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.
Proteochemometric modeling of drug resistance over the mutational space for multiple HIV protease variants and multiple protease inhibitors.
PMID: 19391634
2009
Journal of chemical information and modeling
Abstract: The model revealed the most deleterious mutations in the protease to be D30N, V32I, G48V, I50V, I54V, V82A, I84V, and L90M.
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
Protease inhibitor resistance analysis in the MONARK trial comparing first-line lopinavir-ritonavir monotherapy to lopinavir-ritonavir plus zidovudine and lamivudine triple therapy.
PMID: 19451297
2009
Antimicrobial agents and chemotherapy
Abstract: By week 96 (W96), virus samples from 18 of 33 patients in the monotherapy arm showed changes from baseline sequences, and 5 of these patients had viruses with major protease inhibitor (PI) resistance-associated mutations (M46I at W40, L76V at W48, M46I and L76V at W48, L10F and V82A at W72, and L76V at W84).
Molecular dynamics and free energy studies on the wild-type and mutated HIV-1 protease complexed with four approved drugs: mechanism of binding and drug resistance.
PMID: 19537723
2009
Journal of chemical information and modeling
Abstract: In agreement with virological and clinical data, the structural analysis showed that the single mutations V82A, I84V, and M46I are associated with higher energetic values for all analyzed complexes with respect to wild-type, indicating their decreased stability.
HIV type-1 clade C resistance genotypes in treatment-naive patients and after first virological failure in a large community antiretroviral therapy programme.
Discussion: Other mutations that are more likely to impact on the future use of a protease inhibitor, including D30N, M46I, I47V, I50V and V82A/F, were present, but in a minority of individuals, with only a single mutation noted per individual.
Clinical validation and applicability of different tipranavir/ritonavir genotypic scores in HIV-1 protease inhibitor-experienced patients.
Abstract: Several patterns were frequently observed, including mutations in the NC-p1 cleavage site in combination with I50L, V82A, and I84V within the protease and mutations within the p1-p6 cleavage site in combination with D30N, I50V, and I84V within the protease.
Minority variants associated with transmitted and acquired HIV-1 nonnucleoside reverse transcriptase inhibitor resistance: implications for the use of second-generation nonnucleoside reverse transcriptase inhibitors.
PMID: 19734799
2009
Journal of acquired immune deficiency syndromes (1999)
Result: One patient (8048) was treated with LPV in combination with d4T + abacavir for seven years but was poorly adherent and eventually developed the LPV resistance mutations (I54V and V82A).
Antiretroviral genotypic resistance mutations in HIV-1 infected Korean patients with virologic failure.
PMID: 19949656
2009
Journal of Korean medical science
Result: M41L, I54V, D30N, and V82A/T/S were observed in more than 10 patients and K103N (10/41, 24.4%) was the most frequently observed NNRTI associated mutation.
HIV mutation literature information.
PMID: 
2009
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