Abstract: CONCLUSION: These results demonstrate that ETR and RPV are likely to select for E138K as a major resistance mutation if no or very few other resistance mutations are present and that Y181C may be antagonistic to E138K.
Abstract: However, subtype B viruses containing Y181C generated V179I/F or A62V/A but not E138K following exposure to ETR or RPV, respectively, whereas subtype C viruses containing Y181C developed E138V together with Y188H and V179I under ETR pressure.
Abstract: RESULTS: In wild-type viruses and viruses containing K103N alone at
Prevalence of pre-existing resistance-associated mutations to rilpivirine, emtricitabine and tenofovir in antiretroviral-naive patients infected with B and non-B subtype HIV-1 viruses.
PMID: 23361642
2013
The Journal of antimicrobial chemotherapy
Abstract: Primary rilpivirine RAMs were infrequent (4.6%, n=79) and the most prevalent were E138A (3%, n=52), E138K, (0.3%, n=5), H221Y (0.3%, n=5), E138G (0.2%, n=4) and Y181C (0.2%, n=4).
Abstract: We studied the primary rilpivirine RAMs (K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, H221Y, F227C and M230I/L) and other potential rilpivirine-associated mutations (V90I, L100I, K101T, E138S
Prevalence of primary resistance mutations to integrase inhibitors in treatment-naive and -experienced patients infected with B and non-B HIV-1 variants.
Abstract: According to the geno2pheno algorithm, some of the secondary mutations detected (L74V, E138K, G163RS, and V151I) have been associated with a reduced estimated susceptibility to RAL and only the E138K mutation has been associated with a decreased estimated susceptibility to EGV.
Combination therapies, effectiveness, and adherence in patients with HIV infection: clinical utility of a single tablet of emtricitabine, rilpivirine, and tenofovir.
Abstract: E138K is the most important mutation associated with resistance against rilpivirine and its development must be avoided whenever possible, because this mutation confers broad cross-resistance against all approved members of the non-nucleoside reverse transcriptase inhibitor family of drugs.
Conclusion: Also of concern is that the patients who developed resistant viruses in the ECHO and THRIVE studies commonly had mutations at both the E138K and M184I positions in the HIV reverse transcriptase gene, leading to dual resistance against both rilpivirine and emtricitabine.
Conclusion: The fact that E138K causes cross-resistance among all currently approved members of the non-NRTI family of drugs, including rilpivirine, etravirin
Human APOBEC3G-mediated hypermutation is associated with antiretroviral therapy failure in HIV-1 subtype C-infected individuals.
PMID: 23443042
2013
Journal of the International AIDS Society
Result: In two proviral sequences only, the E138K<
Table: E138K
Discussion: Also, one study has reported the co-presence of M184I and E138K in 24% of hypermutated sequences of treated patients.
Discussion: However, random polymorphisms of E138K/A were observed in the proviral DNA of both therapy-naive and experienced patients.
Discussion: In contrast, co-evolution of M184I and E138K was not found in our hypermutated sequences.
Discussion: Thus, due to a suboptimal anti-APOBEC3G activity of HIV-1 Vif mutants, the HIV drug resistance mutations M184I and E138K may be induced in vitro without any drug exposure.
Effect of mutations at position E138 in HIV-1 reverse transcriptase and their interactions with the M184I mutation on defining patterns of resistance to nonnucleoside reverse transcriptase inhibitors rilpivirine and etravirine.
PMID: 23612196
2013
Antimicrobial agents and chemotherapy
Abstract: Each of the E138A/G/K/Q/R mutations, alone or in combination with M184I, resulted in decreased susceptibility to RPV and etravirine (ETR).
Abstract: Impacts of mutations at position E138 (A/G/K/Q/R/V) alone or in combination with M184I in HIV-1 reverse transcriptase (RT) were investigated.
Abstract: The E138K/Q/R mutations can compensate for M184I in regard to both enzymatic fitness and viral replication capacity.
Abstract: The favored emergence of E138K over other mutations at position E138, together with M184I, is not due to an advantage in either
96-Week resistance analyses of rilpivirine in treatment-naive, HIV-1-infected adults from the ECHO and THRIVE Phase III trials.
Abstract: E138G/A/K conferred 5.1-, 7.1-, and 2.7-fold resistance to rilpivirine, respectively.
Abstract: E138G/A/K in human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) are rilpivirine resistance-associated mutations and can be identified in a few ART-naive patients, although at low frequency.
Abstract: CONCLUSIONS: E138G/A/K can be selected by HLA-B*18-restricted CTLs and confer significant rilpivirine resistance.
Abstract: Here we tested whether E138G/A/K could be selected by HLA-B*18-restricted CTLs.
Abstract: RESULTS: The prevalence of E138G/A/K was 21% and 0.37% in 19 and 1088 patients with and without HLA-B*18, respectively (odds ratio,
Trends in Genotypic HIV-1 Antiretroviral Resistance between 2006 and 2012 in South African Patients Receiving First- and Second-Line Antiretroviral Treatment Regimens.
Method: The following non-polymorphic ARV-selected mutations were classified as drug resistance mutations (DRM): (i) the NRTI resistance mutations M41L, A62V, K65RN, D67NG, T69D, T69 insertions, T69 deletion, K70REGQ, L74VI, V75MT, F77L, Y115F, F116Y, Q151M, M184VI, L210W, T215YFSDCIV, and K219QENR; (ii) the
Molecular Hybridization-Inspired Optimization of Diarylbenzopyrimidines as HIV-1 Nonnucleoside Reverse Transcriptase Inhibitors with Improved Activity against K103N and E138K Mutants and Pharmacokinetic Profiles.
PMID: 23856772
2013
Antimicrobial agents and chemotherapy
Abstract: E138K, a G A mutation in HIV-1 reverse transcriptase (RT), is preferentially selected by etravirine (ETR) and rilpivirine over other substitutions at position E138 that offer greater drug resistance.
Abstract: E138K, as well as E138G, consistently emerged first during ETR selection experiments, followed by E138A and E138Q; E138R was never selected.
Abstract: Surprisingly, E138K was identified as a tiny minority in 23% of drug-naive subtype B patients, a result confirmed by ultradeep sequencing (UDS).
Abstract: This result could reflect a low fitness cost of E138K; however, E138K
HIV mutation literature information.
PMID: 
2013
AIDS (London, England)
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