Integrase Inhibitor Resistance Mechanisms and Structural Characteristics in Antiretroviral Therapy-Experienced, Integrase Inhibitor-Naive Adults with HIV-1 Infection Treated with Dolutegravir plus Two Nucleoside Reverse Transcriptase Inhibitors in the DAWNING Study.
PMID: 34694877
2022
Antimicrobial agents and chemotherapy
Result: Integrase mutants with G118R or G118R plus E138K exhibited faster doluteg
Result: A subcluster of sequences containing K160T in addition to G118R, E138K, and R263K showed the greatest evolutionary distance.
Result: Clonal and population sequences at CVW from participant 3 had multiple evolving pathways with >=2 integrase substitutions, with separate clusters forming for sequences containing H51Y and G118R (bootstrap = 96%) and those containing G118R, E138K, and R263K (bootstrap = 90%).
Integrase Strand Transfer Inhibitor (INSTI) Genotypic Resistance Analysis in Treatment-nNaive, INSTI Free Antiretroviral-Experienced and INSTI-Experienced Turkish Patients Infected with HIV-1.
Abstract: Additional mutations, E92Q, E138K, G140A, S147G, and Q148R were found in elvitegravir; E192Q, E138K/T, G140A/S, S147G, Q148H/R, N155H, E157Q were found in dolutegravir (DTG) experienced patients.
Abstract: Major INSTI-mutations E138K, Y143R, S147G, Q148R, N155H, and E157Q were found in raltegrav
Chemical space exploration of novel naphthyl-carboxamide-diarylpyrimidine derivatives with potent anti-HIV-1 activity.
Abstract: Compound a1 showed exceptionally inhibitory effects with an EC50 value of 3.7 nM against HIV-1 wt strain, and an EC50 of 11 nM targeting mutant E138K.
Abstract: They displayed up to single-digit nanomolar activity against wild-type (WT) and rilpivirine-associated resistant mutant E138K viruses, as well as potent inhibitory ability toward the RT enzyme.
"Design, synthesis, and evaluation of ""dual-site""-binding diarylpyrimidines targeting both NNIBP and the NNRTI adjacent site of the HIV-1 reverse transcriptase."
PMID: 33340914
2021
European journal of medicinal chemistry
Abstract: Of note, 14c exhibited potent activity against the single mutant strain E138K (EC50 = 10.6 nM), being comparable with ETR (EC50 = 9.80 nM) and 3.5-fold more potent than that of compound 7 (EC50 = 37.3 nM).
HIV-1 Subtype C Drug Resistance Mutations in Heavily Treated Patients Failing Integrase Strand Transfer Inhibitor-Based Regimens in Botswana.
Result: Amongst the individuals previously exposed to RAL ART (seven out of eleven), DRMs selected whilst failing their current DTG based regimens were E138K, G140A, Q148R; and N155H Figure 3.
Result: The four individuals failing DTG cART but with no documented prior exposure to RAL, their selected DRMs were E138K, G140A, Q148K, A128T; G118R, E138K; N155ND and T66A, G118R, E138EAKT Figure 3.
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.
Low Frequency of Integrase Inhibitor Resistance Mutations Among Therapy-Naive HIV Patients in Southeast China.
PMID: 33679129
2021
Drug design, development and therapy
Abstract: INSTIs TDRM was rare, with only one primary integrase mutation E138K observed in one sample and one secondary mutation E157Q detected in another sample.
Conclusion: However, TDRM associated with INSTIs-treatment resistance, including E138K and E517Q were also detected in therapy- naive HIV patients in Southeast China.
Result: Only one major INSTIs-resistance mutation (E138K) was detected in one sample.
Table: E138K
Discussion: However, the frequency of INSTIs-resistance mutations may increase with the extensive use of ART, since E
HIV Drug Resistance Mutations Detection by Next-Generation Sequencing during Antiretroviral Therapy Interruption in China.
Result: The most common drug resistance mutation was K103N (13.2%), followed by V179D (6.3%) and E138AGK (3.5%).
Discussion: The minority mutations detected by NGS may have resulted from apolipoprotein B mRNA editing catalytic polypeptide (APOBEC)-mediated G-to-A hypermutation such as E138K, M184I and G190E in RT or spontaneous mutation during viral replication, or from PCR error, which was introduced by error-prone reverse transcriptase or PCR enzymes.
Drug resistance mutations in HIV provirus are associated with defective proviral genomes with hypermutation.
Abstract: Certain Apolipoprotein B Editing Complex 3-related DRMs including reverse transcriptase gene mutations M184I, E138K, M230I, G190E and protease gene mutations M46I, D30N were enriched in hypermutated sequences but not in intact sequences or plasma sequences.
Analysis and Molecular Determinants of HIV RNase H Cleavage Specificity at the PPT/U3 Junction.
Method: Double mutants E138K/M184I and E138K/M184V were prepared from the single-mutant E138K HIV-1 RT, previously described.
Method: Quadruple mutants E138K/M184I/N348I/T369I and E138K/M184V/N348I/T369I were obtained after introducing mutations E138K and M184I/V in sequential order, using as template the plasmid p66RTB containing the p66-coding sequence of mutant N348I/
HIV mutation literature information.
PMID: 
2022
Antimicrobial agents and chemotherapy
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