Abstract: The kinetics of the interaction between drug-resistant variants of HIV-1 protease (G48V, V82A, L90M, I84V/L90M, and G48V/V82A/I84V/L90M) and clinically used inhibitors (amprenavir, indinavir, nelfinavir, ritonavir, and saquinavir) were determined using biosensor technology.
Dual pressure from antiretroviral therapy and cell-mediated immune response on the human immunodeficiency virus type 1 protease gene.
Abstract: In contrast, the mutant PR82A(76-84) epitope is generally not recognized by wild-type-specific CTL, or when recognized it is of low to moderate avidity, suggesting that the protease inhibitor-selected V82A mutation acts both as a CTL and protease inhibitor escape mutant.
Abstract: This epitope, which is HLA-A2 restricted, includes two amino acids that commonly mutate (V82A and I84V) in the face of protease inhibitor therapy.
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.
Analysis of the protease sequences of HIV-1 infected individuals after Indinavir monotherapy.
Abstract: More prevalent detected mutations, thought to contribute to antiretroviral resistance, were L63P (42%), L10I (35%), M36I (30%), V82A/T/F (26%).
Novel enzyme-linked minisequence assay for genotypic analysis of human immunodeficiency virus type 1 drug resistance.
PMID: 14605126
2003
Journal of clinical microbiology
Abstract: ELMA is a combination of hybridization and a 1-base extension reaction, and we designed the assay to detect five mutations conferring nucleoside analogue resistance (M41L, D67N, K70R, T215Y, and M184V) and six mutations conferring protease inhibitor resistance (D30N, M46I, G48V, V82A, I84V, and L90M).
Multidrug resistance to HIV-1 protease inhibition requires cooperative coupling between distal mutations.
Abstract: A mutant containing only the four active site mutations (V82A/I84V/M46I/I54V) only showed a small cooperative effect, suggesting that the mutations at the dimer interface (L10I/L90M) play a major role in eliciting a cooperative response.
Abstract: This mutant (MDR-HM) contains six amino acid mutations (L10I/M46I/I54V/V82A/I84V/L90M) located within and outside the active site of the enzyme.
Abstract: To understand the origin of resistance, three submutants containing mutations in specific regions were also studied, i.e., the active site (
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.
Sexual transmission of HIV-1 isolate showing G-->A hypermutation.
Abstract: The patient's viral genotype showed several mutations related to antiretroviral drug resistance in RT (T69N, M184V, T215F, K219Q) and protease (M36I, G48V, I54V, T63L, V82A) genes.
Low prevalence of primary mutations associated with drug resistance in antiviral-naive patients at therapy initiation.
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).
Evolution of primary protease inhibitor resistance mutations during protease inhibitor salvage therapy.
PMID: 11897594
2002
Antimicrobial agents and chemotherapy
Abstract: D30N persisted less frequently than L90M (50% versus 100%, respectively; P < 0.001) and V82A/F/T (50% versus 81%, respectively; P = 0.05).
Abstract: Among 78 patients meeting study selection criteria, baseline primary PI resistance mutations included L90M (42% of patients), V82A/F/T (27%), D30N (21%), G48V (6%), and I84V (4%).
Abstract: HIV-1 isolates from 38 (49%) patients failing PI salvage therapy developed new primary PI resistance mutations including L90M, I84V, V82A,
HIV mutation literature information.
PMID: 
2003
Antiviral research
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