literature

HIV mutation literature information.

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).

Role of the K101E substitution in HIV-1 reverse transcriptase in resistance to rilpivirine and other nonnucleoside reverse transcriptase inhibitors.

PMID: 24002090 2013 Antimicrobial agents and chemotherapy

Abstract: Previous biochemical and virological studies have shown that compensatory interactions between substitutions E138K and M184I can restore enzyme processivity and the viral replication capacity.

Abstract: Recombinant RT enzymes and viruses containing K101E, but not E138K, were highly resistant to nevirapine (NVP) and delavirdine (DLV) as well as ETR and RPV, but not EFV.

Abstract: Resistance to the recently approved nonnucleoside reverse transcriptase inhibitor (NNRTI) rilpivirine (RPV) commonly involves substitutions at positions E138K and K101E in HIV-1 reverse transcriptase (RT), t

Biochemical analysis of the role of G118R-linked dolutegravir drug resistance substitutions in HIV-1 integrase.

PMID: 24080645 2013 Antimicrobial agents and chemotherapy

Abstract: Homology modeling provided insight into the mechanism of resistance conferred by G118R as well as the effects of H51Y or E138K on enzyme activity.

Abstract: Now, we have characterized the impact of the G118R substitution, alone or in combination with either H51Y or E138K, on 3' processing and integrase strand transfer activity.

Abstract: The addition of H51Y and E138K to G118R partially restored strand trans

[Resistance profile of rilpivirine].

PMID: 24252532 2013 Enfermedades infecciosas y microbiologia clinica

Abstract: In vitro studies and phase III clinical trials have allowed the identification of 16 mutations associated with resistance to RPV K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L.

Abstract: The most common resistance mutation that emerges in this setting is E138K.

PMID: 21997204 2012 Journal of acquired immune deficiency syndromes (1999)

Abstract: Addition of M184I, but not M184V, to E138K, further decreased susceptibility to RPV and maintained FTC resistance.

Abstract: BACKGROUND: The registrational phase III clinical trials of the nonnucleoside reverse transcriptase (RT) inhibitor (NNRTI) rilpivirine (RPV) in combination with two nucleoside/nucleotide RT inhibitors (NRTIs) found a unique genotypic resistance pattern involving the NNRTI mutation E138K with the NRTI mutation M184I.

Abstract: CONCLUSIONS: The higher frequency of E138K and

PMID: 22067667 2012 Journal of acquired immune deficiency syndromes (1999)

Abstract: The absolute number of VFs with treatment-emergent NNRTI resistance-associated mutations (RAMs) was higher for rilpivirine (most commonly E138K or K101E) than efavirenz (most commonly K103N), but relative proportions were similar [63% (39 of 62) vs.

Abstract: The frequent emergence of E138K, especially in combination with M184I, in rilpivirine VFs is a unique finding of these trials.

Prevalence of TMC278 (rilpivirine) associated mutations in the Frankfurt Resistance Database.

PMID: 22209291 2012 Journal of clinical virology

Abstract: OBJECTIVE: Objective of our investigation was to determine the prevalence of mutations E138K, Y181I/V, and K101E/P before the approval of rilpivirine.

Abstract: RESULTS: The E138K, Y181I/V, and the K101E mutations were found in 0.4%, 0.9%, and 2.4% of the patients, respectively.

BF integrase genes of HIV-1 circulating in Sao Paulo, Brazil, with a recurrent recombination region.

PMID: 22485165 2012 PloS one

Result: Other B resistance-associated mutations were L74M (0.8%), T97A (1.6%), E138K (0.8%), M154I (3.9%), M154L (0.8%), E157K (2.3%), G163R (3.1%), and I203M (3.1%).

PMID: 22623801 2012 Journal of virology

Abstract: M184I/V and E138K are signature mutations of clinical relevance in HIV-1 reverse transcriptase (RT) for the nucleoside reverse transcriptase inhibitors (NRTIs) lamivudine (3TC) and emtricitabine (FTC) and the second-generation (new) nonnucleoside reverse transcriptase inhibitor (NNRTI) rilpivirine (RPV), respectively, and the E138K mutation has also been shown to be selected by etravirine in cell culture.

Abstract: The E138K mutation was recently shown to compensate for the low enzyme processivity and viral fitness associated with the M184I/V mutations through enhanced deoxyn

PMID: 22695298 2012 AIDS (London, England)

Abstract: Additionally, analysis of 601 patients PBMCs sequences revealed that the copresence of mutations E138K and M184I were never detected in nonhypermutated sequences, whereas these mutations were found at a high frequency (24%) in the context of APOBEC3 editing and in the absence of exposure to etravirine-rilpivirine.

Abstract: BACKGROUND: Recent clinical trials with rilpivirine combined with emtricitabine and tenofovir revealed that patients failing treatment, frequently, harbored viruses encoding resistance-associated mutations in the HIV-1 reverse transcriptase at position E138K and M184I.

Abstract: CONCLUSION: We demonstrate using in-vitro experiments and analyzing patients PBMCs sequences that M184I and E138K resistance-associat

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