Deep sequencing analysis of HIV-1 reverse transcriptase at baseline and time of failure in patients receiving rilpivirine in the phase III studies ECHO and THRIVE.
Abstract: At failure, two patients without NNRTI RAMs by PS carried minority rilpivirine RAMs K101E and/or E138K; and five additional patients carried other minority NNRTI RAMs V90I, V106I, V179I, V189I, and Y188H.
Abstract: Linkage analysis showed that E138K and K101E were usually not observed on the same viral genome.
Contribution of APOBEC3G/F activity to the development of low-abundance drug-resistant human immunodeficiency virus type 1 variants.
PMID: 26482266
2016
Clinical microbiology and infection
Abstract: APOBEC3G/F-associated E138K, M184I and M230I appeared within clonal sequences containing in-frame STOP codons in 2/3 (66%), 5/5 (100%) and 4/4 (100%) of the samples.
Abstract: In a large pan-European case-control study investigating the clinical relevance of pre-existing DRMVs using 454 pyrosequencing, the six most prevalent plasma DRMVs detected corresponded to G-to-A nucleotide mutations (V90I, V106I, V108I, E138K, M184I and M230I).
Abstract: Mutations E138K, M184I and M230I co-occurred in the same sequence as APOBEC3G/F signatures in 3/9 (33%), 5/11 (
Sub-Epidemics Explain Localized High Prevalence of Reduced Susceptibility to Rilpivirine in Treatment-Naive HIV-1-Infected Patients: Subtype and Geographic Compartmentalization of Baseline Resistance Mutations.
PMID: 26651266
2016
AIDS research and human retroviruses
Method: Major RPV resistance-associated mutations (RPV-RAMs) were defined based on data from the clinical trials, phenotypic RPV resistance analyses, and package inserts: K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C, M230I/L, and the mutational combination of L100I+K103N.
Systematic review to determine the prevalence of transmitted drug resistance mutations to rilpivirine in HIV-infected treatment-naive persons.
Abstract: Pooled results from the Stanford database (n=52,680) correlated with these findings indicating a low prevalence of 8/9 rilpivirine mutations (<0.1%), except for E138A/G/K/Q/R (2.9%, 95% CI 1.8, 4.4).
Abstract: The prevalence of E138A/G/K/Q/R mutations is higher (0.7%) and varies according to geographical region and HIV subtype.
Abstract: Two mutations were mo
Clinical Outcomes of Virologically-Suppressed Patients with Pre-existing HIV-1 Drug Resistance Mutations Switching to Rilpivirine/Emtricitabine/Tenofovir Disoproxil Fumarate in the SPIRIT Study.
Abstract: Mutations potentially affecting RPV activity, including E138A/G/K/Q, Y181C, and H221Y, were detected in isolates from 11 patients by one or both assays.
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: 27070547
2016
Journal of medicinal chemistry
Abstract: Compounds 6a, 14c, and 14d showed high potency against the 1b-resistant E138K mutated viral strain as well as good balance between anti-HIV-1 activity and desirable druglike properties.
Abstract: From the perspective of optimizing future NNRTI compounds as clinical trial candidates, computational modeling results provided valuable information about how the R(1) group might provide greater efficacy against the E138K mutant.
Abstract: Three series (6, 13, and 14) of new diarylaniline (DAAN) analogues were designed, synthesized, and evaluated for anti-HIV potency, especially against the E138K viral strain with a major mutation conferring resistance to the new-generation non-nucleoside reverse transcriptase inhibitor drug rilpivirine (1b).
Introduction: On the other hand, lead 3b had high
Role of Rilpivirine and Etravirine in Efavirenz and Nevirapine-Based Regimens Failure in a Resource-Limited Country: A Cross- Sectional Study.
Introduction: According to the ECHO and THRIVE studies, E138K was the most frequently selected mutation (45%) detected in ARVnaive patients who have failed RPV therapy which is also often seen with M184I (34%), confering resistance to both lamivudine (3TC) and emtricitabine (FTC).
Method: RT-RAMs were identified and analyzed by using the Stanford Drug Resistance Database for V90I, A98G, L100I/V, K101E/P/Q/H/N, K103N/S/T/Q/E/H/R, V106A/M/I, V108I, E138A/K/Q/G/R, PMID: 27124362
2016
Journal of acquired immune deficiency syndromes (1999)
Result: DOR potently inhibited the replication of E40K, K101E, V111A, M184I, M184V, K101E/M184I, K101E/M184V, E138K/M184I, and E138K/M184V (all <3 nM).
Result: In addition, we selected HIV-1 RT mutations in cell culture with a closely related RPV analog (unpublished observations): E40K, D67E, V111A, E138K, Y181C, and PMID: 27130466
2016
Retrovirology
Figure: a K65R series, b L74V series, c K103N series, d E138K series, e M184I series, and f M184V series.
Figure: d E138K series including NL4.3E138K, NL4.3R263K-E138K, and NL4.3H51Y/R263K-E138K.
Discussion: Given that the R263K substitution has been reported in some INSTI-naive patients in the SAILING study and in tissue culture selections, we aimed to investigate the effects of R263K and its secondary mutation H51Y toge
Usefulness of an HIV DNA resistance genotypic test in patients who are candidates for a switch to the rilpivirine/emtricitabine/tenofovir disoproxil fumarate combination.
PMID: 27231280
2016
The Journal of antimicrobial chemotherapy
Abstract: Rilpivirine/emtricitabine/tenofovir disoproxil fumarate RAMs studied were K65R, L100I, K101E/P, E138A/G/K/R/Q, V179L, Y181C/I/V, M184V/I, Y188L, H221Y, F227C and M230I/L in the RT.
HIV mutation literature information.
PMID: 
2016
Journal of medical virology
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