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 HIV mutation literature information.


  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.


  Binding of single walled carbon nanotube to WT and mutant HIV-1 proteases: analysis of flap dynamics and binding mechanism.
 PMID: 23142620       2012       Journal of molecular graphics & modelling
Introduction: In the present study, we have tested the SWCNTs as inhibitors in WT as well as in three primary mutants (I50VPR, V82APR and I84VPR) of HIV-1-PR by docking the SWCNT in the active site region, and then performed all-atom molecular dynamics (MD) simulations for the complexes.
Method: The PDB entries are: 1T3R for the wild type (WT), 2F8G for the I50VPR, 2QD7 for the V82APR, and 2NNP for the I84VPR mutants.
Result: Although the WT, I50VPR, V82APR and I84VPR mutant trajectories have significant overlaps, some differences can still be observed (Figure 6a).


  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).


  Interpretation of genotypic resistance to predict darunavir/ritonavir failure in antiretroviral experienced patients.
 PMID: 22067663       2012       Journal of acquired immune deficiency syndromes (1999)
Abstract: Four mutations (V32I, I50V, L76V, I84V) were predictive of failure, the hazard ratio progressively increased by detecting 1 (hazard ratio: 2.0, 95% confidence interval: 1.3 to 3.0), 2 (3.6, 2.0 to 6.6), or 3 of them (9.7, 2.8 to 33.5).


  Genotypic resistance profiles associated with virological failure to darunavir-containing regimens: a cross-sectional analysis.
 PMID: 22237471       2012       Infection
Abstract: DISCUSSION: The higher statistical difference at baseline between failing versus non-failing patients was observed for the V32I and I84V mutations.


  Interaction of I50V mutant and I50L/A71V double mutant HIV-protease with inhibitor TMC114 (darunavir): molecular dynamics simulation and binding free energy studies.
 PMID: 22239286       2012       The journal of physical chemistry. B
Introduction: The resistance of the inhibitor GRL-98065, an analog of TMC114 just aniline group replaced by a 1,3-benzodioxole group, to mutants I50V and V82A was attributed to a higher entropic contribution than in the wild type (WT) HIV-pr, and the reduced van der Waals may be responsible to the drug resistance of I84V to GRL-98065.
Result: For example, L90M and V82F/I84V mutations open the flap a bit more in the mutant than the WT, whereas M46I mutation makes the flap more closed.


  Low prevalence of transmitted drug resistance in patients newly diagnosed with HIV-1 infection in Sweden 2003-2010.
 PMID: 22448246       2012       PloS one
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


  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


  Transition states of native and drug-resistant HIV-1 protease are the same.
 PMID: 22493227       2012       Proc Natl Acad Sci U S A
Abstract: The KIEs measured for the native and I84V enzyme indicate nearly identical transition states, implying that a true transition-state analogue should be effective against both enzymes.
Abstract: We have measured primary (14)C and (15)N KIEs and secondary (3)H and (18)O KIEs for native and multidrug-resistant HIV-1 protease (I84V).
Abstract: We observed (14)C KIEs ((14)V/K) of 1.029 +- 0.003 and 1.025 +- 0.005, (15)N KIEs ((15)V/K) of 0.987 +- 0.004 and 0.989 +- 0.003, (18)O KIEs ((18)V/K) of 0.999 +- 0.003 and 0.993 +- 0.003, and (3)H KIEs ((3)V/K) KIEs of 0.968 +- 0.001 and 0.976 +- 0.001 for the native and I84V enzyme, respectively.


  Three main mutational pathways in HIV-2 lead to high-level raltegravir and elvitegravir resistance: implications for emerging HIV-2 treatment regimens.
 PMID: 23028968       2012       PloS one
Table: I84V



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