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.
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
Clinical validation and applicability of different tipranavir/ritonavir genotypic scores in HIV-1 protease inhibitor-experienced patients.
Abstract: The following variables were significantly associated (p<0.05) to failure with multivariate analysis: WS, log peak of HIV-RNA, IAS mutations: L33F, I54AMV, Q58E, and non-IAS mutation: N37DES.
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.
Evolution of the HIV-1 protease region in heavily pretreated HIV-1 infected patients receiving Atazanavir.
Abstract: In two of these subjects new mutations (I54V and A71V) conferring cross-resistance emerged after 3 months of therapy.
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.
HIV type 1 pol gene diversity and antiretroviral drug resistance mutations in Santos, Brazil.
PMID: 18327988
2008
AIDS research and human retroviruses
Abstract: Drug resistance mutations identified in common to subtypes B, F, and recombinants B/F were protease inhibitors M46I/L (29%), I54V (24%), A71V (22%), and V82A/F (31%); reverse transcriptase nucleoside resistance mutations M41L (52%), D67N (30%), K70R (26%), M184V (88%), L210W (29%), T215Y/I/F (65%), and K219Q/E/N (28%); and reverse transcriptase nonnucleoside resistance mutation K103N (52%).
Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir.
PMID: 18390885
2008
The Journal of antimicrobial chemotherapy
Abstract: Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations.
HIV mutation literature information.
PMID: 
2009
The Biochemical journal
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