literature

HIV mutation literature information.

Low Frequency of Integrase Inhibitor Resistance Mutations Among Therapy-Naive HIV Patients in Southeast China.

PMID: 33679129 2021 Drug design, development and therapy

Discussion: E157Q has been shown to act as a compensatory mutation due to its ability to restore damaged enzymatic activity caused by N155H or R263K substitution.

Transmitted HIV drug resistance and subtype patterns among blood donors in Poland.

PMID: 34140600 2021 Scientific reports

Discussion: This variant may reduce integrase susceptibility if present in combination with other DRMs within this region, especially R263K.

Integrase Strand Transfer Inhibitor Resistance in Integrase Strand Transfer Inhibitor-Naive Persons.

PMID: 33683148 2021 AIDS research and human retroviruses

Abstract: Two surveillance DRMs, E138K and R263K occurred in 0.15% and 0.10% of naive sequences, respectively.

HIV-1 Subtype C Drug Resistance Mutations in Heavily Treated Patients Failing Integrase Strand Transfer Inhibitor-Based Regimens in Botswana.

PMID: 33807382 2021 Viruses

Introduction: INSTI-naive highly treatment-experienced patients failing DTG cART have been found to have a virus with DRMs including G118R, D67N; H51H/Y, G118R, E138E/K, and less commonly R263R/K, V260I, R263R, N155H, G118R, and E138E.

Method: The mutations of interest included: T66A/I/K, Discussion: Compared with a similar cohort of patients from clinical trials, the selection of major integrase DRM- R263K was common.

Interaction analysis of statistically enriched mutations identified in Cameroon recombinant subtype CRF02_AG that can influence the development of Dolutegravir drug resistance mutations.

PMID: 33892628 2021 BMC infectious diseases

Abstract: RESULTS: We observed 12.8% (37/287) sequences to contain RAMs, with only 1.0% (3/287) of the sequences having major INSTI RAMs: T66A, Q148H, R263K and N155H.

Abstract: The interaction analysis revealed that DTG bound to DNA, 2MG ions and DDE motif residues for T66A, T97A, Q148H, N155H and R263K comparable to the WT structure.

Result: Moreover, T66A, Q148H, N155H, D232N and R263K mutations all indicated a loss of interactions with neighbouring resid

Virologic outcomes of switching to dolutegravir functional mono- or dual therapy with a non-cytosine nucleoside analog: a retrospective study of treatment-experienced, patients living with HIV.

PMID: 33941212 2021 AIDS research and therapy

Method: Patients with the following baseline mutations associated with reduced susceptibility to DTG: T66K, E92Q, G118R, E138 K/A/T, G140 S/A/C, Q148 H/R/K, N155H and R263K were excluded.

Altered HIV-1 mRNA Splicing Due to Drug-Resistance-Associated Mutations in Exon 2/2b.

PMID: 35008581 2021 International journal of molecular sciences

Result: Additionally, R263K was recently described to decrease HIV integration and to be associated with therapy failure using Dolutegravir in HIV-1 treated patients.

Result: As expected from the HEXplorer prediction, the silent R263R mutation led to a similar splicing pattern as R263K, albeit, in contrast to the missense version R263K, a slight band for the most abundant mRNA species Tat2b was still present (Figure 3C).

Result: Compared with the parental sequence, the V260I mutation is predicted to have little effect on splice site recognition with a DeltaHZEI of -37.79, whereas R263K is predicted to result in a more severe change in splicing outcome with a DeltaHZEI of -132.16.

HIV Pretreatment Drug Resistance Trends in Mexico City, 2017-2020.

PMID: 34959542 2021 Pathogens (Basel, Switzerland)

Result: Resistance in IN was mainly due to R263K (1.6%) and E138AKT, G140ACS, Q148HKR (0.8% each) (Figure 6c).

Case Report: Emergent Resistance in a Treatment-Naive Person With Human Immunodeficiency Virus Under Bictegravir-Based Therapy.

PMID: 34189182 2021 Open forum infectious diseases

Discussion: However, a recent 2020 case report did document treatment-emergent resistance in a treatment-experienced individual who had received crushed BIC/FTC/TAF tablets through a nasogastric tube, which the authors speculate may have resulted in inadequate blood levels of the drug that led to the R263K mutation.

Discussion: In treatment-naive individuals, the R263K (INI) mutation is very rare and has most commonly been observed by ultra-deep sequencing.

Discussion: Most cases of treatment failure with development of R263K (INI) mutations have been documented in the context of DTG administration, with failure most often linked to low serum drug levels from drug-drug interactions with rifampin or rifabutin.

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