ArticleAntimicrobial agents and chemotherapy2008
Factors associated with the selection of mutations conferring resistance to protease inhibitors (PIs) in PI-experienced patients displaying treatment failure on darunavir.
Article in Antimicrobial agents and chemotherapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- An Enzymatic Route to the Synthesis of Tricyclic Fused Hexahydrofuranofuran P2-Ligand for a Series of Highly Potent HIV-1 Protease Inhibitors.Tetrahedron letters · 2024Article
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- Structure-Based Design of Highly Potent HIV-1 Protease Inhibitors Containing New Tricyclic Ring P2-Ligands: Design, Synthesis, Biological, and X-ray Structural Studies.Journal of medicinal chemistry · 2020Article
- Molecular Determinants of Epistasis in HIV-1 Protease: Elucidating the Interdependence of L89V and L90M Mutations in Resistance.Biochemistry · 2019Article
- Novel Protease Inhibitors Containing C-5-ModifiedAntimicrobial agents and chemotherapy · 2019Article
- Article
- Evaluation of novel protease inhibitors against darunavir-resistant variants of HIV type 1.FEBS open bio · 2017Article
- The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.Biochemistry and biophysics reports · 2015Article
- The role of mutations at codons 32, 47, 54, and 90 in HIV-1 protease flap dynamics.Discoveries (Craiova, Romania) · 2014Article
- Description of the L76V resistance protease mutation in HIV-1 B and "non-B" subtypes.PloS one · 2013Article
- Genotypic resistance profiles associated with virological failure to darunavir-containing regimens: a cross-sectional analysis.Infection · 2012Article
- Prevalence, mutation patterns, and effects on protease inhibitor susceptibility of the L76V mutation in HIV-1 protease.Antimicrobial agents and chemotherapy · 2010Article
- In vitro selection of highly darunavir-resistant and replication-competent HIV-1 variants by using a mixture of clinical HIV-1 isolates resistant to multiple conventional protease inhibitors.Journal of virology · 2010Article
- Computational mutation scanning and drug resistance mechanisms of HIV-1 protease inhibitors.The journal of physical chemistry. B · 2010Article
- Managing treatment-experienced pediatric and adolescent HIV patients: role of darunavir.Therapeutics and clinical risk management · 2009Article
- Both a protective and a deleterious role for the L76V mutation.Antimicrobial agents and chemotherapy · 2009Article
- Review
- Effect of flap mutations on structure of HIV-1 protease and inhibition by saquinavir and darunavir.Journal of molecular biology · 2008Article
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11 authors.
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Abstract
The objective of this study was to characterize the mutations selected by darunavir (DRV) use in protease inhibitor (PI)-experienced patients and the associated factors. We analyzed treatment failure in 54 PI-experienced human immunodeficiency virus (HIV)-infected patients on a DRV- and ritonavir-containing regimen. Viral genotyping was carried out at the baseline, at between 1 and 3 months of treatment, and at between 3 and 6 months of treatment to search for the selection of mutations conferring resistance to PIs. The median baseline HIV RNA level was 4.9 log(10) copies/ml, and the median CD4 count was 87 cells/mm(3). At the baseline, the median numbers of resistance mutations were as follows: 3 DRV resistance mutations, 4 major PI resistance mutations, and 10 minor PI resistance mutations. The most common mutations that emerged at rebound included V32I (44%), I54M/L (24%), L33F (25%), I84V (21%), and L89V (12%). Multivariate analysis showed that higher baseline HIV RNA levels and smaller numbers of nucleoside reverse transcriptase inhibitor simultaneously used with DRV were associated with a higher risk of DRV resistance mutation selection. By contrast, L76V, a known DRV resistance mutation, was found to decrease the risk of selection of another DRV resistance mutation. The occurrence of virological failure while a patient was on DRV was associated with the selection of mutations that increased the level of DRV resistance without affecting susceptibility to tipranavir (TPV). In these PI-treated patients who displayed treatment failure while they were on a DRV-containing regimen, we confirmed the set of emerging mutations associated with DRV failure and identified the factors associated with the selection of these mutations. TPV susceptibility does not seem to be affected by the selection of a DRV resistance mutation.
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