Result: In this study,19 substitutions conferring major resistance to DTG at 10 amino acid positions in the IN (T66A/I/K, E92G, G118R, E138K/A/T, G140S/A/C, Y143R/C/H, S147G, Q148H/R/K, N155H, and R263K) were assessed to explore the genetic barrier to DTG.
Could Long-Acting Cabotegravir-Rilpivirine Be the Future for All People Living with HIV? Response Based on Genotype Resistance Test from a Multicenter Italian Cohort.
PMID: 35207677
2022
Journal of personalized medicine
Method: We also excluded PWH with the following INSTI mutations: T66I, E92Q, G118R, G140S, Y143A/C/G/H/K/R/S, S147G, Q148H/K/N/R, N155H/S/T, and R263K.
Impact of Integrase Sequences from HIV-1 Subtypes A6/A1 on the In Vitro Potency of Cabotegravir or Rilpivirine.
PMID: 34978890
2022
Antimicrobial agents and chemotherapy
Introduction: Although L74I has not been observed in association with INSTI resistance (https://hivdb.stanford.edu/dr-summary/resistance-notes/INSTI/), the L74M mutation in combination with INSTI resistance-associated mutations (RAMs) T66I/K, E92V, Y143C, or N155H reduced susceptibility 14- to >200-fold to raltegravir or elvitegravir.
Brief Report: Bictegravir/Emtricitabine/Tenofovir Alafenamide Efficacy in Participants With Preexisting Primary Integrase Inhibitor Resistance Through 48 Weeks of Phase 3 Clinical Trials.
PMID: 34897227
2022
Journal of acquired immune deficiency syndromes (1999)
Introduction: Primary INSTI drug resistance reported in surveillance studies are mainly substitutions that cause resistance to RAL and EVG (T66A/I, E92Q, Y143C/H/R, S147G, Q148H/K/R, and N155H pathways) and R263K, which confers low-level reduced susceptibility to EVG, DTG, and bictegravir (BIC).
Table: T66I/A
Emergence of Resistance in HIV-1 Integrase with Dolutegravir Treatment in a Pediatric Population from the IMPAACT P1093 Study.
PMID: 34694878
2022
Antimicrobial agents and chemotherapy
Result: Four of 5 participants with G118R had 1 additional treatment-emergent INSTI-associated substitution of L74M, E138E/K, E92E/Q, or T66I, respectively.
Table: T66I
Discussion: Thus, V75A and the known INSTI resistance-associated substitutions L74M and T66I may cooperate with G118R to exacerbate INSTI resistance and reduce viral replication capacity.
Discussion: Treatment-emergent G118R in combination with either L74M or PMID: 34694877
2022
Antimicrobial agents and chemotherapy
Table: T66A/I
Table: T66I
Interaction analysis of statistically enriched mutations identified in Cameroon recombinant subtype CRF02_AG that can influence the development of Dolutegravir drug resistance mutations.
Discussion: The close proximity of the T66A/I/K variants to the viral DNA 3' end and mutation N155H, could sterically hamper viral DNA binding and/or metal ion coordination with DTG.
Transmitted HIV-1 drug resistance in a large international cohort using next-generation sequencing: results from the Strategic Timing of Antiretroviral Treatment (START) study.
Abstract: INSTI DRMs were detected almost exclusively below the 20% detection threshold, most commonly Y143H (0.4%), Q148R (0.4%) and T66I (0.4%).
Method: INSTI mutations, which are not included on this list, were defined as those on the Stanford HIVdb surveillance DRM list, namely T66AIK, E92Q, F121Y, G140ACS, Y143CHR, S147G, Q148HKR and N155HS.
Increased acquired protease inhibitor drug resistance mutations in minor HIV-1 quasispecies from infected patients suspected of failing on national second-line therapy in South Africa.
Discussion: Previous studies on HIV-1C have shown major INI mutations at baseline in less than 5% of patients from Ethiopia (T66I, E138K, Q148R, and Q148H) and South Africa (Q148H, T66S, E92G, S147G, T66A, Y143YF and Y143H).
HIV-1 Subtype C Drug Resistance Mutations in Heavily Treated Patients Failing Integrase Strand Transfer Inhibitor-Based Regimens in Botswana.
HIV mutation literature information.
PMID: 
2022
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