Introduction: I54V in combination with other mutations, especially V82A, decreases the susceptibility to PI therapy.
Prevalence, mutation patterns, and effects on protease inhibitor susceptibility of the L76V mutation in HIV-1 protease.
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%).
Human immunodeficiency virus type 1 protease inhibitor drug-resistant mutants give discordant results when compared in single-cycle and multiple-cycle fitness assays.
PMID: 20826651
2010
Journal of clinical microbiology
Abstract: When all the mutants were ranked in order from most to least fit for both assays, 4 protease mutants moved more than 5 positions in rank: the D30N, I54L, I54M, and V82A mutants.
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.
Method: HIV (HXB2) viral stocks containing either the WT protease gene or mutations coding for single amino acid substitutions (I54V, V82A, or L90M) of the protease gene were produced as follows: Mutant PR coding sequences were generated from a pGEM vector containing the HIV-1 LAI (clone HXB2)
In Vivo validation of a bioinformatics based tool to identify reduced replication capacity in HIV-1.
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: Nonetheless, the differences in these results may also suggest that virus containing the D30N mutation is less able to replicate in the thymus than virus containing the V82A mutation (as is suggested by our bioinformatics model).
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 w
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: V82A
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.
Mutations associated with virological response to darunavir/ritonavir in HIV-1-infected protease inhibitor-experienced patients.
PMID: 19147519
2009
The Journal of antimicrobial chemotherapy
Abstract: Cochran-Armitage procedure identified eight mutations with a negative impact on the virological response, namely K14R, K20I, E34Q, I47V, I54M, K55R, T74P and I84V; and two mutations (E35D and V82A) with a positive impact.
Gag mutations strongly contribute to HIV-1 resistance to protease inhibitors in highly drug-experienced patients besides compensating for fitness loss.
Introduction: Interestingly, some of these mutations appear to depend upon the presence of specific mutations in PR: Mutation A431V is mostly observed in PI-resistant viruses carrying mutations V82A and/or M46I in PR.
Discussion: The mechanism of this compensation has been documented for mutation A431V, which emerges mostly in viruses carrying resistance mutation V82A in PR.
HIV mutation literature information.
PMID: 
2010
The FEBS journal
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