Complex patterns of protease inhibitor resistance among antiretroviral treatment-experienced HIV-2 patients from Senegal: implications for second-line therapy.
PMID: 23571535
2013
Antimicrobial agents and chemotherapy
Abstract: Common protease substitutions included V10I, V47A, I54M, V71I, I82F, I84V, L90M, and L99F, and most patients harbored viruses containing multiple changes.
Abstract: In addition, the triple mutant that included I54M plus I84V plus L90M was resistant to all three PIs (31-, 10-, and 3.8-fold increases in the mean EC50 for darunavir, saquinavir, and lopinavir, respectively).
Abstract: Relative to wild-type HIV-2, the V47A mutant was resistant to lopinavir (6.3-fold increase in the mean 50% effectiv
"Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."
Method: In our study, samples with at least one of the major PI RAM of the IAS-USA list as follows: D30N, V32I, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V,
Result: Among subtype B samples, the major PI RAM significantly correlating as pairs with L76V were: M46I, I54L/M, Q58E, V82F, I84V, and L90M.
Novel P2 tris-tetrahydrofuran group in antiviral compound 1 (GRL-0519) fills the S2 binding pocket of selected mutants of HIV-1 protease.
PMID: 23298236
2013
Journal of medicinal chemistry
Abstract: Mutations V82A and I54M showed compensating structural changes consistent with 6-7-fold lower inhibition.
Abstract: The high resolution X-ray crystal structures of inhibitor 1 in complexes with single substitution mutants PR(R8Q), PR(D30N), PR(I50V), PR(I54M), and PR(V82A) were analyzed in relation to kinetic data.
Introduction: In order to study the molecular basis for the potency of inhibitor 1 against drug resistant viral strains, crystal structures of inhibitor 1 complexes with PR mutants bearing single substitutions of <
Cooperative effects of drug-resistance mutations in the flap region of HIV-1 protease.
Introduction: I54A has a PI susceptibility profile similar to I54V, unlike other substitutions such as I54L and I54M.
Transmitted drug resistance and phylogenetic relationships among acute and early HIV-1-infected individuals in New York City.
PMID: 22592583
2012
Journal of acquired immune deficiency syndromes (1999)
4Method: ARV resistance was defined by mutations at the following positions: M41L, A62V, K65R, D67N, T69ins, K70R, L74VI, Y115F, F116Y, Q151M, M184VI, T210W, T215YF and K219QE for Nucleoside Reverse Transcriptase Inhibitors (NRTI), L100I, K101EP, K103NS, V106AM
Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.
Method: The following resistance mutations were scored: to nucleoside reverse transcriptase inhibitors (NRTIs): M41L, K65R, D67N/G/E, T69D/insertion, K70R/E, L74V/I, V75M/T/A/S, F77L, Y115F, F116Y, Q151M, M184V/I, L210W, T215Y/F/I/S/C/D/V/E, K219Q/EN/R; to non-nucleoside revers
Energetic basis for drug resistance of HIV-1 protease mutants against amprenavir.
PMID: 22350569
2012
Journal of computer-aided molecular design
Abstract: Drug resistance arises from an increase in the energetic contribution from the van der Waals interactions between APV and PR (V32I, I50V, and I84V mutant) or a rise in the energetic contribution from the electrostatic interactions between the inhibitor and its target (I54M and I54V mutant).
Abstract: However, the affinities of the drug resistant protease variants V32I, I50V, I54V, I54M, I84V and L90M to amprenavir are decreased 3 to 30-fold compared to the wild-type.
Virological response to darunavir in patients infected with HIV is linked to darunavir resistance-associated mutations corrected by the count of mutations with positive impact and is not associated with pharmacological and combined virological/pharmacological parameters.
PMID: 21545648
2012
Fundamental & clinical pharmacology
Abstract: Darunavir GIQ is defined as the ratio between darunavir trough plasma concentration and the count of darunavir resistance-associated mutations (V11I, V32I, L33F, I47V, I50V, I54L/M, T74P, L76V, I84V, L89V) corrected or not corrected by the count of mutations with positive impact (V82A and E35D).
The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
HIV mutation literature information.
PMID: 
2013
Antimicrobial agents and chemotherapy
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