literature

HIV mutation literature information.

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.

PMID: 27039930 2016 Biochemistry

Result: Only five of the mutations in PR22 are identical with those in PRS17, namely, E35D, M36I, S37D, I54V, and L90M.

Result: Other mutations in this region, E35D and M36I in both mutants, and S37D in PRS17, are located in the flap hinge loop and likely contribute to altered flap conformation and dynamics.

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

Abstract: In PRS17, the hinge loop cluster of mutations, E35D, M36I and S37D, contributes to the altered flap dynamics by a mechanism similar to that of PR20.

Result: Comparison of PRS17/DRV with PR20/DRV complex, which has E35D, M36I, S37N and I62V mutations, reveals that the hinge loop conformation of PR20 in subunit A is similar to PRS17 except for absence of the K20R mutation and consequent absence of the ion pair interactions observed between Arg20 and Asp35 in

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

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

Abstract: Protease substitutions I13V, E35D, M36I, R57K, H69K, and L89M, which serve as drug-resistance support mutations in subtype B, were present in the majority of subtype-A1 sequences of the population.

Result: Specifically, the E35D and M36I substitutions were present in 100% of cases, followed by substitutions H69K (99%), I13V (96%), L89M (95%), and R57K (93%), indicating that these sequence alterations may occur as genetic signatures in subtype A1.

Result: This involved six protease amino acid su

Viral Genetic Diversity and Polymorphisms in a Cohort of HIV-1-Infected Patients Eligible for Initiation of Antiretroviral Therapy in Abuja, Nigeria.

PMID: 25582324 2015 AIDS research and human retroviruses

Abstract: Eleven polymorphic mutations (G16E, K20I, L23P, E35D, M36I, N37D/S/T, R57K, L63P, and V82I) were detected in the PR that were subtype or CRF specific while only three mutations (D123N, I135T, and I135V) were identified in the RT.

Result: Of the 271 sequences analyzed, 11 polymorphic mutations (G16E, K20I, L23P, E35D, M36I

Mutations in the reverse transcriptase and protease genes of human immunodeficiency virus-1 from antiretroviral naive and treated pediatric patients.

PMID: 25674767 2015 Viruses

Table: E35D

Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.

PMID: 26107265 2015 PloS one

Table: E35D

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

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: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I, I47V, V82AS, D30N, G48V; and accompanied by minor mutations like- L10I, I13V, L63P, A71V, L89M, I93L, E35DN, I15V, D60E, L24I etc.

Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.

PMID: 25575025 2014 Retrovirology

Table: E35D

HIV-1 diversity, transmission dynamics and primary drug resistance in Angola.

PMID: 25479241 2014 PloS one

Result: Similar findings were obtained for K14R, E35D and R57K in subtype A and for L89M in subtype G.