Result: The Q148K + E138K combination was evident at month 3, and though this combination is reported to be a potent RAL escape variant, it was not detected subsequently.
Interaction of reverse transcriptase (RT) mutations conferring resistance to lamivudine and etravirine: effects on fitness and RT activity of human immunodeficiency virus type 1.
Abstract: Clinical trials of RPV administered with lamivudine or emtricitabine showed the emergence of E138K together with M184I, which confers lamivudine and emtricitabine resistance in most patients with virologic failure.
Abstract: Fitness profiles and growth competition experiments showed that the E138K/M184I mutant had a significant replicative advantage over the E138K/M184V mutant in the presence of etravirine and lamivudine.
Abstract: Resistance to the nonnucleoside reverse transcriptase inhibitors etravirine and rilpivirine (RPV) is conferred by the E138K mutation in human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (M184 V/I.
Abstract: E138K restored viral replication capacity (RC) in the presence of M184I/V, and this was confirmed in cell-free RT processivity assays.
Abstract: Recently, several phase 3 clinical trials (ECHO and THRIVE) showed that E138K and M184I were the most frequent mutations to emerge in patients who failed therapy with rilpivirine (RPV) together with two nucleos(t)ide reverse transcriptase inhibitors, emtricitabine (FTC) and tenofovir (TDF).
Abstract: Structural modeling shows that the addition of E138K to M184I/V promotes tighter dNTP binding.
Abstract: The results of phenotyping showed that viruses containing both the E138K and Nonnucleoside Reverse Transcriptase Inhibitors with Improved Activity against K103N and E138K Mutants and Pharmacokinetic Profiles.
Prevalence and patterns of HIV transmitted drug resistance in Guatemala.
PMID: 22358416
2011
Revista panamericana de salud publica
Abstract: Major NNRTI mutations such as K101E, K103N, and E138K showed higher frequencies than expected in ART-naive populations.
TMC278, a next-generation nonnucleoside reverse transcriptase inhibitor (NNRTI), active against wild-type and NNRTI-resistant HIV-1.
PMID: 19933797
2010
Antimicrobial agents and chemotherapy
Abstract: NNRTI RAMs emerging in HIV-1 under selective pressure from TMC278 included combinations of V90I, L100I, K101E, V106A/I, V108I, E138G/K/Q/R, V179F/I, Y181C/I, V189I, G190E, H221Y, F227C, and M230I/L.
IDX-899, an aryl phosphinate-indole non-nucleoside reverse transcriptase inhibitor for the potential treatment of HIV infection.
PMID: 20112173
2010
Current opinion in investigational drugs (London, England
Abstract: Two pathways of resistance have been identified for IDX-899 in vitro that include Glu138Lys and Val90Ile/Tyr181Cys mutations.
Impact of human leukocyte antigen-B*51-restricted cytotoxic T-lymphocyte pressure on mutation patterns of nonnucleoside reverse transcriptase inhibitor resistance.
Abstract: Computational analysis indicated that I135T and E138K cooperatively extend the gap between the binding site of reverse transcriptase and NNRTI.
Abstract: RESULTS: E138K emerged during the cultural passages of HIV-1I135V, HIV-1I135T, and HIV-1I135R, but not during the passages of HIV-1WT.
Abstract: The HIV-1I135L/E138K and HIV-1I135R/<
Abstract: The combination of I135T, the most frequent escape mutation, and E138K (HIV-1I135T/E138K) conferred significant resistance to efavirenz, nevirapine, and etravirine.
In vitro resistance development for RO-0335, a novel diphenylether nonnucleoside reverse transcriptase inhibitor.
Abstract: Two pathways to loss of susceptibility to RO-0335 were observed, containing patterns of amino acid changes at either V106I/A plus F227C (with additional contributions from A98G, V108I, E138K, M230L and P236L) or V106I/Y188L (with a potential contribution from L100I, E138K and Y181C).
HIV mutation literature information.
PMID: 
2011
AIDS (London, England)
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