literature

HIV mutation literature information.

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.

PMID: 26761642 2016 Antiviral therapy

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: Rilpivirine mutations assessed were: L100I, K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L.

Abstract: The prevalence of E138A/G/K/Q/R mutations is higher (0.7%) and varies according to geographical region and HIV subtype.

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.

PMID: 26899540 2016 HIV clinical trials

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.

Novel HIV-1 Non-nucleoside Reverse Transcriptase Inhibitor Agents: Optimization of Diarylanilines with High Potency against Wild-Type and Rilpivirine-Resistant E138K Mutant Virus.

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).

Role of Rilpivirine and Etravirine in Efavirenz and Nevirapine-Based Regimens Failure in a Resource-Limited Country: A Cross- Sectional Study.

PMID: 27120449 2016 PloS one

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)

Discussion: Although DOR apparently did not select for the E138K mutation in cell culture, we found that this mutation did reduce the susceptibility of HIV-1 to DOR by about 20-fold.

Discussion: Although the E138 residue does not make any direct contacts with DOR, the binding of DOR within the pocket caused the position of this residue to shift substantially, which could prevent the interaction between E138K of the p51 subunit and K101 of the p66 subunit.

Discussion: As has already been reported, the E138K mutation does not cause a significant reduction in susceptibility to RPV in cell culture assays (including ours).

Effect on HIV-1 viral replication capacity of DTG-resistance mutations in NRTI/NNRTI resistant viruses.

PMID: 27130466 2016 Retrovirology

Result: 3a, b, f), or undetectable levels in H51Y/R263K-K103N, H51Y/R263K-E138K and H51Y/R263K-M184I viruses.

Result: In viruses carrying K65R, E138K, or M184V, the additional presence of R263K in IN coding sequence caused a further impact on viral replication than was associated with any of these RT mutations on their own.

Result: Our results show that the addition of R263K to the K65R-,

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.

Rilpivirine as a Treatment for HIV-infected Antiretroviral-naive Adolescents: Week 48 Safety, Efficacy, Virology and Pharmacokinetics.

PMID: 27294305 2016 The Pediatric infectious disease journal

Abstract: Eight patients experienced virologic failure, including 5 who developed rilpivirine resistance-associated mutations, mostly E138K, K101E and M230L.

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