HIV mutation literature information.


  Altered error specificity of RNase H-deficient HIV-1 reverse transcriptases during DNA-dependent DNA synthesis.
 PMID: 23444139       2013       Nucleic acids research
Result: All tested RTs showed similar or increased catalytic efficiencies (measured as the ratio kcat/Km) in comparison with the O_WT RT, and the mutant enzyme V75I (O_V75I), as well as with the BH10_WT RT.
Result: Although position +149 could be considered as a common hot spot location for both mutant RTs, identified errors were one-nucleotide deletions in the case of O_V75I/D443N RT and base substitutions (mostly G T mutations) in the case of O_V75I/E478Q RT.
Result: For example, the spectrum of O_D443N  PMID: 23840622       2013       PloS one
Method: The Q151M complex of mutations was defined as Q151M alone or in combination with one or more of the following mutations: A62V, V75I, F77L, and F116Y.


  Chemical system biology based molecular interactions to identify inhibitors against Q151M mutant of HIV-1 reverse transcriptase.
 PMID: 24015311       2013       PloS one
Result: In our study, other NRTI-RAMs known to be associated with Q151M-mediated multi-nucleoside resistance including A62V, V75I, F77L, and F116Y, were also significantly more common in patients harboring the Q151M mutation (p<0.001).


  Major groove binding track residues of the connection subdomain of human immunodeficiency virus type 1 reverse transcriptase enhance cDNA synthesis at high temperatures.
 PMID: 24303887       2013       Biochemistry
Abstract: Some of them (e.g., F61A, K65R, K65R/V75I, and V148I) had a negative effect on reverse transcription efficiency above 65C.


  Biochemical, inhibition and inhibitor resistance studies of xenotropic murine leukemia virus-related virus reverse transcriptase.
 PMID: 21908397       2012       Nucleic acids research
Discussion: In HIV, decreased binding of AZT is conferred initially in the presence of the primary Q151M mutation, followed by secondary mutations F77L, A62V, V75I and F116Y.


  Low rates of nucleoside reverse transcriptase inhibitor resistance in a well-monitored cohort in South Africa on antiretroviral therapy.
 PMID: 22293461       2012       Antiviral therapy
Result: At time of failure the following NRTI mutations were observed: A62V (n=1; 1%), K65R (n=2; 3%), D67G/N (n=2; 3%), T69L (n=1; 1%), K70R (n=1; 1%), V75I (n=1; 1%), M184V (n=46; 66%) and K219K (n=1; 1%).


  Lys66 residue as a determinant of high mismatch extension and misinsertion rates of HIV-1 reverse transcriptase.
 PMID: 22925131       2012       The FEBS journal
Introduction: showed that the mutation Val75Ile increased the mismatch extension fidelity 3-fold while showing no apparent effect on misinsertion fidelity.


  Differential in vitro kinetics of drug resistance mutation acquisition in HIV-1 RT of subtypes B and C.
 PMID: 23056372       2012       PloS one
Discussion: Q151M is a primary mutation that in vivo can be co-selected together with a group of secondary mutations (A62V, V75I, F77L and F116Y) that confers a cross-resistance with all NRTIs.


  Monitoring HIV viral load in resource limited settings: still a matter of debate?
 PMID: 23236346       2012       PloS one
Result: Among patients carrying RAMs, 12/15 (80.0%) harboured RAMs associated to thymidine analogues (TAMs) (M41L, D67N, K70R, V75I, L210W, T215F/Y) (Table 3).
Result: The most frequent TAMs were T215F/Y (11/12, 91.7%), M41L (10/12, 83.3%), L210W (3/12, 27,3%), D67N (3/12, 25.0%), K70R (1/12, 8.3%) and V75I (1/12, 8.3%) (Table 3).
Table: V75I


  Effect of translocation defective reverse transcriptase inhibitors on the activity of N348I, a connection subdomain drug resistant HIV-1 reverse transcriptase mutant.
 PMID: 23273211       2012       Cellular and molecular biology (Noisy-le-Grand, France)
8Discussion: The A62V/V75I/F77L/F116Y/Q151M set of mutations is known as the ""Q151M"" complex RT, and has been known as a multidrug-resistance mutation, since the latter mutations are known to be involved in resistant variants with reduced susceptibility to dideoxynucleotides and to AZT."
Result: In addition, another mutant HIV-1 RT (A62V/V75I/F77L/F116Y/Q151M) was included in drug susceptibility assays.
Discussion: We report that both EFdA-TP and ENdA-TP are very potent inhibitors of N348I,



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