Result: For example, M41L and D67N had 16 (D218E, E44A, G190S, G196E, H221Y, I142V, K101E, L210W, L228R, L74V, M184V, R211K, T215F, V108I, V118I, and V179I) and nine (E44A, H208Y, H221Y, K70R, L210W
HIV-1 drug-resistant mutations and related risk factors among HIV-1-positive individuals experiencing treatment failure in Hebei Province, China.
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)
Discussion: To our knowledge, the differences we found in the other NNRTI DRMs, K101E (rilpivirine and etravirine resistance), Y181C (resistance to all NNRTIs), V108I (efavirenz and nevirapine resistance), and P225H (efavirenz resistance) have not been reported previously.
High level of HIV-1 drug resistance mutations in patients with unsuppressed viral loads in rural northern South Africa.
Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
Abstract: Fourteen major mutations of codon 99-191 on the RT gene were selected (K103N, V106A/M, V108I, Q151M, Y181C/I, M184V/I, Y188C/L/H, and G190S/A) at a cost of testing of 35 USD.
Abstract: The prevalence of each HIVDR mutation were K103N 6.0%, V106I 1.1%, V108I 0.4%, Y181C 2.3%, Y181I 0.7%, Y181V 0.4%, M184V 3.0%, M184I 1.5%, and PMID: 26651266
2016
AIDS research and human retroviruses
Method: In addition, we defined a list of minor RPV-RAMs that have been observed in in vitro or in vivo selection studies and are included in one or more of clinically widely used genotypic resistance interpretation algorithms ANRS (V24), Rega (V9.1.0), and HIVdb (V7.0.1), encompassing V90I, A98G, L100I/V, K101H/Q/T, K103R/S, V106A/I, V108I, E138S, V179D/E/F/I/T, Y181F/G/S, Y188F, V189I, G190A/C/E/Q/S/T/V, and M230V
Discovery, characterization, and lead optimization of 7-azaindole non-nucleoside HIV-1 reverse transcriptase inhibitors.
Introduction: Both drugs selected for mutations on RT, as the V108I mutant emerged after 69 weeks of treatment with 8 and E138K arose after 39 weeks of treatment with 9 (Supp.
Introduction: However, none of the compounds inhibited the V108I mutant selected by 8, indicating that there may be conserved binding features among all three molecules that are disrupted by this mutation.
Introduction: It did demonstrate some potency against the Y181C RT mutant in the cell-free assay (IC50 = 6.69 muM, data not shown), but was inactive against the K103N, V108I, and E138 K forms of the enzyme.
Introduction: The three most active compounds against wild type