Role of atazanavir in the treatment of HIV infection.
PMID: 19436623
2009
Therapeutics and clinical risk management
Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and
Analysis and characterization of dimerization inhibition of a multi-drug-resistant human immunodeficiency virus type 1 protease using a novel size-exclusion chromatographic approach.
Result: PRMDR contains multiple drug-resistant mutations (L10I, K45R, I54V, L63P, A71V, V82T, L90M and I93L) and is highly resistant to a number of active-site inhibitors, although it remains sensitive to the experimental active-site inhibitor JE-2147.
Discordant genotypic interpretation and phenotypic role of protease mutations in HIV-1 subtypes B and G.
PMID: 19136678
2009
The Journal of antimicrobial chemotherapy
Abstract: Indinavir-associated mutations M46I/L, I84V and V82A/F/T developed earlier in subtype B across the time of exposure to that drug when compared with subtype G counterparts.
Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
PMID: 18992847
2009
Infection, genetics and evolution
Method: Mutations D30N (NFV), V32I (LPV), M46I/L (IDV/RTV), I47V/A (LPV/RTV), G48V (SQV), I50L/V (APV), V82A/F/T/S (LPV/IDV/RTV), I84V (APV/IDV/RTV) and L90M (SQV/NFV) were considered as major resistance mutations and were analyzed separately for each PI as well as quantitatively all together.
Result: Ninety-seven percent of isolates with V82A/F/T/S mutations were from patients treated with IDV, RTV and/or LPV, and 89% of those with L90M were from patients treated with NFV and/or SQV.
Table: V82T
Transmission networks of drug resistance acquired in primary/early stage HIV infection.
Result: In addition, cluster C represents an MDR transmission network, wherein all four PHIs harboured K103N and three of the four also harboured L10I, I54V, A71V, V82A/I/T, I84I/V, and L90M.
HIV type 1 subtype C drug resistance among pediatric and adult South African patients failing antiretroviral therapy.
PMID: 19000027
2008
AIDS research and human retroviruses
Abstract: Of the patients who received PIs, the most common mutations were V82A/T (12%), M46I (11%), and L90M (8%).
Population trends in the prevalence and patterns of protease resistance related to exposure to unboosted and boosted protease inhibitors.
Abstract: Individual mutations L33F, M461/L, V82A/F/T/S/L and 184V became relatively more frequent over the period of study.
HIV drug resistance pattern among HAART-exposed patients with suboptimal virological response in Ouagadougou, Burkina Faso.
PMID: 18667925
2008
Journal of acquired immune deficiency syndromes (1999)
Abstract: Dominant mutations included M46I (37%), 154V (26%), V82A/T/F (30%) in PR; K103N (44%), G190A/S (16%) and T215F/Y (48%) (NRTIs) in RT.
Abstract: Some resistance mutations, notably D67N/G, K70R and L210W (thymidine analogue mutations-TAMs); K101E, V179E in RT, 154V, V82A/T/F and L90M in PR were significantly higher among CRF06_cpx than CRF02_AG strains (P
The HIV-1 protease substitution K55R: a protease-inhibitor-associated substitution involved in restoring viral replication.
PMID: 18252693
2008
The Journal of antimicrobial chemotherapy
Abstract: RESULTS: The K55R mutation, which is not a natural polymorphism, was identified to be strongly associated with protease mutations M46I/L and to a lesser extent L24I, I54V and V82A/T/S/F.
Genotypic resistance profile and clinical progression of treatment-experienced HIV type 1-infected patients with virological failure.
PMID: 18240962
2008
AIDS research and human retroviruses
Abstract: In multivariable models adjusting for prior AIDS, baseline CD4 counts, HIV-1 RNA, and calendar year, viral resistance variables associated with increased hazards of clinical progression were the presence of reverse transcriptase substitution T215F (p = 0.002) and the presence of three or more protease substitutions among L33F/I/V, V82A/F/L/T, I84V, and L90M (p = 0.003).
HIV mutation literature information.
PMID: 
2009
Therapeutics and clinical risk management
Browser Board
Co-occurred Entities
Filtrator
ViMRT