E92Q/G, T97A, Y143HCR, S147G, Q148H/R/K, and N155H) nor silent mutations known to change the genetic barrier were observed.

Conclusion: None of the previously reported major mutations (T66AIK, E92Q, Y143RCH, S147G, Q148HRK and N155H) associated with resistance to INIs were observed in HIV-1C Ethiopian isolates, indicating that

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