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 HIV mutation literature information.


  In vitro resistance selections using elvitegravir, raltegravir, and two metabolites of elvitegravir M1 and M4.
 PMID: 22197635       2012       Antiviral research
Abstract: Additional resistance selection experiments using elvitegravir led to the development of previously reported integrase inhibitor resistance mutations (T66I, F121Y, and S153Y) as well as a novel R263K integrase mutation.


  Subtype diversity associated with the development of HIV-1 resistance to integrase inhibitors.
 PMID: 21360548       2011       Journal of medical virology
Abstract: Of note, the remaining patients on RAL regimens for 14 +- 3 months harbored no or only minor integrase mutations/polymorphisms (T66I, T97A, H114P, S119P, A124S, G163R, I203M, R263K).


  The HIV-1 integrase mutations Y143C/R are an alternative pathway for resistance to Raltegravir and impact the enzyme functions.
 PMID: 20436677       2010       PloS one
Introduction: In vitro, several mutations have been introduced into the IN gene and activities of mutants have been determined (T66I, L74M, E92Q, F121Y, Q148K, S153Y, N155H).


  Evaluation of HIV-1 integrase inhibitors on human primary macrophages using a luciferase-based single-cycle phenotypic assay.
 PMID: 20558207       2010       Journal of virological methods
Abstract: IN inhibitors were also tested using a lentiviral vector containing an IN with introduced T66I/S153Y mutations, known to affect the activity of azido-group-containing diketo acid (DKA) IN inhibitors.


  Physical trapping of HIV-1 synaptic complex by different structural classes of integrase strand transfer inhibitors.
 PMID: 20799722       2010       Biochemistry
Introduction: In the patients enrolled for elvitegravir (EVG) studies, T66I, E92Q, Q148R and N155H mutations are primary contributors to EVG resistance.


  Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.
 PMID: 19918099       2009       Antiviral therapy
Introduction: Elvitegravir, which remains in the final stages of clinical development, is additionally associated with T66I and E92Q in primary resistance.
Result: Of the 38 major and minor integrase inhibitor resistance associated codons, 44, 61, 66, 92, 121, 140, 143, 147, 148, 155, 226 and 263 were the only positions absolutely conserved across all 342 sequences and these included six primary resistance-associated mutations for raltegravir and elvitegravir (T66I, E92Q, G140S, Y143C/H/R Q148H/R/K and N155S/H).
Discussion: In this population-based review of all sites associated with integrase inhibitor


  Characterization and structural analysis of HIV-1 integrase conservation.
 PMID: 19290031       2009       AIDS reviews
Abstract: All primary signature mutations emerging in patients failing raltegravir (Y143R, Q148H/K/R, N155H) or elvitegravir (T66I, E92Q, S147G, Q148H/K/R, N155H), as well as secondary mutations (H51Y, T66A/K, E138K, G140S/A/C, Y143C/H, K160N, R166S, E170A, S230R, D232N, R263K) were complete


  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: 19178153       2009       Biochemistry
Abstract: T66I/M154I exhibited little if any time-dependent inhibition by any of the six INIs, as measured by differences in potency upon preincubation or by progress curve analysis.


  Defining the DNA substrate binding sites on HIV-1 integrase.
 PMID: 19014951       2009       Journal of molecular biology
Discussion: Changes at position 230 are reported to appear in conjunction with T66I and M74L substitutions in cells.
Discussion: We have not analyzed substitutions at position 66 in vitro, but Lee and Robinson reported that the T66I substitution caused a small decrease in 3' processing.


  Natural variation of HIV-1 group M integrase: implications for a new class of antiretroviral inhibitors.
 PMID: 18687142       2008       Retrovirology
Result: Among the CCD mutations shown to directly reduce raltegravir or elvitegravir susceptibility - H51Y, T66I, E92Q, F121Y, G140S, Y143C/H/R, Q146P, S147G, Q148H/R/K, S153Y, N155H/S, and E157Q - only positions 153 and 157 are polymorphic (prevalence >= 0.5%) with S153A and E157Q each present in 1% of sequences (Figures 1).
Discussion: Nearly all INI-resistance mutations known to directly reduce HIV-1 susceptibility were nonpolymorphic i



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