literature

HIV mutation literature information.

Resistance to HIV Integrase Inhibitors: About R263K and E157Q Mutations.

PMID: 29346270 2018 Viruses

Introduction: They showed that the presence of the E92Q or N155H resistance mutations was compatible with the emergence of R263K, whereas no R263K selection was observed in presence of G140S-Q148R, E92Q-N155H, G140S, Y143R and Q148R resistance mutations.

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.

Result: Emergent high-level resistance to RAL were associated with the Y143R/G and Q148R pathways.

Table: Y143R

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.

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%).

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

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

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.

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

PMID: 28923862 2017 Antimicrobial agents and chemotherapy

Abstract: In both single and multiple rounds of HIV-1 infections, BIC remained active against the Y143R, N155H, R263K, R263K/M50I, and R263K/E138K mutants (<=4-fold increase in EC50).

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.

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

Drug resistant integrase mutants cause aberrant HIV integrations.

PMID: 27682062 2016 Retrovirology

Introduction: We tested the effects of three IN mutations, Y143R, N155H, and the double mutation G140S/Q148H, all of which reduce the susceptibility of HIV-1 to RAL, on viral DNA integration.

Result: Although the data suggest that a suboptimal concentration of RAL appears to increase the propensity of the Y143R mutant to make aberrant integrations, the differences in the fraction of integration sites that were aberrant for the Y143R mutant, comparing the presence and absence of RAL, were not statistically significant.

Result: In the absence of any added RAL, we found aberrant integrations in infections that were done using the Y143R mutant; howeve

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