Method: Plasma samples contained a median of 3 [Q1-Q3: 2-4] Figure: FC resistance was evaluated based on the contribution of the number of RPV-associated mutations (L100I, K101E/P, E138A/G/K/Q/R, V179L, Y181C/I/V, Y188L, H221Y, F227C and M230I/L) per sample with and without K103N.
Discussion: Other studies have reported an association of RPV resistance with K103N combined with other NNRTI resistance mutations, especially L100I, in clinical samples.
Targeting the entrance channel of NNIBP: Discovery of diarylnicotinamide 1,4-disubstituted 1,2,3-triazoles as novel HIV-1 NNRTIs with high potency against wild-type and E138K mutant virus.
PMID: 29635166
2018
European journal of medicinal chemistry
Method: HIV-1 (IIIB, K103 N/Y181C (RES056), F227L/V106A, L100I, K103 N, E138K, Y181C, and Y188L) or HIV-2 (ROD) stock (50 muL at 100-300 CCID50) (50% cell culture infectious dose) or culture medium was added to either the infected or mock-infected wells of the microtiter tray.
Result: All six compounds showed same sensitivity order against the six mutant viruses as follows: Y188L (least sensitive to these compounds) < L100I < F227L + V106A < K103 N < Y181L < E138K (
"Discovery of Novel Diarylpyrimidine Derivatives as Potent HIV-1 NNRTIs Targeting the ""NNRTI Adjacent"" Binding Site."
Abstract: Especially, 20 showed marked antiviral activity, which was 1.5-fold greater against WT and 1.5- to 3-fold greater against L100I, K103N, Y181C, Y188L, and E138K when compared with ETV.
HIV Reverse Transcriptase and Protease Genes Variability Can Be a Biomarker Associated with HIV and Hepatitis B or C Coinfection.
Discussion: Patient 91_co (HIV/HCV) has the codons T12S, L19I, L74V, K103R, E122K, D123E, I135T, S163C, M184V, L214F, K219E, E224K, V245M, L100I, V106I, V179D and M230L and used the drugs 3TC, EFV and TDF for treatment.
Characterization of minority HIV-1 drug resistant variants in the United Kingdom following the verification of a deep sequencing-based HIV-1 genotyping and tropism assay.
Result: Most of the minority mutations in viruses from both groups of naive patients were observed in the RT, e.g., M41L, E44D, A62V, K65R, D67N, D67G, V75I, L100I, K103N, K103R, V188I, M184I, L210W, K219Q, Y318F, etc., although a number of minority mutations associated with resistance to PI (L10F, V11I, M46I/
Acquisition of tenofovir-susceptible, emtricitabine-resistant HIV despite high adherence to daily pre-exposure prophylaxis: a case report.
Abstract: The HIV genotype revealed Met184Val, Leu7
Result: Genotypic testing (GenoSure MG) for the HIV strain isolated from this patient showed notable RT mutations of L74V, L100I, M184V, and K103N, none of which are known to confer resistance to TDF, although M184V confers high-level resistance to FTC.
Result: SGS was consistent with the standard genotype in detecting RT mutations: specifically L74V, L100I, M184V, and K103N were detected, but K65R and K70E were not.
Long-term virological outcome in children receiving first-line antiretroviral therapy.
Result: K103N (48%), Y181C (37%), G190A/S (25%), Y188C/L (10%), V106M/A (8%), K65R (8%) and L100I (4%) were the major NNRTI DRMs observed in these 52 children.
HIV Drug Resistance Mutations in Non-B Subtypes After Prolonged Virological Failure on NNRTI-Based First-Line Regimens in Sub-Saharan Africa.
PMID: 28129253
2017
Journal of acquired immune deficiency syndromes (1999)
Result: After adjustment, participants on zidovudine at failure were more likely to have T215F, T215Y, M41L, K70R, D67N, L210W, type-1 thymidine analog, type-2 thymidine analog, and any thymidine analogue mutations (TAMs); those on tenofovir to have K65R, K70E, Y115F, and M184I; those on efavirenz to have K103N, P225H, Y188L, and L100I; and those on nevirapine to have Y181C and G190A.
Virological response, HIV-1 drug resistance mutations and genetic diversity among patients on first-line antiretroviral therapy in N'Djamena, Chad: findings from a cross-sectional study.
Abstract: Overall, 32% (37/116) patients presented >= one major drug resistant mutation(s), with 29% (34/116) to nucleos(t)ide reverse transcriptase inhibitors (67% [29/43] M184V/I, 30% [13/43] T215Y/F, 19% [8/43] V75A/F/I/L/M, 9% [4/43] K70P/R/W, 9% [4/43] K219E/N/Q and 5% [2/43] Result: Out of the 43 sequences generated, the most prevalent DRMs were: 30% [13/43] K103N/S/E, 26% [11/43] Y181C/V/F/L, 2% [1/43] L100I, 2% [1/43] F227L and 2% [1/43] P225H, followed by other DRMs observed at lower rates.
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.
HIV mutation literature information.
PMID: 
2018
Antiviral chemistry & chemotherapy
Browser Board
Co-occurred Entities
Filtrator
ViMRT