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 HIV mutation literature information.


  Resistance against Integrase Strand Transfer Inhibitors and Relevance to HIV Persistence.
 PMID: 26198244       2015       Viruses
Table: Q148H


  Combination of two pathways involved in raltegravir resistance confers dolutegravir resistance.
 PMID: 26205139       2015       The Journal of antimicrobial chemotherapy
Abstract: CONCLUSIONS: Combination of N155H, G140S and Q148H mutations originating from two distinct resistance pathways to raltegravir or elvitegravir led to a high level of dolutegravir resistance.
Abstract: RESULTS: Our data showed that the combination of N155H, G140S and Q148H mutations led to strong resistance to dolutegravir.


  Discordant predictions of residual activity could impact dolutegravir prescription upon raltegravir failure.
 PMID: 26305833       2015       Journal of clinical virology
Abstract: A total of 141 unique mutational patterns were observed, with N155H (25.4%), Q148H (16.2%) and Y143R (8.3%) the most prevalent signature mutations.


  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
Abstract: Among raltegravir recipients with viraemia (median 3523 HIV-1 RNA copies/mL), 113/255 (44.3%) had one or more major INI RAMs, most commonly N155H (45/255, 17.6%), Q148H/R/K + G140S/A (35/255, 13.7%) and Y143R/C/H (12/255, 4.7%).
Abstract: Comparing subtype B with non-B clades, Q148H/R/K occurred in 42/209 (20.1%) versus 2/46 (4.3%) subjects (P = 0.009) and G140S/A occurred in 36/209 (17.2%) versus 1/46 (2.2%) subjects (P = 0.005).
Abstract: Reduced occurrence of Q148H/R/K + G140S/A was seen in non-B clades versus subtype B, and was explained by the higher genetic barrier to the


  Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
 PMID: 26626277       2015       Journal of translational medicine
Abstract: Neither major resistance-associated IN mutations (T66I/A/K, E92Q/G, T97A, Y143HCR, S147G, Q148H/R/K, and N155H) nor silent mutations known to change the genetic barrier were observed.
Discussion: This includes T66IAK, E92Q, F121Y, G140SA, Y143HCR, Q146P, S147G, Q148KHR, and N155HS; (2) minor


  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.


  HIV-1-infected patients with advanced disease failing a raltegravir-containing salvage regimen in Sao Paulo, Brazil.
 PMID: 24359837       2014       International journal of antimicrobial agents
Abstract: At failure, major RAL resistance mutations included Q148H/R/K (21/47; 45%), N155H (14/47; 30%), Y143R/H/C (3/47; 6%) and E92Q (1/47; 2%).
Abstract: Most samples with Q148H/R/K also showed G140S/A/C (21/47; 45%).


  Bicyclic 1-hydroxy-2-oxo-1,2-dihydropyridine-3-carboxamide-containing HIV-1 integrase inhibitors having high antiviral potency against cells harboring raltegravir-resistant integrase mutants.
 PMID: 24471816       2014       Journal of medicinal chemistry
Abstract: Importantly, some of these new inhibitors retain greater antiviral efficacy compared to that of RAL when tested against a panel of IN mutants that included Y143R, N155H, G140S/Q148H, G118R, and E138K/Q148K.
Conclusion: Several compounds have selectivity indices of greater than 20,000, and certain of these inhibitors have greater antiviral efficacies than RAL against a panel of IN mutants that included Y143R, N155H, G118R, and the double mutants G140S/Q148H and E1


  Comparison of illumina and 454 deep sequencing in participants failing raltegravir-based antiretroviral therapy.
 PMID: 24603872       2014       PloS one
Method: Patients with more than one darunavir resistance-associated mutation or with known major integrase resistance-associated mutations (N155H, Q148H/R/K, Y143C/R, and G140S) were excluded from the study.


  Preclinical profile of BI 224436, a novel HIV-1 non-catalytic-site integrase inhibitor.
 PMID: 24663024       2014       Antimicrobial agents and chemotherapy
Abstract: BI 224436 also retains full antiviral activity against recombinant viruses encoding INSTI resistance substitutions N155S, Q148H, and E92Q.



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