HIV mutation literature information.


  Tissue culture drug resistance analysis of a novel HIV-1 protease inhibitor termed PL-100 in non-B HIV-1 subtypes.
 PMID: 20541566       2010       Antiviral research
Abstract: One of these involved the V82A and L90M resistance mutations while the other involved a mutation at position T80I, with other mutations being observed at positions M46I/L, I54M, K55R, L76F, P81S and I85V.


  Darunavir: a review of its use in the management of HIV infection in adults.
 PMID: 19323590       2009       Drugs
Abstract: In a 24-week analysis of pooled data from the POWER 1 and 2 studies in treatment-experienced patients, 11 protease mutations associated with a reduced response to boosted darunavir were identified (V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V and L89V).


  Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
 PMID: 18992847       2009       Infection, genetics and evolution
Method: Mutations L10F/I/R/V, K20M/R, L24I, L33F, M36I, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73C/S/T/A, V77I and N88D/S were considered as minor resistance mutations and were also analyzed separately and together as a group.
Result: The major protease mutations V32I and I47V/A and the minor mutations L10R, I54M, and  PMID: 19143530       2009       Clinical infectious diseases
Result: Because patients in our cohort were exclusively treated with indinavir during the study, we focused on HIV-2 PR mutations K7R, I54M, V62A, I82F, L90M, and L99F, which have been associated with phenotypic PI resistance to indinavir in previous, albeit limited, studies.
Result: Eight of 23 patients had virus strains with PI mutations (K7R, I54M, V62A, I82F, L90M, and L99F) suggestive of indinavir resistance; 4 of these patients had virus strains that harbored multiple


  Mutations associated with virological response to darunavir/ritonavir in HIV-1-infected protease inhibitor-experienced patients.
 PMID: 19147519       2009       The Journal of antimicrobial chemotherapy
Abstract: CONCLUSIONS: Among the eight mutations with a negative impact on the virological response, I47V, I54M, T74P and I84V were previously described as darunavir resistance-associated mutations.
Abstract: Cochran-Armitage procedure identified eight mutations with a negative impact on the virological response, namely K14R, K20I, E34Q, I47V, I54M, K55R, T74P and I84V; and two mutations (E35D and V82A) with a positive impact.


  Role of atazanavir in the treatment of HIV infection.
 PMID: 19436623       2009       Therapeutics and clinical risk management
Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and


  Evolution and predictors of HIV type-1 drug resistance in patients failing combination antiretroviral therapy in Italy.
 PMID: 19474470       2009       Antiviral therapy
Abstract: There was an increase of type-1 thymidine analogue and of protease mutations L33F, I47A/V, I50V and I54L/M, whereas L90M decreased over calendar years.


  Clinical validation and applicability of different tipranavir/ritonavir genotypic scores in HIV-1 protease inhibitor-experienced patients.
 PMID: 19601778       2009       Current HIV research
Abstract: The following variables were significantly associated (p<0.05) to failure with multivariate analysis: WS, log peak of HIV-RNA, IAS mutations: L33F, I54AMV, Q58E, and non-IAS mutation: N37DES.


  Structural basis for the resilience of Darunavir (TMC114) resistance major flap mutations of HIV-1 protease.
 PMID: 20640812       2009       Interdisciplinary sciences, computational life sciences
Abstract: Good affinity of Darunavir accounts for the additive effects of well accommodation at binding site, good ligand-receptor electrostatic and van der waals energy while, the low susceptibility to I50V and I54M can be rationalized in terms of flexibility in the binding site residues that do not permit drug accommodation to the binding site distortions created by the mutation.
Abstract: Our research indicates that the observed effectiveness of Darunavir against the wild type HIV-1 protease is due to an extremely high affinity towards the wild-type and a relatively mild effect to the I50V and I54M mutations is due to low affinity towards the inhibitor.
Abstract: The major flap mutations I50V and I54M lower the binding affinity of Darunavir b


  Factors associated with the selection of mutations conferring resistance to protease inhibitors (PIs) in PI-experienced patients displaying treatment failure on darunavir.
 PMID: 18039922       2008       Antimicrobial agents and chemotherapy
Abstract: The most common mutations that emerged at rebound included V32I (44%), I54M/L (24%), L33F (25%), I84V (21%), and L89V (12%).



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