HIV mutation literature information.


  Effects of drug-resistant mutations on the dynamic properties of HIV-1 protease and inhibition by Amprenavir and Darunavir.
 PMID: 26012849       2015       Scientific reports
Introduction: Kinetic experiments show that the L90M, G48V, and L90M/G48V variants could reduce the binding affinity of inhibitors, which is caused by an increase in dissociation rates.


  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
Result: Three subjects harboured major protease mutations (V32I, M46I, I47V, L90M), selected in prior failures.
Table: L90M


  Treatment-Emergent Mutations and Resistance in HIV-Infected Children Treated with Fosamprenavir-Containing Antiretroviral Regimens.
 PMID: 26157536       2015       The open AIDS journal
Discussion: This patient's virus had the major PI mutations M46L, V82A and L90M at baseline, and the I54L mutation emerged during therapy.


  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
Result: Although major PI resistance mutations was not detected in the non-drug users, three major PI resistance mutations including L90M, M46I and D30N were detected in 4 (5.1 %) IDUs.
Result: Interestingly, mutation L90M co-existed with K20R minor mutation in 1 (2.1 %) ART-experienced IDU, while D30N co-existed with T74S+K20R minor mutations in 1 (3.1 %) ART-naive IDU.
Discussion: Importantly, phenotypic and/or clinical evidence indicate that D30N mutation confers high-level resistance to nelfinavir; L90M imparts resistance to nelfinavir, sequinavir, indinavir, and lopin


  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 Drug Resistance Mutations: Potential Applications for Point-of-Care Genotypic Resistance Testing.
 PMID: 26717411       2015       PloS one
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.
Table: L90M


  Development of Nevirapine Resistance in Children Exposed to the Prevention of Mother-to-Child HIV-1 Transmission Programme in Maputo, Mozambique.
 PMID: 26161559       2015       PloS one
Result: PI resistance mutations were M46I (n = 5, 62.5%) and Q58E (n = 1, 12.5%), L90M (n = 2, 25.0%) (Fig 1).


  HIV-1 subtype characteristics of infected persons living in southwestern Greece.
 PMID: 26715861       2015       HIV/AIDS (Auckland, N.Z.)
Result: The 22 cases experiencing virologic failure presented with the following DRMs: M46I, F53LY, I54LTV, G73ST, L76V, V82AT, I84V, I185V, N88D, and L90M for PIs; L100I, K103NS, V179F Y181C, G190AS, V106A, K103N, and P225H for NNRTIs; and


  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: L23I, D30N, E35G, M46I/L/V, G48V, I54L, G73S/T/C/A, T74S, V82A/F/S/T, I84V, N88D/S and L90M are other mutations correlated to NFV resistance.
Introduction: The other mutations which were co-occurring with DBM and TPM included major mutations like- M46IL, I54MV, I84V, L90M, N88S, V32I,  PMID: 26633459       2015       Viruses
Result: L90M exerts little or no effect on the susceptibility to tipranavir in HIV-1 isolates, while I54M was associated with a reduced susceptibility to the inhibitor.
Result: Further statistical analysis was also performed to complete the linear correlation analysis of data showing non-normal distribution, which revealed that there are no significant differences between the values determined by the different assays (p > 0.05) (wild-type: z = 1.35 and p = 0.22; I54M/L90M mutant: z = 0.51 and p = 0.69).
Result: Introduction of the double mutation I54M and L90M greatly decreased the efficacy of the inhibitors, with the exception of tipranavir, which remained indifferent to the mutations.



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