Introduction: Although substitutions at positions M50I, H51Y or E138K emerged under DTG pressure after R263K, none of these was able to restore viral replicative capacity to wild-type levels.
Recent Transmission Clustering of HIV-1 C and CRF17_BF Strains Characterized by NNRTI-Related Mutations among Newly Diagnosed Men in Central Italy.
Abstract: All carried R5-tropic viruses, with evidence of atypical or resistance amino-acidic mutations related to NNRTI-drugs (K103Q in C-cluster, and K101E+E138K in CRF17_BF-cluster).
Result: Analysing the HIV-1 CRF17_BF cluster, all strains carried the NNRTI resistance mutations K101E and E138K in the RT, thus showing the transmission of a resistant viral strain.
Discussion: By contrast, the CRF17_BF cluster has been characterized by HIV-1 strains resistant to both first and second NNRTIs generations, due to the presence of the RT mutations K101E and E138K
Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades.
PMID: 26311843
2015
The Journal of antimicrobial chemotherapy
Method: Dolutegravir resistance categories were as follows: (i) no resistance, absence of Q148H/R/K; (ii) low-level resistance, Q148H/R/K in the absence of G140S/A/C, L74I and E138A/K/T; (iii) intermediate-level resistance, Q148H/R/K with one of the mutations G140S/A/C, L74I or E138A/K/T; and (iv) high-l
Result: Of these, L74M, T97A, E138K, V151I and G163R were significantly associated (P < 0.01) with raltegravir exposure.
The Combination of the R263K and T66I Resistance Substitutions in HIV-1 Integrase Is Incompatible with High-Level Viral Replication and the Development of High-Level Drug Resistance.
Abstract: E138K is a common secondary substitution observed with various primary resistance substitutions in RAL- and EVG-treated individuals.
Abstract: In order to determine how different combinations of integrase resistance mutations can influence the outcome of therapy, we report here the effects of the T66I, E138K, and R263K substitutions, alone and in combination, on viral replicative capacity and resistance to integrase inhibitors.
Abstract: The addition of the E138K substitution partially compensated for these deficits and resulted in high levels of resistance against EVG but not against DTG or RAL.
The dolutegravir R263K resistance mutation in HIV-1 integrase is incompatible with the emergence of resistance against raltegravir.
Abstract: DESIGN AND METHODS: We performed tissue culture selection experiments using DTG-resistant viruses containing integrase substitutions at positions R263K, H51Y/R263K, E138K/R263K, G118R and H51Y/G118R in the presence of increasing concentrations of either RAL or EVG.
Abstract: In contrast, resistance against EVG appeared earlier than in wild-type virus in viruses containing the R263K and E138K/R263K DTG-associated resistance substitutions.
Abstract: RESULTS: The presence of the R263K substitution delayed the emergence of
Comparison of 454 Ultra-Deep Sequencing and Allele-Specific Real-Time PCR with Regard to the Detection of Emerging Drug-Resistant Minor HIV-1 Variants after Antiretroviral Prophylaxis for Vertical Transmission.
Method: By analysing five samples of recombinant wild-type virus NL4.3 with viral loads ranging from 103 to 109 copies/ml, we found the highest error rate for unknown drug resistance mutations detected in our sample panel to be 0.25% for E138K.
Result: Twenty-eight NVP-selected mutations (V90I, K101E, K103N/R, V106A/I/M, V108I, E138A/G/K/R, Y181C, Y188C, G190A or P225H) were detected in 19 samples at levels of 1.1% to 99.1%.
Table: E138K
Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
PMID: 26626277
2015
Journal of translational medicine
Discussion: This includes T66IAK, E92Q, F121Y, G140SA, Y143HCR, Q146P, S147G, Q148KHR, and N155HS; (2) minor INI-resistance mutations were defined as non-polymorphic or minimally polymorphic mutations that reduce INI susceptibility H51Y, L74 M, T97A, E138AK, S153Y,
HIV-1 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.
Discussion: A POC test for RPV resistance would also require a different set of NNRTI-associated DRMs than those described here because K101E, E138K, and Y181C appear to be the DRMs occurring most commonly in individuals receiving first-line RPV-containing regimens.
The connection domain mutation N348I in HIV-1 reverse transcriptase enhances resistance to etravirine and rilpivirine but restricts the emergence of the E138K resistance mutation by diminishing viral replication capacity.
Abstract: N348I also enhanced levels of resistance conferred by E138K against RPV and ETR by 2.2- and 2.3-fold, respectively.
Abstract: Clinical resistance to rilpivirine (RPV), a novel nonnucleoside reverse transcriptase (RT) inhibitor (NNRTI), is associated an E-to-K mutation at position 138 (E138K) in RT together with an M184I/V mutation that confers resistance against emtricitabine (FTC), a nucleoside RT inhibitor (NRTI) that is given together with RPV in therapy.
Abstract: Now, we show that both N348I alone and N348I/ PMID: 24379202
2014
Antimicrobial agents and chemotherapy
Abstract: Furthermore, E138K, Y181C, and K101E mutant viruses that are associated with ETR and RPV were susceptible to MK-1439 with a fold change (FC) of <3.
HIV mutation literature information.
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2015
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