literature

HIV mutation literature information.

Gag-Protease Sequence Evolution Following Protease Inhibitor Monotherapy Treatment Failure in HIV-1 Viruses Circulating in East Africa.

PMID: 26258548 2015 AIDS research and human retroviruses

Abstract: Before bPI, significant variation in Protease and Gag was observed at positions previously associated with PI exposure and resistance including Gag mutations L449P, S451N, and L453P and Protease K20I an

Introduction: Of particular relevance to this study were mutations associated with resistance to boosted lopinavir: L10I (three subtype A patients), L10V (one subtype A), K20R (five subtype As and 1 subtype C), L33V (one subtype D), L63P (one subtype A, two subtype Cs, and three subtype Ds).

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

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

Method: MDR769 L33F is based on the previously studied multi-drug resistant variant 769, MDR769, which contains the mutations Q7K, L10I, M36V, M46L, I54V, I62V, L63P, A71V, V82T, I84V, L90M.

HIV-1 subtype characteristics of infected persons living in southwestern Greece.

PMID: 26715861 2015 HIV/AIDS (Auckland, N.Z.)

Result: Finally, several polymorphic sites were identified, with L63PSA being the most prevalent (96% of cases).

The Evolving Genotypic Profile of HIV-1 Mutations Related to Antiretroviral Treatment in the North Region of Brazil.

PMID: 26543866 2015 BioMed research international

Result: In contrast, several secondary mutations were found to differ between B and non-B subtypes: L63P (p < 0.001) and A71T (p = 0.021) were higher in subtype B, and M36I (p < 0.001), K20R (p < 0.001), L10V (p = 0.004), L89 M (p < 0.001), and F53L (p = 0.011) were higher in non-B subtypes.

Result: With respect to accessory or secondary mutations, the most frequent were L63P (60.7%), M36I (41.1%), I93L (40.1%), I62V (39%), V77I (35.8%), A71V (24.9%), and L10I (24.7%) (Figure 1(d)).

Discussion: L63P and

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

Abstract: Minor PI mutations including A71T, G48E, G48R, I13V, K20I, K20R, L10I, L10V, L33F, L63P, T74S, V11I, and V32L were detected among the ART-experienced (36.2 vs.

Table: L63P

Discussion: In addition, our results corroborate previous studies showing K20I/M/R, L10I/V, I13V, and L63P minor mutations among

Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.

PMID: 24586665 2014 PloS one

Abstract: Polymorphism mutation sites with mutation rates in the protease region higher than 60.0% were: L63A/P/S/T 89.7%, V77I 82.2%, I72E/M/K/T/V 80.4%, I93L 75.7%, and E35D 72.9%.

Result: The sites with mutation rates higher than 60.0% included: L63A/P/S/T 89.7% (96/107), among which L63P was 70.1% (75/107); V77I 82.2% (88/107); I72E/M/K/T/V 80.4% (86/107), among which I72V was 63.6% (75/107); I93L 75.7%; E35D 72.9%.

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

PMID: 24738918 2014 ACS chemical biology

Method: The PRP51 construct contains 14 mutations (L10I, I15V, K20R, L24I, V32I, L33F, M36I, M46L, I54M, L63P, K70Q, V82I, I84V, and L89M) plus three other mutations Q7K to minimize autoproteolysis and C67A and C95A to prevent cysteine-induced aggregation.

Result: Mutations L63P and K70Q also alter surface si

Natural polymorphisms and unusual mutations in HIV-1 protease with potential antiretroviral resistance: a bioinformatic analysis.

PMID: 24629078 2014 BMC bioinformatics

Result: According to the IAS-USA, the mutations associated with drug resistance, with a p >10%, were L10I, M36I, I62V, L63P, I64V, A71V/T, V77I, L90M, and I93L.

Result: Although the study of mutations in this position has been limited to L63P to assess the effect of mutations that provide non-hydrophobic characteristics, alternative mechanisms could be shown by which HIV-1 PR compensates for pharmacological stressors.

Result: The L63P mutation has a compensatory effect that increases catalytic activity from 110% to 530%; when L63P is

The M50I polymorphic substitution in association with the R263K mutation in HIV-1 subtype B integrase increases drug resistance but does not restore viral replicative fitness.

PMID: 24433497 2014 Retrovirology

Result: Furthermore, the pre-existing polymorphism L63P which emerges during treatment with PIs has been shown to be compensatory when combined with a primary resistance mutation .

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