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
Development of Nevirapine Resistance in Children Exposed to the Prevention of Mother-to-Child HIV-1 Transmission Programme in Maputo, Mozambique.
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.
Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.
Single Genome Analysis for the Detection of Linked Multiclass Drug Resistance Mutations in HIV-1-Infected Children After Failure of Protease Inhibitor-Based First-Line Therapy.
PMID: 25923117
2015
Journal of acquired immune deficiency syndromes (1999)
Discussion: Age adjusted full-dose RTV can select M46I, I54V, and V82A in children, as well as L10F, M46L, and Q58E in adults.
Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.
Abstract: Three patients (5%) had major protease inhibitor (PI) resistance mutations: all three had the V82A mutation, and one patient (Clade J virus) had a concurrent M46I, Q58E, and L76V DRM.
Result: V82A was detected in all three patients, with concurrent M46I, Q58E, and L76V in one of the three patients harboring the clade J HIV-1 virus.
Cobicistat-boosted darunavir in HIV-1-infected adults: week 48 results of a Phase IIIb, open-label single-arm trial.
Result: At baseline, one or more primary PI RAMs were found in 10 patients (3%; nine treatment-naive, and one treatment-experienced), most commonly M46I/L (three treatment-naive and one treatment-experienced) and Q58E (four treatment-naive).
Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.
Result: Q58E led to TPV/r potential low-level resistance, with a resistance rate of 1.9% (2/107).
Result: The mutation positions were A71T, L10I, A71V, and Q58E, with A71T and L10I happening simultaneously, leading to NFV potential low resistance.
Table: Q58E
Discussion: Results from the HIV-1 drug resistance mutation research by the International AIDS Society-USA (updated in March 2013) have revealed that PI resistance mutation sites are L10I, K20M, V32I, M36I, PMID: 24629078
2014
BMC bioinformatics
Result: We modelled the proteins with unusual mutations (L5F, D29V, L63G, L63R, P79L and T91V), natural polymorphisms (L63H andL63S), and drug-resistant mutant PRs with single mutations or patterns of mutations (D30N, V32I, M36I, M46I, I47V, G48V, I50V, I50L, I54M, Q58E, T74P, L76V, V82A
A uniquely prevalent nonnucleoside reverse transcriptase inhibitor resistance mutation in Russian subtype A HIV-1 viruses.
Result: Of the 243 patients who received one or more protease inhibitors, 32 (13%) had a study-defined protease inhibitor-resistance mutation most commonly L10F, K20T, V32I, L33F, M46I/L, I47V/A, I50L, F53L, I54V/L, Q58E, L76V, V82A/C, I84V, L89V, and L90M.