literature

HIV mutation literature information.

Lack of impact of pre-existing T97A HIV-1 integrase mutation on integrase strand transfer inhibitor resistance and treatment outcome.

PMID: 28212411 2017 PloS one

Method: Primary INSTI RAMs against EVG and/or RAL were based on IAS-USA Guidelines of RAMs with some modifications to remove secondary INSTI RAMs (i.e., L74M, F121Y, E138A/K, and G140A/S) (Fig 1).

Prevalence of integrase inhibitor resistance mutations in Austrian patients recently diagnosed with HIV from 2008 to 2013.

PMID: 27530391 2017 Infection

Abstract: Two patients carried the accessory mutations E138K and G140A, respectively, where both lie on the Q148 pathway.

Recent trends and patterns in HIV-1 transmitted drug resistance in the United Kingdom.

PMID: 27476929 2017 HIV medicine

Method: In this report, the term 'transmitted drug resistance mutations' (TDRMs) is used to describe (a) for pol, the presence of one or more mutations from the World Health Organisation (WHO) 2009 surveillance list 19 with the addition of E138K, a mutation known to cause resistance to the second-generation nonnucleoside reverse transcriptase inhibitor (NNRTI) rilpivirine, and all changes at codon T215 as they are likely to be ancestrally related to T215F or Y mutations 20; (b) for integrase, the presence of mutations from the IAS-USA 2013 list or accessory mutations reported by the Stanford HIVdb algorithm v7.0 (HIV Drug Resistance Database, Stanford University, Stanford, CA).

Discovery of uracil-bearing DAPYs derivatives as novel HIV-1 NNRTIs via crystallographic overlay-based molecular hybridization.

PMID: 28254696 2017 European journal of medicinal chemistry

Abstract: Activity against the clinic prevalent mutant strains was also tested, suggesting that 16d was sensitive to E138K (EC50 = 34.2 nM).

Etravirine combined with antiretrovirals other than darunavir/ritonavir for HIV-1-infected, treatment-experienced adults: Week 48 results of a phase IV trial.

PMID: 28382208 2017 SAGE open medicine

Result: Other etravirine RAMs that each emerged in <5 VFs were V90I, E138G, E138K, and E138Q.

Drug-like property-driven optimization of 4-substituted 1,5-diarylanilines as potent HIV-1 non-nucleoside reverse transcriptase inhibitors against rilpivirine-resistant mutant virus.

PMID: 28465101 2017 Bioorganic & medicinal chemistry letters

Abstract: Newly synthesized p-cyanovinyl-DAANs (8a-8g) with different R1 side chains plus prior active p-cyanoethyl-DAANs (4a-4c) were evaluated not only for anti-HIV potency against both wild-type HIV virus and rilpivirine-resistant (E138K, E138K+M184I) viral replication, but also for multiple drug-like properties, including aqueous solubility, lipophilicity, and metabolic stability in human liver microsomes and human plasma.

Abstract: This study revealed that both ester and amide R1 substituents led to low nanomolar anti-HIV potency against wild-type and rilpivirine-resistant viral strains (E138K-resistance fold changes<3).

Introduction: Furthermore, these same DAANs also inhibited the E138K+M184I viral strain with resistance FCs ranging from 1.4 to 6.3, better than or sim

HIV-1 strains belonging to large phylogenetic clusters show accelerated escape from integrase inhibitors in cell culture compared with viral isolates from singleton/small clusters.

PMID: 28472323 2017 The Journal of antimicrobial chemotherapy

Discussion: The emergence of select mutations under dolutegravir pressure, including R263K (AGA AAA or AGG AAG), G163R (GGA AGA or GGG AGG) and E138K (GAA AAA, GAG AAG), may be related to APOBEC-mediated G A hypermutation.

Structure-Based Optimization of Thiophene[3,2-d]pyrimidine Derivatives as Potent HIV-1 Non-nucleoside Reverse Transcriptase Inhibitors with Improved Potency against Resistance-Associated Variants.

PMID: 28481112 2017 Journal of medicinal chemistry

Abstract: Compound 25a was exceptionally potent against the whole viral panel, affording 3-4-fold enhancement of in vitro antiviral potency against WT, L100I, K103N, Y181C, Y188L, E138K, and K103N+Y181C and 10-fold enhancement against F227L+V106A relative to the reference drug etravirine (ETV) in the same cellular assay.

Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.

PMID: 29137637 2017 Virology journal

Method: Major INSTI resistance mutations (T66I, E92Q, F121Y, Y143CHR, S147G, Q148HKR, N155H) that confer substantial phenotypic resistance to at least one of the currently approved INSTI as well as minor INSTI resistance mutations (T66AK, L74 M, E92G, T97A, E138AK, G140AS, R263K) that increase INSTI resistance and/or viral

M184I/V substitutions and E138K/M184I/V double substitutions in HIV reverse transcriptase do not significantly affect the antiviral activity of EFdA.

PMID: 28961903 2017 The Journal of antimicrobial chemotherapy

Abstract: CONCLUSIONS: These findings help to alleviate concern that EFdA may not be active against viruses that contain both the M184I/V and E138K substitutions in RT.

Abstract: In other clinical trials that evaluated rilpivirine together with emtricitabine in first-line therapy, the emergence of both the M184I/V and E138K mutations in RT was demonstrated.

Abstract: METHODS: Recombinant viruses containing the M184I/V and/or E138K substitutions were generated by site-directed mutagenesis and evaluated in tissue culture for susceptibility to various nucleoside compounds, including EFdA.

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