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 HIV mutation literature information.


  Resistance profile of the HIV-1 maturation inhibitor GSK3532795 in vitro and in a clinical study.
 PMID: 31622432       2019       PloS one
Method: Participants with a history of genotypic/phenotypic drug resistance to protease inhibitors (PIs) or with HIV-1 genotypic drug resistance to PIs at baseline (including D30N, M46I/L, I47V/A, G48V, I50L, I54M/L, Q58E, T74P, L76V, V82A/F/L/T/S, N83D, I84V, N88S, or L90M) were excluded, despite any reported effects of PI resistance or resistance


  Switching to bictegravir/emtricitabine/tenofovir alafenamide maintained HIV-1 RNA suppression in participants with archived antiretroviral resistance including M184V/I.
 PMID: 31430369       2019       The Journal of antimicrobial chemotherapy
Method: Primary PI-R substitutions were D30N, V32I, M46I/L, I47V/A, G48V, I50V/L, I54M/L, Q58E, T74P, L76V, V82A/F/L/S/T, N83D, I84V, N88S and L90M in PR.


  Highly Drug-Resistant HIV-1 Protease Mutant PRS17 Shows Enhanced Binding to Substrate Analogues.
 PMID: 31172041       2019       ACS omega
Abstract: G48V resistance mutation induces curled flap tips in PRS17-D25N structure.
Abstract: The steric hindrance caused by G48V mutation in the flap of PRS17 contributes to altered binding interactions of P3 Arg, P4' norleucine of CA-p2, and P4 and P3' of p2-NC with the addition of new hydrogen bonds and van der Waals contacts.
Result: Also, PR with individual mutations of M46L, G48V, and I54V in the flaps showed worse inhibition constants (Ki) for DRV and saquinavir relative to the wild-type PR.


  Consistent Prediction of Mutation Effect on Drug Binding in HIV-1 Protease Using Alchemical Calculations.
 PMID: 29847122       2018       Journal of chemical theory and computation
Abstract: In this study, we analyze ten different protease-inhibitor complexes carrying major resistance-associated mutations (RAMs) G48V, I50V, and L90M using molecular dynamics simulations.


  Room Temperature Neutron Crystallography of Drug Resistant HIV-1 Protease Uncovers Limitations of X-ray Structural Analysis at 100 K.
 PMID: 28195728       2017       Journal of medicinal chemistry
Introduction: In a few instances, however, drug resistant mutations lead to possible formation of unfavorable interactions, with a stark example of saquinavir-specific substitution G48V.


  Week 48 resistance analysis of Elvitegravir/Cobicistat/Emtricitabine/Tenofovir DF versus Atazanavir + Ritonavir + Emtricitabine/Tenofovir DF in HIV-1 infected women (WAVES study GS-US-236-0128).
 PMID: 28891788       2017       HIV clinical trials
Method: Primary PI-R substitutions assessed were D30N, V32I, L33F, M46I/L, I47A/V, G48V, I50L/V, I54L/M, Q58E, T74P, L76V, V82A/F/L/S/T, I84V, N88S, and L90M in PR.


  Antiviral Activity of Bictegravir (GS-9883), a Novel Potent HIV-1 Integrase Strand Transfer Inhibitor with an Improved Resistance Profile.
 PMID: 27645238       2016       Antimicrobial agents and chemotherapy
Method: The protease inhibitor (PI)-resistant mutant viruses encoding mutations in the HIV-1 protease-coding sequence, L10F/M46I/I50V, I84V/L90M, G48V/I54V/V82S, and G48V/V82A/L90M, were produced in electroporated SupT1 cells via homologous recombination.


  The Antiviral Activity of Approved and Novel Drugs against HIV-1 Mutations Evaluated under the Consideration of Dose-Response Curve Slope.
 PMID: 26930645       2016       PloS one
Method: M46I, I54V, V82A, M46IN88S, G48VI54V, M46IV82TI84V, and G48VI54VV82A mutations were introduced into the PR coding region, and K103N, Y181C, K103NY181C, K101Q, K101QY181C, K101QH221Y,  PMID: 27039930       2016       Biochemistry
Abstract: Three of five mutations in PR(S17) correlating with major drug resistance, M46L, G48V, and V82S, and five of 11 natural variations differ from the mutations in two clinically derived extreme mutants, PR20 and PR22 bearing 19 and 22 mutations, respectively.
Result: Mutations in PRS17 associated with resistance to multiple drugs are M46L, G48V, I54V, V82S and L90M.
Result: Similarly SQV binds to PRS17 with ~10-fold poorer affinity relative to PR20, possibly also reflecting effects of SQV resi


  Structural Studies of a Rationally Selected Multi-Drug Resistant HIV-1 Protease Reveal Synergistic Effect of Distal Mutations on Flap Dynamics.
 PMID: 27992544       2016       PloS one
Result: G48V is also a minor mutation for atazanavir.
Result: Comparison of the inhibitor-free PRS17 structure with wild-type PR open form (2PC0) shows that the tip of the flaps in PRS17 is twisted from residues G48V to Gly52 (Fig 4B).
Result: Conformational changes associated with mutation cluster of M46L, G48V and I54V are illustrated in Fig 4.



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