Prevalence and clinical impact of minority resistant variants in patients failing an integrase inhibitor-based regimen by ultra-deep sequencing.
PMID: 29873733
2018
The Journal of antimicrobial chemotherapy
Abstract: Among 53 patients harbouring at least one resistance mutation detected by both techniques, the most dominant INSTI resistance mutations were N155H (45%), Q148H/K/R (23%), T97A (19%) and Y143C (11%).
Prevalence of Integrase Strand Transfer Inhibitors Resistance Mutations in Integrase Strand Transfer Inhibitors-Naive and -Experienced HIV-1 Infected Patients: A Single Center Experience.
PMID: 29631420
2018
AIDS research and human retroviruses
Abstract: Among them, 10 harbored N155H, 4 Q148H, 2 Q148R, 2 Y143C/S, and 2 T66A/I/T, respectively.
Primary resistance to integrase strand transfer inhibitors in patients infected with diverse HIV-1 subtypes in sub-Saharan Africa.
PMID: 29462322
2018
The Journal of antimicrobial chemotherapy
Abstract: Major INSTI resistance mutations were detected only at <20% threshold, at a prevalence of 2.4% (2.5% in subtype A, 2.4% C, 0% D, 8.3% G and 2.4% in recombinants) and included T66A/I (0.7%), E92G (0.5%), Y143C/S (0.7%), S147G (0.2%) and Q148R (0.5%).
Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.
Introduction: Resistance is commonly associated with selection of one of the signature raltegravir resistance mutations Y143C/R/H, Q148H/K/R or N155H.
Result: 2), including T97A and Y143C (both 0.2%).
Result: In a sample taken 28 days later, 77.5% of the population contained N155H, 15.4% had T97A and variants with Y143C were not detected anymore.
Result: In the subsequent sample 70 days after start of raltegravir therapy, N155H had increased to 88.6% and Y143C had reappeared in 11.8% of the reads.
Result: Interestingly, in the two other cultures, N155H emerge
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).
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.
Integrase strand-transfer inhibitor polymorphic and accessory resistance substitutions in patients with acute/recent HIV infection.
PMID: 27624569
2017
The Journal of antimicrobial chemotherapy
Abstract: CONCLUSIONS: Although signature InSTI substitutions (such as Y143R/C, N155H or Q148K/R/H) were not detected, polymorphisms and substitutions conferring low-level resistance to raltegravir and elvitegravir were frequently found in a baseline genotypic test.
Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.
Introduction: As a secondary INSTI RAM, T97A further reduces INSTI susceptibility and/or rescues viral fitness in association with Y143C/R, Q148H+G140S, or N155H.
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
Temporal Patterns and Drug Resistance in CSF Viral Escape Among ART-Experienced HIV-1 Infected Adults.
PMID: 28328546
2017
Journal of acquired immune deficiency syndromes (1999)
Result: Two studies reported sequencing the integrase gene in CSF; N155H, L74I, and Q148R mutations were observed as single mutations in the integrase gene, and Y143C was observed in combination with T66I.
Discussion: Three CSF integrase mutations were identified in CSF (N155H, Y143C, and Q148R).
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.
Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.
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
HIV mutation literature information.
PMID: 
2018
The Journal of antimicrobial chemotherapy
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