ViMRT
}  
 
Home   
< Docs   

 HIV mutation literature information.


  Differential Flap Dynamics in Wild-type and a Drug Resistant Variant of HIV-1 Protease Revealed by Molecular Dynamics and NMR Relaxation.
 PMID: 23144597       2012       Journal of chemical theory and computation
Introduction: Flap+ is a multi-drug-resistant HIV-1 protease variant with a combination of flap and active site mutations (L10I, G48V, I54V, and V82A) that occur simultaneously in sequences of patients undergoing drug therapy (Figure 1).
Method: As described above, Flap+ contains additional mutations of L10I, G48V, I54V, and V82A, and was expressed and purified similar to that of the WT.
Method: The initial coordinates of the Flap+ variant were also from 1HHP and 2HB4, with the mutations (L10I, G48V, I54V, and V82A) modeled in using geomet


  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


  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


  Correlation between resistance profile and immunosuppression in heavily treated HIV-1 infected Romanian patients.
 PMID: 22180722       2011       Romanian biotechnological letters
Abstract: A significantly higher total number of mutations were encountered in severely immunosuppressed patients, who presented also major mutations in the protease gene (V82A, I54V, G48V) and the major M184V mutation associated with type 2 thymidine analogs mutations in reverstranscriptase gene.CONCLUSION: A good immune status seems to be associated with a low range of mutations, indicating the impact of immune restoration or preservation on the therapeutic success rate.
Result: Five out of the 21 patients with severe immunosuppression harbored major PI mutations V82A, I54V, and G48V associated with phenotypic resistance to ritonavir.


  The new and less toxic protease inhibitor saquinavir-NO maintains anti-HIV-1 properties in vitro indistinguishable from those of the parental compound saquinavir.
 PMID: 21763726       2011       Antiviral research
Abstract: The following recombinant viruses were generated and tested: L33F, M46I, G48V, I54V, I84V + L90M, M46I + L90M, G48V + L90M, M46I + I54V + L90M, L33F + M46I + L90M.


  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).


  Influence of major HIV-1 protease inhibitor resistance mutations on CTL recognition.
 PMID: 21107269       2011       Journal of acquired immune deficiency syndromes (1999)
Abstract: CONCLUSIONS: PI mutations, G48V, M46I, and I47A, can abrogate CTL recognition, indicating potential interactions between development of drug resistance and CTL response.
Abstract: RESULTS: G48V abolished KF9 recognition by CTL in all 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).


  Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
 PMID: 21297946       2011       PloS one
Method: The final list of mutations included M41L, E44D, D67N, T69D, K70R, L74V, L100I, K103N, V108I, V118I, Y181C, M184V, G190A, L210W, T215F, T215Y and K219Q in RT; and L33F, L33I, M46I, M46L, G48V, <


  Human immunodeficiency virus type 1 protease inhibitor drug-resistant mutants give discordant results when compared in single-cycle and multiple-cycle fitness assays.
 PMID: 20826651       2010       Journal of clinical microbiology
Abstract: Five protease mutants showed statistically different fitness values by the MCA versus the SCA: the D30N, G48V, I50V, I54L, and I54M mutants.


  Revealing the drug resistance mechanism of saquinavir due to G48V and V82F mutations in subtype CRF01_AE HIV-1 protease: molecular dynamics simulation and binding free energy calculations.
 PMID: 20471372       2010       Biochemical and biophysical research communications
Abstract: Recently, G48V mutation is found to co-exist with the mutation C95F in AIDS patients treated with saquinavir.
Abstract: The mutation G48V in HIV-1 protease is a major resistance mutation against the drug saquinavir.
Abstract: The present structure also provides a rationale for the clinical observation that the resistance mutations C95F/G48V/V82A occur as a cluster in AIDS patients.



Browser Board

 Co-occurred Entities




   Filtrator