Comparison of genotypic and virtual phenotypic drug resistance interpretations with laboratory-based phenotypes among CRF01_AE and subtype B HIV-infected individuals.
Abstract: PRS17 has none of the major mutations (I47V, I50V, I54ML, L76V and I84V) associated with darunavir resistance, but has 10,000-fold weaker binding affinity relative to the wild type PR.
Abstract: Comparable binding affinity of 8000-fold weaker than PR is seen for drug resistant mutant PR20, which bears 3 mutations associated with major resistance to darunavir (I47V, I54L and I84V).
Result: Despite the presence of a large number of mutations, PRS17 shares only one mutation (L90M) and a si
Binding of Clinical Inhibitors to a Model Precursor of a Rationally Selected Multidrug Resistant HIV-1 Protease Is Significantly Weaker Than That to the Released Mature Enzyme.
Result: I54L (in PR20) and I54V (in PRS17) are major mutations associated with high-level resistance to most PIs, with the possible exception of DRV (for I54V).
Result: Although PR20 bears major DRV resistance mutations V32I, I47V, I54L, there are no corresponding mutations in PRS17 to explain the similar Ki values shown by these 2 enzymes.
Result: In contrast, mutations D30N, V32I, L33F, I47V, I54L, and
Unique Flap Conformation in an HIV-1 Protease with High-Level Darunavir Resistance.
Introduction: The latest International AIDS Society (IAS)-USA panel list shows 11 mutations associated with DRV resistance: V11I, V32I, L33F, I47V, I50V, I54M/L, T74P, L76V, I84V, and L89V (Wensing et al.,).
The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.
PMID: 29124158
2015
Biochemistry and biophysics reports
Introduction: L33F was initially identified as an accessory mutation to I54L/M, V32I+I47V, and I84V/I but is now recognized as a nonpolymorphic major drug resistance mutation.
Treatment-Emergent Mutations and Resistance in HIV-Infected Children Treated with Fosamprenavir-Containing Antiretroviral Regimens.
Result: The major PI treatment-emergent mutations selected at VF in virus from Patient-1 included M46M/L, I50I/V, I54I/L, and Q58Q/E, while virus from Patient-2 selected the V82V/A mutation.
Discussion: This patient's virus had the major PI mutations M46L, V82A and L90M at baseline, and the I54L mutation emerged during therapy.
Assessing transmissibility of HIV-1 drug resistance mutations from treated and from drug-naive individuals.
Discussion: We show here that D30N, N88D/S and L90 M also have high transmissibility and that other SDRMs have higher (M41L, T215Rev and K219E/N/Q/R for NRTIs and K101E/P for the NNRTIs) or lower transmissibility (K70E/R, L74I/V, and T215Y/F for NRTIs; Y181C/I/V for NNRTIs and I84 V and I54A/L/M/S/T/V for protease inhibit
Conformational variation of an extreme drug resistant mutant of HIV protease.
PMID: 26397743
2015
Journal of molecular graphics & modelling
Method: Plasmid DNA encoding PR (subtype B of group M) with 20 mutations Q7K; L10F; I13V; I15V; D30N; V32I; L33F; E35D; M36I; S37N; I47V; I54L; Q58E; I62V; L63P; A71V; I84V; N88D; L89T and L90M (termed PR20) cloned between the Nde1 and BamH1 sites
HIV-1 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.
Result: The remaining 8% of viruses with predicted intermediate or high-level LPV resistance had a combination of two or more PI DRMs with lower mutation scores, including V32I, M46I, I54M/L/V, I47V, V82S/T/M and L90M.
HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.
HIV mutation literature information.
PMID: 
2016
Journal of medical virology
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