literature

HIV mutation literature information.

Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.

PMID: 26695135 2015 BMC bioinformatics

Introduction: L33I is a less commonly occurring mutation with similar effects to L33F, while L33V mutation has not been related to any kind of drug resistance in PI therapy.

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: Clinical isolates previously obtained from the Wayne State University Infectious Disease Clinic in Detroit, MI contain major drug resistance mutations L33F, I47V, I50V, I54M, L76V, V82I/F, and I84F as well as nonpolymorphicaccessory mutations L10V/G, V11I, I13V, K20T/R, L33I/M, K43T, F53L, A71L, T74P, and L89V.

HIV-1 protease inhibitor drug resistance in Kenyan antiretroviral treatment-naive and -experienced injection drug users and non-drug users.

PMID: 26279669 2015 AIDS research and therapy

Discussion: The detection of A71T, G48E/R, I13V, K20I/R, L10I/V, L33F, L63P, T74S, V11I, and V32L minor mutations in this study is, in part, consistent with previous studies that reported K20R, L10I/V, L33F/I, and L63P minor mutations among HIV-positive women attending antenatal clinics in a large HIV treatment study in western Kenya.

Defective hydrophobic sliding mechanism and active site expansion in HIV-1 protease drug resistant variant Gly48Thr/Leu89Met: mechanisms for the loss of saquinavir binding potency.

PMID: 25513833 2015 Biochemistry

Abstract: HIV drug resistance continues to emerge; consequently, there is an urgent need to develop next generation antiretroviral therapeutics.1 Here we report on the structural and kinetic effects of an HIV protease drug resistant variant with the double mutations Gly48Thr and Leu89Met (PRG48T/L89M), without the stabilizing mutations Gln7Lys, Leu33Ile, and Leu63Ile.

Result: Neither structure contains stabilizing mutations Gln7Lys, Leu33Ile, or Leu63Ile.

The role of mutations at codons 32, 47, 54, and 90 in HIV-1 protease flap dynamics.

PMID: 32309558 2014 Discoveries (Craiova, Romania)

Introduction: The DetMDRs also contain previously identified non-polymorphic accessory mutations L10V/G, V11I, I13V, K20T/R, L33F/I/M, K43T, F53L, A71L, T74P, and L89V.

HIV-1 transmitted drug resistance-associated mutations and mutation co-variation in HIV-1 treatment-naive MSM from 2011 to 2013 in Beijing, China.

PMID: 25510523 2014 BMC infectious diseases

Table: L33I

Effects of PRE and POST therapy drug-pressure selected mutations on HIV-1 protease conformational sampling.

PMID: 24983495 2014 FEBS letters

Method: The L63P construct was generated using site-directed mutagenesis kit (Strategene) and made within the subtype B background of a pentamutated protease containing the stabilizing mutations Q7K, L33I, L63I and substitution of native cysteines to alanine: C67A, C95A.

Result: Given the conformational ensemble for L63P resembles that of PRE, results shows that it is not the absence of the stabilizing mutations, namely Q7K, L33I, and L63I that are present in our subtype B constructs but not in PRE/POST, that cause the alteration to the more closed-like state in PRE.

Structures of darunavir-resistant HIV-1 protease mutant reveal atypical binding of darunavir to wide open flaps.

PMID: 24738918 2014 ACS chemical biology

Result: The optimized wild-type PR bears the mutations L33I and L63I shown to significantly restrict autoproteolysis of wild-type PR in addition to Q7K, which exists in PRP51.

Figure: Note that the wild-type PR sequence used for structural comparison includes mutations Q7K, L33I, and L63I to prevent autoproteolysis, and both proteins include C67A and C95A to eliminate potential cysteine-thiol oxidation.

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

Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and

Discussion: Although there was a high frequency (7/39) of PI substitutions (including L33I/F and L90M, which we did not observe) in this subgroup, many patients were on NRTI-sparing dual-PI regimens and it is not possible to assess whether the substitutions observed were selected by atazanavir or by the other PI in the regimen.

Elucidating a relationship between conformational sampling and drug resistance in HIV-1 protease.

PMID: 23566104 2013 Biochemistry

Method: Seven stabilized (Q7K, L33I, L63I) and inactive (D25N) constructs (Bsi) with engineered labeling sites (K55C) were made using the QuikChange site-directed mutagenesis kit by Stratagene: D30N, M36I, A71V, D30N/M36I, D30N/A71V, M36I/A71V, and D30N/M36I/A71V.

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