literature

HIV mutation literature information.

Retrospective study on the outcome of two-drug regimens based on dolutegravir plus one reverse transcriptase inhibitor in virologically-suppressed HIV-infected patients.

PMID: 31926287 2020 International journal of antimicrobial agents

Abstract: One VF to DTG+RPV occurred because of historical resistance to RPV, accompanied by newly selected G140A and Q148R mutations.

Expanded Spectrum of Antiretroviral-Selected Mutations in Human Immunodeficiency Virus Type 2.

PMID: 31965175 2020 The Journal of infectious diseases

Abstract: In IN, 11 nonpolymorphic TSMs occurred in >=4 persons: Q91R, E92AQ, T97A, G140S, Y143G, Q148R, A153G, N155H, H156R, R231 5-amino acid insertions.

HIV-1 acquired drug resistance to integrase inhibitors in a cohort of antiretroviral therapy multi-experienced Mexican patients failing to raltegravir: a cross-sectional study.

PMID: 32041622 2020 AIDS research and therapy

Discussion: On the other hand, we do not find a significant difference between the mean viral load of the subjects with DTG resistance compared to the subjects without DTG resistance (n = 22), nor with samples harbouring a G140S/A + Q148H/R/K combination (n = 3) as described in that study.

High prevalence of integrase mutation L74I in West African HIV-1 subtypes prior to integrase inhibitor treatment.

PMID: 32105319 2020 The Journal of antimicrobial chemotherapy

Introduction: At VF the major integrase mutation Q148R occurred in two and G140R in one.

Impact of genotypic diversity on selection of subtype-specific drug resistance profiles during raltegravir-based therapy in individuals infected with B and BF recombinant HIV-1 strains.

PMID: 32125378 2020 The Journal of antimicrobial chemotherapy

Abstract: INI DRMs differed between B and F IN subtypes, with Q148K/R/H, G140S and E138K/A being more prevalent in subtype B (63% versus 0%, P = 0.0021; 50% versus 0%, P = 0.0096; and 50% versus 0%, P = 0.0096, respectively).

Characterization of viral rebounds on dual etravirine/raltegravir maintenance therapy (ANRS-163 ETRAL trial).

PMID: 32259255 2020 The Journal of antimicrobial chemotherapy

Abstract: Some RT variants became dominant at VF (K101E, 86.3%; Y181C, 100.0%; G190A, 100.0%) and others emerged in integrase (Y143C, 2.4%; Q148R, 6.2%; N155H, 18.8%).

Evidence for Disruption of Mg(2+) Pair as a Resistance Mechanism Against HIV-1 Integrase Strand Transfer Inhibitors.

PMID: 32974383 2020 Frontiers in molecular biosciences

Introduction: There are three commonly frequent resistance pathways among the resistance mutations: N155H, Q148HRK, and Y143HC; interestingly, N155H and Q148HRK are mutually exclusive.

First case of Dolutegravir and Darunavir/r multi drug-resistant HIV-1 in Cameroon following exposure to Raltegravir: lessons and implications in the era of transition to Dolutegravir-based regimens.

PMID: 32843050 2020 Antimicrobial resistance and infection control

Conclusion: Another GRT, covering HIV-1 integrase (IN) region, performed on the sample plasma aliquot, revealed major RAMs, L74I, E138KQ, G140A, Q148R, and E157Q, to integrase strand transfer inhibitors (INSTI) including raltegravir, dolutegravir, bictegravir and elvitegravir.

Discussion: Specifically, previous exposure to RAL (a drug with a low-genetic barrier to resistance) in a context of poor adherence contributed to selecting mutations (E138KQ, G140A, Q148R) conferring cross-resistance to DTG.

Accumulation of integrase strand transfer inhibitor resistance mutations confers high-level resistance to dolutegravir in non-B subtype HIV-1 strains from patients failing raltegravir in Uganda.

PMID: 32853364 2020 The Journal of antimicrobial chemotherapy

Abstract: Two patients, one with E138A/G140A/Q148R/G163R and one with E138K/G140A/S147G/Q148K, displayed the highest reported resistance to raltegravir, elvitegravir and even dolutegravir.

Molecular dynamic simulations to investigate the structural impact of known drug resistance mutations on HIV-1C Integrase-Dolutegravir binding.

PMID: 32379830 2020 PloS one

Introduction: Genetic resistance pathways including primary mutations at codons Y143C/H/R, Q148H/K/R or N155H together with one or more additional associated secondary mutations at L74M, E92Q, T97A, E138E/A/K or G140S/A, has been reported to result in higher levels of resistance with RAL treatment.

Table: Q148R

Discussion: showed the structural impact of mutations Q148H/R and G140S/A on the flexibility of the HIV-1 IN as a mechanism for RAL resistance.

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