Abstract: We have previously selected mutations at position R263K, G118R, H51Y, and E138K as being associated with low-level resistance to DTG.
Bicyclic 1-hydroxy-2-oxo-1,2-dihydropyridine-3-carboxamide-containing HIV-1 integrase inhibitors having high antiviral potency against cells harboring raltegravir-resistant integrase mutants.
PMID: 24471816
2014
Journal of medicinal chemistry
Abstract: Importantly, some of these new inhibitors retain greater antiviral efficacy compared to that of RAL when tested against a panel of IN mutants that included Y143R, N155H, G140S/Q148H, G118R, and E138K/Q148K.
Method: The double mutant E138K + Q148K was made by using the Q148K mutant and the appropriate oligonucleotide to introduce the second mutation, E138K.
Method: The following sense with cognate antisense (not shown) oligonucleotides (Integrated DNA Technologies, Coralville, IA) was used in the mutagenesis: G118R, 5'
Comparison of illumina and 454 deep sequencing in participants failing raltegravir-based antiretroviral therapy.
Abstract: The only raltegravir-resistant MV detected was an E138K mutation in one participant by Illumina sequencing, but not by 454.
Result: The only raltegravir-resistant MV detected was an E138K mutation detected at a frequency of 0.15% in one participant by Illumina sequencing, but not by 454.
Prevalence in the USA of rilpivirine resistance-associated mutations in clinical samples and effects on phenotypic susceptibility to rilpivirine and etravirine.
Abstract: METHODS: In total, 15,991 samples submitted to Monogram Biosciences (South San Francisco, CA, USA) for routine resistance testing between January 2010 and June 2011 were assessed for the presence of known rilpivirine RAMs K101E/P, E138A/G/K/Q/R, V179L, Abstract: Median FC values >2.0 were observed for clinical isolates with rilpivirine RAMs K101P, E138Q/R, Y181C/I/V, Y188L or M230L, and for the combination of E138K with M184I/V, and K101E with M184I.
Transmitted drug resistance to rilpivirine among antiretroviral-naive patients living with HIV from northern Poland.
PMID: 24746180
2014
Journal of the International AIDS Society
Abstract: RPV-associated mutations were divided into RPV resistance mutations (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L) according to the International AIDS Society-USA (IAS-USA) mutation list and variants potentially affecting RPV susceptibility (L100I, K101H/T, E138S, V179F/D/G/T, G190A/E/S, F227L and M230V) based on the
E138A in HIV-1 reverse transcriptase is more common in subtype C than B: implications for rilpivirine use in resource-limited settings.
Introduction: Although RPV has been reported to have higher in vitro genetic barrier to resistance, at least 17 single substitutions in HIV-1 RT (L100I, K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C, and M230I/L) have been associated with a decreased virologic response to this NNRTI.
Introduction: In contrast to E138A, the frequencies of other substitutions at codon 138 (i.e., E138G/K/Q) were similar in both subtypes B and C.
Introduction: In subtype
Rilpivirine resistance and the dangerous liaisons with substitutions at position 184 among patients infected with HIV-1: analysis from a national drug-resistance database (ARCA).
Abstract: Among Italian patients the susceptibility to RPV is widespread since some severe substitutions (e.g., E138K are rare), whereas issues exist for others (i.e., E138A, Y181C) which are more frequent.
Abstract: Rilpivirine (RPV) is a novel NNRTI with a mutational pattern different from first-generation drugs of the same class: 16 resistance-associated mutations (RAM) are listed, but the combination E138K + M184I seems to be the most important.
Abstract: The combination E138K + M184I is absent in both naive and experienced subjects.
Effects of the W153L substitution in HIV reverse transcriptase on viral replication and drug resistance to multiple categories of reverse transcriptase inhibitors.
PMID: 24867966
2014
Antimicrobial agents and chemotherapy
Abstract: Biochemical assays demonstrated that W153L alone or in combination with K65R, M184I, K101E, K103N, E138K, and Y181C impaired enzyme processivity and polymerization efficiency but did not diminish RNase H activity, providing mechanistic insights into the low replicative fitness associated with these substitutions.
Abstract: To investigate the impact of W153L, alone or in combination with the clinically relevant RT resistance substitutions K65R (change of Lys to Arg at position 65), M184I, K101E, K103N<
Optimization of the antiviral potency and lipophilicity of halogenated 2,6-diarylpyridinamines as a novel class of HIV-1 NNRTIS.
Abstract: In particular, (E)-6-(2''-bromo-4''-cyanovinyl-6''-methoxy)phenoxy-N(2) -(4'-cyanophenyl)pyridin-2,3-diamine (8 c) displayed low-nanomolar antiviral potency (3-7 nM) against wild-type and drug-resistant viral strains bearing the E138K or K101E mutations, which are associated with resistance to rilvipirine (1 b).
Result: K101E and E138K are the most important mutations associated with resistance against new-generation NNRTI drug
Result: Its structure with two different X groups (Br and OMe) might be critical in influencing antiviral potency against these drug-resistant viral strains, especially for E138K and K101E, two major mutations associated with next-generation NNRTI drugs 1a and 1b.
Altered viral fitness and drug susceptibility in HIV-1 carrying mutations that confer resistance to nonnucleoside reverse transcriptase and integrase strand transfer inhibitors.
Abstract: Conversely, RT-E138K and -Y181C mutations improved the fitness of the IN-G140S/Q148H mutant virus in the presence of raltegravir (RAL); the RT-K103N mutation had no effect.
Abstract: However, both the RT-K103N plus IN-G140S/Q148H and the RT-E138K plus IN-G140S/Q148H mutant viruses had significantly greater fold increases in 50% inhibitory concentrati
HIV mutation literature information.
PMID: 
2014
AIDS (London, England)
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