Abstract: RESULTS: In protease (PR), resistance-associated mutations M46I/L, I54M/L/V/A/S and V82A/F/T/S/M/I were associated with each other and with minor mutations at codons 10, 24 and 71.
Comparison of protease inhibitor (PI) resistance-associated mutations between PI-naive and PI-experienced HIV-1 infected patients in Thailand where subtype A/E is predominant.
Abstract: The most common primary PI-RAMs in the latter group were V82A (10%), I54V (7%) and G48V (4.8%).
HIV-1 protease mutations and protease inhibitor cross-resistance.
PMID: 20660676
2010
Antimicrobial agents and chemotherapy
Abstract: Of the mutations with the greatest effect on PI susceptibility, I84AV was associated with decreased susceptibility to eight PIs; V32I, G48V, I54ALMSTV, V82F, and L90M were associated with decreased susceptibility to six to seven PIs; I47A, G48M, I50V, L76V, V82ST, and N88S were associated with decreased susceptibility to four to five PIs; and D30N, PMID: 20695887
2010
The FEBS journal
Abstract: Mutation to smaller side chains eliminated hydrophobic interactions in the PR(I50V) and PR(I54V) structures.
Abstract: The structural and kinetic effects of amprenavir (APV), a clinical HIV protease (PR) inhibitor, were analyzed with wild-type enzyme and mutants with single substitutions of V32I, I50V, I54V, I54M, I84V and L90M that are common in drug resistance.
Introduction: Conservative mutations of hydrophobic residues are common in PI resistance, including V32I, PMID: 20805393
2010
Antimicrobial agents and chemotherapy
Abstract: Common partner mutations included M46I, I54V, V82A, I84V, and L90M.
Frequency and diversity of human immunodeficiency virus type 1 mutations associated with antiretroviral resistance among patients from Southern Brazil failing highly active antiretroviral therapy (HAART).
PMID: 20818500
2010
International journal of molecular medicine
Abstract: Mutations associated with resistance to protease inhibitor (PI) were detected in 124 tests (97.6%), the main ones were L90M in 28 (22.0%), V82A in 27 (21.2%), M46I in 26 (20.5%), and I54V in 23 (18.1%).
Patients with discordant responses to antiretroviral therapy have impaired killing of HIV-infected T cells.
Abstract: In such patients, two protease mutations, I54V and V82A, occur more frequently.
Abstract: Primary CD4 T cells expressing I54V or V82A protease underwent less cell death than with WT or other mutant proteases.
Result: We tested WT HIV protease or the following point mutations: D25G (active site dead), T26S (catalytically impaired), D30N, F53L, or L90M; or the DAMs I54V and V82A produced in E-coli.
Result: Whereas expression of YFP WT PMID: 21603285
2010
The open medical informatics journal
Discussion: However, comparison is difficult due to the presence of different mutations in the HIV protease (D30N versus I54V+V82A), as well as the variability inherent in experiments employing SCID-hu mice in which a chimeric organ is created by engraftment of primary human tissues.
Discussion: who found that mice infected with a virus (210P) containing protease mutation at I54V and V82A had a higher level of viremia than mice infected with wild-type virus.
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 L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.
Result: Conversely, mutations I54V and V77I were significantly more prevalent in subtype B-infected children.
Table: I54V
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: Likewise, the pattern I54V/L-L90M did not reduce the susceptibility of subtype G to indinavir and saquinavir.
Abstract: RESULTS: Mutation I54V/L was selected by nelfinavir in subtype G isolates, a mutation not previously described for this drug in subtype B.
HIV mutation literature information.
PMID: 
2010
Antiviral therapy
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