Longitudinal use of a line probe assay for human immunodeficiency virus type 1 protease predicts phenotypic resistance and clinical progression in patients failing highly active antiretroviral therapy.
PMID: 12019110
2002
Antimicrobial agents and chemotherapy
Abstract: Combinations of protease mutations (M46I, G48V, I54V, V82A or -F, I84V, and L90M) predicted phenotypic resistance to the protease inhibitor and to nelfinavir.
Genetic variation of the protease and reverse transcriptase genes in HIV-1 CRF04_cpx strains.
PMID: 12079565
2002
AIDS research and human retroviruses
Abstract: Substitutions classically associated with resistance to antiretroviral drugs were observed in six of seven samples, including G48V, V82A, L90M, M46I in the protease protein, and K70R, D69D/N, M184V, T215F, K103N in the reverse transcriptase protein.
Resistance profiles of cyclic and linear inhibitors of HIV-1 protease.
Abstract: Kinetic analysis of the mutants revealed that catalytic efficiency was 1-30% of that for the wild-type enzyme, a consequence of reduced kcat in all cases and an increased KM for all mutants except for the G48V enzyme.
Abstract: The greatest increase in Ki was generally observed for the 184V mutant and least for the G48V/L90M mutant, and additional combinations of mutations did not result in improved inhibition profiles for the cyclic compounds.
Abstract: The overall structure-inhibitory profiles of the cyclic compounds were similar, and the inhibition of the V82A, 184V and G48V/L90M mutants were less efficient than of the wild-type enzyme.
Abstract: To allow a detailed structure-inhibition analysis, enzyme with single, double, triple and quadruple combinations o
Genotypic and phenotypic cross-resistance patterns to lopinavir and amprenavir in protease inhibitor-experienced patients with HIV viremia.
PMID: 12396453
2002
AIDS research and human retroviruses
Abstract: Mutations L10I, G48V, I54T, I54V, and V82A were significantly associated with decreased LPV susceptibility (p < 0.001 for each) and had increased RIs of 2.2, 4.4, 13, 4.6, and 3.2, respectively.
Comparison of DNA sequencing and a line probe assay for detection of human immunodeficiency virus type 1 drug resistance mutations in patients failing highly active antiretroviral therapy.
PMID: 11158089
2001
Journal of clinical microbiology
Abstract: Mutations M461, G48V, and L90M were often transient and drug pressure related.
Structure-activity studies of FIV and HIV protease inhibitors containing allophenylnorstatine.
Abstract: VLE776 also exhibited potent antiviral activities against the drug-resistant HIV mutants (G48V and V82F) and the TL3-resistant HIV mutants.
High prevalence of genotypic and phenotypic HIV-1 drug-resistant strains among patients receiving antiretroviral therapy in Abidjan, Cote d'Ivoire.
PMID: 11391173
2001
Journal of acquired immune deficiency syndromes (1999)
Abstract: The prevalence of mutations associated with resistance to ARV drugs was: 29 (42.6%) to zidovudine, 10 (14.7%) to lamivudine, one (1.5%) to didanosine, one K103N mutation (associated with resistance to delavirdine, nevirapine, and efavirenz), one Y181C mutation (associated with resistance to delavirdine and nevirapine), two to both indinavir (M46I/L and V82A) and saquinavir (G48V and L90M), and one each to ritonavir (V82A) and nelfinavir (D30N).
Genotypic and phenotypic evidence of different drug-resistance mutation patterns between B and non-B subtype isolates of human immunodeficiency virus type 1 found in Brazilian patients failing HAART.
Abstract: A strong cross-resistance phenotype among all four PI was associated with the mutation L90M in the subtype-B isolates, and with G48V and V82A/F in the non-B counterparts.
Abstract: Although all patients were treated with similar P1 drug regimen, the non-B subtype isolates did not present the L90M and 184V mutations and used mainly G48V and V82A/F to achieve drug resistance.
Baseline antiretroviral drug susceptibility influences treatment response in patients receiving saquinavir-enhancing therapy.
Abstract: Genotypic resistance to SQV was defined by the presence of G48V and/or L90M mutations in the protease gene.
Susceptibility to PNU-140690 (Tipranavir) of human immunodeficiency virus type 1 isolates derived from patients with multidrug resistance to other protease inhibitors.
PMID: 10770770
2000
Antimicrobial agents and chemotherapy
Abstract: The substitutions among the amino acid residues of the protease included L10I, K20R, L24I, M36I, N37D, G48V, I54V, L63P, I64V, A71V, V77I, V82A, I84V, and L90M.
HIV mutation literature information.
PMID: 
2002
Antimicrobial agents and chemotherapy
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