HIV mutation literature information.


  Relatively high prevalence of drug resistance among antiretroviral-naive patients from Henan, Central China.
 PMID: 23800338       2014       AIDS research and human retroviruses
Abstract: The unexpectedly high percentage of drug resistance in Henan province is mainly due to the prevalence of minor mutations in the protease and integrase regions, especially A71T/V and L68V/I/IM/LV.


  "Description of the L76V resistance protease mutation in HIV-1 B and ""non-B"" subtypes."
 PMID: 23349869       2013       PloS one
5Result: Likewise, this cluster was confirmed also in HIV-1 ""non-B"" sequences, where the major PI RAM L76V, M46I, I54L and I84V grouped together with the secondary one A71V (bootstrap value = 0.86)."


  A Comparative Molecular Dynamics, MM-PBSA and Thermodynamic Integration Study of Saquinavir Complexes with Wild-Type HIV-1 PR and L10I, G48V, L63P, A71V, G73S, V82A and I84V Single Mutants.
 PMID: 26587633       2013       Journal of chemical theory and computation
Abstract: Finally, it was indicated that a water-mediated hydrogen bond between saquinavir and Asp29 in the active site (wild-type, A71V, G73S) facilitates a proper placement of the drug into the binding cavity that favors binding.
Abstract: In this work, we examine L10I, G48V, L63P, A71V, G73S, V82A, and I84V single mutant HIV-1 PR strains in complexes with saquinavir to elucidate drug-protease interactions and dynamics.
Abstract: The preservation of hydrogen bonds of saquinavir with both the active site and flap residues in the wild-type and certain single mutants (


  Structural and thermodynamic basis of amprenavir/darunavir and atazanavir resistance in HIV-1 protease with mutations at residue 50.
 PMID: 23365446       2013       Journal of virology
Abstract: Reduced affinity to both I50V/A71V and I50L/A71V double mutants is largely due to decreased binding entropy, which is compensated for by enhanced enthalpy for ATV binding to I50V variants and APV binding to I50L variants, leading to hypersusceptibility in these two cases.
Abstract: To explain how APV, DRV, and ATV susceptibility are influenced by mutations at residue 50 in HIV-1 protease, structural and binding thermodynamics studies were carried out on I50V/L-substituted protease variants in the compensatory mutation A71V background.


  Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
 PMID: 23469241       2013       PloS one
Result: The latter differed significantly in the frequencies of the major resistance RT mutations T215FY and K219QE (NRTI) and of several secondary/accessory mutations, including: the protease mutations I13V, M36I, I62V, L63P, A71V, V77I, L89M and I93L (Table 6) and the RT mutations A98S, K101N, K103R and V179I (Table 5).
Table:  PMID: 23566104       2013       Biochemistry
Result: An example of the Gaussian reconstruction of the distance profile for M36I/A71V is shown in Figure 3A.
Result: For A71V, D30N/M36I, D30N/A71V, and M36I/A71V the most probable distance occurs at a shorter distance of ~ 33 A (solid line); which is a distance consistent with a closed-like or closed conformation.
Result: For A71V, D30N/M36I, M36I/A71V and D30N/M36I/A71V, a small but distinct peak in


  Extreme multidrug resistant HIV-1 protease with 20 mutations is resistant to novel protease inhibitors with P1'-pyrrolidinone or P2-tris-tetrahydrofuran.
 PMID: 23590295       2013       Journal of medicinal chemistry
Introduction: Recently, we characterized a clinically derived HIV-1 protease (PR20) bearing 20 mutations [Q7K, L10F, I13V, I15V, D30N, V32I, L33F, E35D, M36I, S37N, I47V, I54L, Q58E, I62V, L63P, A71V, I84V, N88D, L89T and L90M] and extremely resist


  Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.
 PMID: 23711895       2013       The Journal of antimicrobial chemotherapy
Abstract: The minor mutations most strongly associated with atazanavir experience were M36I, M46I, F53L, A71V, V82T and I85V (P < 0.05).


  Potential elucidation of a novel CTL epitope in HIV-1 protease by the protease inhibitor resistance mutation L90M.
 PMID: 24015196       2013       PloS one
Method: Equations 1, 2, 3, 4 and 5 represent L90M frequency estimators trained from the V82A, I54V, A71V
Result: The frequencies commonly occurring PR mutations, M46I, I54V, A71V, V82A and I84V were also tested in both B*48 and B*15 subtype sequence sets.
Result: This is likely due the strong association of PR:90M with some substitutions that correlated with both drug resistance and HLA-B*15, namely PR:A71V and PR:L10I.


  Highly-sensitive allele-specific PCR testing identifies a greater prevalence of transmitted HIV drug resistance in Japan.
 PMID: 24358257       2013       PloS one
Discussion: Moreover, accumulation of compensatory mutations such as L63P and A71V in protease have been demonstrated to increase or restore replicative fitness of PI resistant variants, and that once compensation has taken place reversion to wildtype is prohibited by a less fit intermediate.



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