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 HIV mutation literature information.


  [Study of resistance using the TRUGENE HIV-1 genotyping system and analysis of agreement between rule-based algorithms and virtual phenotyping].
 PMID: 15757587       2005       Enfermedades infecciosas y microbiologia clinica
Abstract: For the IP: key mutations L90M (26.1%), M46I (18.1%) and V82AFTS (12.9%); and accessory mutations L63P (50.5%), A71V (27.2%), L10I (25.2%) and M36I (19.2%).


  Amprenavir or fosamprenavir plus ritonavir in HIV infection: pharmacology, efficacy and tolerability profile.
 PMID: 15748098       2005       Drugs
Abstract: When used with ritonavir, the accumulation of six or more mutations among L10F/I/V, K20M/R, E35D, R41K, I54V, L63P, V82A/F/T/S and I84V leads to clear decrease in viral response to treatment.


  Clinically relevant interpretation of genotype and relationship to plasma drug concentrations for resistance to saquinavir-ritonavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients.
 PMID: 15561845       2004       Antimicrobial agents and chemotherapy
Abstract: Adjusted in a multivariate analysis, taking into account all the confounding factors, such as the nucleoside used, five mutations were combined in a resistance score associated with a reduced virological response to an SQV-plus-RTV regimen: L24I, I62V, V82A/F/T/S, I84V, and L90IM.


  Impact of insertions in the HIV-1 p6 PTAPP region on the virological response to amprenavir.
 PMID: 15134184       2004       Antiviral therapy
Abstract: Insertions (P459Ins) within p6 protein, leading to partial or complete duplication of the PTAPP motif, were significantly associated with a decreased VR (P459Ins versus wild-type; -0.3 +/- 0.8 vs -1.1 +/- 1.2 log copies/ml, P=0.007) and were more frequent when the V82A/F/T/S PR mutation was present (P=0.020).


  Epidemiologic and molecular characterization of human immunodeficiency virus type 1 in southern Brazil.
 PMID: 14657764       2003       Journal of acquired immune deficiency syndromes (1999)
Abstract: The overall analysis of drug resistance mutations in viruses from treated subjects has highlighted some associations between subtypes and particular mutations, such as V82A/F/T/S in protease and subtype F1 and M41L and L210W in RT and subtype B.


  HIV-1 phenotypic susceptibility to lopinavir (LPV) and genotypic analysis in LPV/r-naive subjects with prior protease inhibitor experience.
 PMID: 12869832       2003       Journal of acquired immune deficiency syndromes (1999)
Abstract: Current PI therapy (P = 0.002) and indinavir administration (P < 0.001), >5 LPV/r mutations (P < 0.0012), and detection of L10FIRV, K20MR, M46IL, I54VL, A71VT, G73SA, V82AFTS, I84V, and M90L were associated with LPV resistance in univariate analysis.


  Improving lopinavir genotype algorithm through phenotype correlations: novel mutation patterns and amprenavir cross-resistance.
 PMID: 12700444       2003       AIDS (London, England)
Abstract: Several previously defined LPV mutations were found to have a stronger than average effect (e.g., M46I/L, I54V/T, V82A/F), and new variants at known positions (e.g., I54A/M/S, V82S) were identified.


  Genotypic inhibitory quotient as predictor of virological response to ritonavir-amprenavir in human immunodeficiency virus type 1 protease inhibitor-experienced patients.
 PMID: 12543665       2003       Antimicrobial agents and chemotherapy
Abstract: Baseline PI resistance mutations (L10F/I/V, K20M/R, E35D, R41K, I54V, L63P, V82A/F/T/S, I84V) identified by univariate analysis and included in a genotypic score and APV C(min) at week 8 were predictive of the virological response at week 12.


  Persistence of earlier HIV-1 drug resistance mutations at new treatment failure.
 PMID: 12376953       2002       Journal of medical virology
Abstract: In contrast, after changing from indinavir to saquinavir or nelfinavir, the M46I/L and/or V82A/F/ST disappeared in only 9 of 21 occasions at the new treatment failure.


  Combining mutations in HIV-1 protease to understand mechanisms of resistance.
 PMID: 12012342       2002       Proteins
Abstract: D30N/V82S mutant showed lower stability than either of the two individual mutations, which is possibly due to concerted changes in the central P2-P2' and S2-S2' sites.
Abstract: Four double mutants, K45I/L90M, K45I/V82S, D30N/V82S, and N88D/L90M were selected for analysis on the basis of observations of increased or decreased stability or enzymatic activity for the respective single mutants.
Abstract: Mutations D30N, K45I, and V82S showed altered interactions with inhibitor residues at P2/P2', P3/P3'/P4/P4', and P1/P1', respective



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