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 HIV mutation literature information.


  Virologic failures on initial boosted-PI regimen infrequently possess low-level variants with major PI resistance mutations by ultra-deep sequencing.
 PMID: 22355307       2012       PloS one
Abstract: Overall, 3/36(8.3%) subjects had DRMs identified with Stanford-HIVdb weights >12 for ATV or LPV: N88S (at 0.43% level-mutational load 1,828) in 1 subject on ATV; I50V (0.44%-mutational load 110) and L76V (0.52%-mutational load 20) in 1 subject each, both on LPV.
Abstract: The most common UDS-detected DRM were NRTI in 18 subjects: M184V/I (11), TAMs(7) & K65R(4); PI DRMs were detected in 9 subjects: M46I/V(5), F53L(2), I50V(1), D30N(1), and N88S(1).
Result: Nineteen of 24 (79.2%) had any PI,


  HIV-1 protease with 20 mutations exhibits extreme resistance to clinical inhibitors through coordinated structural rearrangements.
 PMID: 22404139       2012       Biochemistry
Method: The PR20/SQV crystal structure was solved by molecular replacement with the structure of PR mutant I50V in complex with DRV (2F8G) using MOLREP.


  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


  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
Result: Although the WT, I50VPR, V82APR and I84VPR mutant trajectories have significant overlaps, some differences can still be observed (Figure 6a).
Result: Average distances for the WT-, I50VPR-, V82APR-, and I84VPR-SWCNT complexes are 6.55 A, 6.42 A, 6.79 A and 6.23 A, with SD 0.60 A, 0.40 A, 0.87 A and 0.35 A, respectively.
Result: Besides the mutation residue I50V/I50'V, Figure 12 and Table 3 show that Arg08 and Gly27' contributes to the binding decrease by over 1.0kcal/mol, which is basically consistent with the longer distance between the residue and the SWCNT as shown in Figures 13a.


  Influence of major HIV-1 protease inhibitor resistance mutations on CTL recognition.
 PMID: 21107269       2011       Journal of acquired immune deficiency syndromes (1999)
Abstract: Furthermore, M46I, I47A, and I50V could impair or abolish CTL recognition in many patients.
Abstract: Recently, we identified KMIGGIGGF (KF9) as a HLA-B*1501-restricted CTL epitope, including several major PI resistance mutations (M46I/L, I47A/V, G48V, I50V).


  The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
 PMID: 21314993       2011       AIDS research and therapy
Table: I50V


  Interpretation of genotypic HIV-1 resistance to darunavir and virological response: validation of available systems and of a new score.
 PMID: 21685536       2011       Antiviral therapy
Abstract: The DRV-2009 score V11I+L33F+R41K+I47V+2*I50V+2*I54M+K55R+D60E+L74P+L76V+N88D+2*L89V-L10I/V-I13V-G16E-G48V-F53I/L-I62V-I66F-V77I (<0 indicating susceptibility, 0-1 intermediate resistance and >=2 resistance) correlated with VR in the derivation set (n=132, R=0.395; P<0.001).


  Studies on adaptability of binding residues and flap region of TMC-114 resistance HIV-1 protease mutants.
 PMID: 21696230       2011       Journal of biomolecular structure & dynamics
Abstract: We provide insight into the molecular basis of TMC-114 resistance major flap mutations (I50V and I54M) in HIV-1 protease.


  TMC310911, a novel human immunodeficiency virus type 1 protease inhibitor, shows in vitro an improved resistance profile and higher genetic barrier to resistance compared with current protease inhibitors.
 PMID: 21896904       2011       Antimicrobial agents and chemotherapy
Abstract: IVRS performed with r13025 in the presence of DRV required less time and resulted in more PI resistance-associated mutations (V32I, I50V, G73S, L76V, and V82I; FC in DRV EC(50) = 258).



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