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 HIV mutation literature information.


  The Combination of the R263K and T66I Resistance Substitutions in HIV-1 Integrase Is Incompatible with High-Level Viral Replication and the Development of High-Level Drug Resistance.
 PMID: 26311878       2015       Journal of virology
Abstract: HIV drug-resistant mutations in integrase that can arise in individuals treated with elvitegravir commonly include the T66I substitution, whereas R263K is a signature resistance substitution against dolutegravir.
Abstract: In order to determine how different combinations of integrase resistance mutations can influence the outcome of therapy, we report here the effects of the T66I, E138K, and R263K substitutions, alone and in combination, on viral replicative capacity and resistance to integrase inhibitors.
Abstract: Our observations support the use of DTG in second-line therapy for individuals who experience treatment failure with EVG due to the T66I substitutio


  Integrase inhibitor (INI) genotypic resistance in treatment-naive and raltegravir-experienced patients infected with diverse HIV-1 clades.
 PMID: 26311843       2015       The Journal of antimicrobial chemotherapy
Method: Major RAMs comprised T66A/I/K, E92Q/G/V, F121Y, G140S/A/C, Y143H/R/C/K, S147G, Q148H/R/K and N155H/S/T.


  Resistance against Integrase Strand Transfer Inhibitors and Relevance to HIV Persistence.
 PMID: 26198244       2015       Viruses
Introduction: Under such circumstances, extensive genotypic characterisation of resistant strains from two large clinical studies, i.e., Studies 102 and 103, revealed the emergence of the T66I, E92Q, T97A, Q148R and N155H resistance mutations in integrase, mostly in combination with the M184I/V substitutions in RT.
Table: T66T/I


  [Resistance profile and genetic barrier of dolutegravir].
 PMID: 25858608       2015       Enfermedades infecciosas y microbiologia clinica
Abstract: Dolutegravir displays in vitro activity against mutant HIV-1 harboring any isolated resistance mutations selected during failures to raltegravir or elvitegravir (Y143C/H/, N155H, Q148H/K/R, E92G/Q, T66A/I/K, T97A, E138A/K, G140A/S).


  Lack of resistance to integrase inhibitors among antiretroviral-naive subjects with primary HIV-1 infection, 2007-2013.
 PMID: 24831260       2015       Antiviral therapy
4Method: Sequences were assembled with Sequencher (version 4.9; Gene Codes Corp, Ann Arbor, Ml) and submitted to the Stanford University HIV Drug Resistance Database (version 6.3.0; http://hivdb.stanford.edu on August 21, 2013) to identify ""major"" INSTI mutations (T66I, E92Q, G140S, Y143C/H/R, S147G, Abstract: Consensus sequencing identified no subjects with major INSTI mutations (T66I, E92Q, G140S, Y143C/H/R, S147G, Q148H/K/R, N155H).


  Week 144 resistance analysis of elvitegravir/cobicistat/emtricitabine/tenofovir DF versus efavirenz/emtricitabine/tenofovir DF in antiretroviral-naive patients.
 PMID: 25321623       2015       Antiviral therapy
Abstract: Emergent substitutions were E92Q (n=7), N155H (n=3), Q148R (n=1) and T66I (n=1) in IN, and M184V/I (n=10) and K65R (n=4) in RT.


  HIV-1 group O integrase displays lower susceptibility to raltegravir and has a different mutational pathway for resistance than HIV-1 group M.
 PMID: 25397483       2014       Journal of the International AIDS Society
Abstract: Mutations selected in HIV-O can be classified as follows: (1) mutations described for HIV-M such as T97A, Q148R, V151A/I (RAL), T66I, E92Q, E157Q (EVG) and M50I, R263K (DTG) and (2) signature mutations for HIV-O.


  Resistance to HIV integrase strand transfer inhibitors among clinical specimens in the United States, 2009-2012.
 PMID: 24145878       2014       Clinical infectious diseases
Abstract: Major integrase mutations included T66AIK, E92QV, F121Y, Y143CHR, S147G, Q148HKR, and N155H; multiple accessory mutations were also assessed.


  Week 144 resistance analysis of elvitegravir/cobicistat/emtricitabine/tenofovir DF versus atazanavir+ritonavir+emtricitabine/tenofovir DF in antiretroviral-naive patients.
 PMID: 25350960       2014       HIV clinical trials
Abstract: Emergent substitutions were E92Q, N155H, or Q148R (n = 2 each) and T66I or T97A (n = 1 each) in IN and M184V/I (n = 7) and K65R (n = 1) in RT.


  Impact of primary elvitegravir resistance-associated mutations in HIV-1 integrase on drug susceptibility and viral replication fitness.
 PMID: 23529738       2013       Antimicrobial agents and chemotherapy
Abstract: Primary INSTI resistance-associated mutations (RAMs) at six IN positions have been identified in HIV-1-infected patients failing EVG-containing regimens in clinical studies: T66I/A/K, E92Q/G, T97A, S147G, Q148R/H/K, and N155H.
Abstract: Recombinant viruses containing the six most common mutations exhibited a range of reduced EVG susceptibility: 92-fold for Q148R, 30-fold for N155H, 26-fold for E92Q, 10-fold for T66I, 4-fold for S147G, and 2-fold for



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