HIV mutation literature information.


  Brazilian Network for HIV Drug Resistance Surveillance (HIV-BResNet): a survey of chronically infected individuals.
 PMID: 12700457       2003       AIDS (London, England)
Abstract: Accessory mutations were found in the PR gene at the following positions: L63P/V/T/A/I [153/345 (44.3%)], M36I/L [149/345 (43.2%)], L10I/F/V [82/345 (23.8%)], V77I [60/345 (17.4%)], A71V/T [11/345 (3.2%)], K20M/R [10/345 (2.9%)], and V82I [4/345 (1.2%)].


  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.


  A potent human immunodeficiency virus type 1 protease inhibitor, UIC-94003 (TMC-126), and selection of a novel (A28S) mutation in the protease active site.
 PMID: 11773409       2002       Journal of virology
Abstract: Upon selection of HIV-1 in the presence of UIC-94003, mutants carrying a novel active-site mutation, A28S, in the presence of L10F, M46I, I50V, A71V, and N88D appeared.


  Amprenavir-resistant HIV-1 exhibits lopinavir cross-resistance and reduced replication capacity.
 PMID: 11953467       2002       AIDS (London, England)
Abstract: Certain amprenavir-selected mutants conferred greater than 10-fold cross-resistance to lopinavir, including PrL10F/M46I/I50V-GagL449F (19-fold) and PrL10F/M46I/I47V/I50V-GagL449F (31-fold).
Abstract: Moreover, one isolate with only two mutations in the protease (L10F/84V) and GagL449F displayed a 7.7-fold increase in lopinavir IC50.
Abstract: The order of relative replication capacity was wild-type > L10F > L10F/<


  Low prevalence of primary mutations associated with drug resistance in antiviral-naive patients at therapy initiation.
 PMID: 11873006       2002       AIDS (London, England)
Abstract: Primary mutations associated with substantial resistance to protease inhibitors were found in only five of 347 patients (1.4%) (M46V/L, I54V, V82A/I); all the other patients carried only secondary mutations (L10F/I/V, M36I, L63P, A71T/V, V77I).


  Identification of genotypic changes in human immunodeficiency virus protease that correlate with reduced susceptibility to the protease inhibitor lopinavir among viral isolates from protease inhibitor-experienced patients.
 PMID: 11462018       2001       Journal of virology
Abstract: Two statistical tests showed that specific mutations at 11 amino acid positions in protease (L10F/I/R/V, K20M/R, L24I, M46I/L, F53L, I54L/T/V, L63P, A71I/L/T/V, V82A/F/T, I84V, and L90M) were associated with reduced susceptibility.


  Absence of zidovudine resistance in antiretroviral-naive patients following zidovudine/lamivudine/protease inhibitor combination therapy: virological evaluation of the AVANTI 2 and AVANTI 3 studies.
 PMID: 10894284       2000       AIDS (London, England)
Abstract: There was a high frequency (4 of 11) of the protease L10F substitution in ZDV/3TC/IDV-treated patients that was associated with virological failure but did not result in phenotypic resistance to any of the PIs tested.


  In vitro selection and characterization of VX-478 resistant HIV-1 variants.
 PMID: 9561202       1998       Advances in experimental medicine and biology
Abstract: By direct PCR analysis of selected viruses, a number of mutations were identified (L10F, M46I, I47V, I50V and I84V) in the protease gene.


  In vitro selection and characterization of human immunodeficiency virus type 1 variants with increased resistance to ABT-378, a novel protease inhibitor.
 PMID: 9696850       1998       Journal of virology
Abstract: Selection of viral variants with increasing concentrations of ABT-378 revealed a sequential appearance of mutations in the protease gene: I84V-L10F-M46I-T91S-V32I-I47V.


  A mutation in human immunodeficiency virus type 1 protease at position 88, located outside the active site, confers resistance to the hydroxyethylurea inhibitor SC-55389A.
 PMID: 9055985       1997       Antimicrobial agents and chemotherapy
Abstract: Passaging of virus first in SC-55389A alone and then in combination with SC-52151 resulted in the accumulation of more mutations in the protease gene (L10F, D35E, D37M, I47V, 154L, A71V, V82I, and S88D) and in the selection of a variant that was cross-resistant to multiple protease inhibitors.



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