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 HIV mutation literature information.


  Prevalence of darunavir resistance mutations in HIV-1-infected patients failing other protease inhibitors.
 PMID: 17646201       2007       The Journal of antimicrobial chemotherapy
Abstract: The prevalence of major darunavir resistance mutations was I50V 2.1%, I54M 1.3%, L76V 2.7% and I84V 14.5%.


  Potent new antiviral compound shows similar inhibition and structural interactions with drug resistant mutants and wild type HIV-1 protease.
 PMID: 17696515       2007       Journal of medicinal chemistry
Abstract
Abstract: PR(D30N) and PR(V82A) showed compensating interactions with inhibitor 1 relative to those of PR, while reduced hydrophobic contacts were observed with PR(I50V) and PR(I84V).
Abstract: Compound 1 had inhibition constants of 17-fold, 8-fold, 3-fold, and 3-fold, respectively, for PR(D30N), PR(I50V), PR(V82A), and PR(I84V) relative to wild type PR.


  Impact of the number of failed therapeutic regimes on the development of resistance mutations to HIV-1 in northeast Brazil.
 PMID: 17962868       2007       The Brazilian journal of infectious diseases
Abstract: There was a significant increase in resistance mutations V82A/F/L/T, I84V, L90M, M41L, K70R, L210W, T215Y/F and K219Q/E in MF.


  [Study on genotypic resistance mutations to antiretroviral drugs on HIV strains of treated and treatment-naive HIV-1 infectious patients in Hubei province].
 PMID: 18396668       2007       Zhonghua liu xing bing xue za zhi
Abstract: Some protease (PR) drug-resistant mutations were found in these samples, such as D30N (2.27%), D30G (2.27%), M46I (4.55%), M46N (2.27%), I47V (4.55%), I84V (4.55%), I84L (2.27%), N88S (2.27%) and L90S (2.27%) that all belonged to major drug-resistant but A71T (29.55%) belonged to minor resistance mutations Five treated patients were detected having mutations associated RT drug resistance: M41L (5.26%), A62V (5.26%),D67N (5.26%),  PMID: 16426053       2006       Journal of chemical information and modeling
Abstract: The best results were obtained in the case of the I84V mutant for which a high number of predictions was achieved.
Abstract: This paper describes the use of the multivariate statistical procedure principal component analysis as a tool to explore the inhibitory activity of classes of protease inhibitors (PIs) against HIV-1 viruses (wild type and more-frequent single mutants, V82A, V82F, and I84V) and against protease enzymes.


  Restrained molecular dynamics simulations of HIV-1 protease: the first step in validating a new target for drug design.
 PMID: 16508951       2006       Biopolymers
Abstract: To test the anticorrelated relationship that was recently displayed in conventional molecular dynamics (MD) simulations, several different restrained MD simulations on a wild type and on the V82F/I84V drug-resistant mutant of HIV-1 protease were performed.


  Non-infectious fluorimetric assay for phenotyping of drug-resistant HIV proteinase mutants.
 PMID: 16527535       2006       Journal of clinical virology
Abstract: RESULTS: We cloned a set of GFP-PR reporters, some of which possess a simple, well-defined drug-resistant PR mutant (G48V L90M, V82A, A71V V82T I84V, D30N, K45I); another four complex PR mutants were obtained from patients undergoing HAART.


  Gated binding of ligands to HIV-1 protease: Brownian dynamics simulations in a coarse-grained model.
 PMID: 16533835       2006       Biophysical journal
Abstract: The computed gated association rate constants of three protease mutants, G48V/V82A/I84V/L90M, G48V, and L90M with three drugs, amprenavir, indinavir, and saquinavir, yield good agreements with experiments.
Abstract: The simulations suggest that the flap flexibility and the opening frequency of the wild-type, the G48V and L90M mutants are similar, but the flaps of the variant G48V/V82A/I84V/L90M open less frequently, resulting in a lower gated rate constant.


  Analysis of a long-term discrepancy in drug-targeted genes in plasma HIV-1 RNA and PBMC HIV-1 DNA in the same patient.
 PMID: 16632914       2006       Japanese journal of infectious diseases
Abstract: In plasma HIV-1 RNA, D67N, K70R, T215Y, and Y188L were present in the reverse transcriptase (RT) region, and two primary mutations, I84V and L90M, were noted in the protease (Pro) region.


  Analysis of HIV-1 CRF_01 A/E protease inhibitor resistance: structural determinants for maintaining sensitivity and developing resistance to atazanavir.
 PMID: 16634628       2006       Biochemistry
Abstract: This structure also explains why the I50L and I84V mutations are important in decreasing the binding affinity of atazanavir.



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