ArticleJournal of virology2009
Selective-advantage profile of human immunodeficiency virus type 1 integrase mutants explains in vivo evolution of raltegravir resistance genotypes.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed.
- Efficacy and safety of raltegravir for treatment of HIV for 5 years in the BENCHMRK studies: final results of two randomised, placebo-controlled trials.The Lancet. Infectious diseases · 2013Trial
- Analysis of low-frequency mutations associated with drug resistance to raltegravir before antiretroviral treatment.Antimicrobial agents and chemotherapy · 2011Trial
- Review
- Structural Biology of HIV Integrase Strand Transfer Inhibitors.Trends in pharmacological sciences · 2020Review
- Raltegravir-Induced Adaptations of the HIV-1 Integrase: Analysis of Structure, Variability, and Mutation Co-occurrence.Frontiers in microbiology · 2019Article
- Impact of the HIV-1 genetic background and HIV-1 population size on the evolution of raltegravir resistance.Retrovirology · 2018Article
- Usefulness of Integrase resistance testing in proviral HIV-1 DNA in patients with Raltegravir prior failure.BMC infectious diseases · 2016Observational
- Drug Susceptibility and Viral Fitness of HIV-1 with Integrase Strand Transfer Inhibitor Resistance Substitution Q148R or N155H in Combination with Nucleoside/Nucleotide Reverse Transcriptase Inhibitor Resistance Substitutions.Antimicrobial agents and chemotherapy · 2016Article
- Different Pathways Leading to Integrase Inhibitors Resistance.Frontiers in microbiology · 2016Review
- Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.Journal of translational medicine · 2015Article
- Integrase inhibitor reversal dynamics indicate unintegrated HIV-1 dna initiate de novo integration.Retrovirology · 2015Article
- Altered viral fitness and drug susceptibility in HIV-1 carrying mutations that confer resistance to nonnucleoside reverse transcriptase and integrase strand transfer inhibitors.Journal of virology · 2014Article
- Efficacy of raltegravir switching strategies in HIV-infected patients with suppressed viraemia according to the genotypic sensitivity score.Infection · 2014Article
- Impact of primary elvitegravir resistance-associated mutations in HIV-1 integrase on drug susceptibility and viral replication fitness.Antimicrobial agents and chemotherapy · 2013Article
- Quantitative prediction of integrase inhibitor resistance from genotype through consensus linear regression modeling.Virology journal · 2013Article
- Article
- HIV integrase inhibitors: 20-year landmark and challenges.Advances in pharmacology (San Diego, Calif.) · 2013Review
- Substitutions at amino acid positions 143, 148, and 155 of HIV-1 integrase define distinct genetic barriers to raltegravir resistance in vivo.Journal of virology · 2012Article
- HIV-1 antiretroviral drug therapy.Cold Spring Harbor perspectives in medicine · 2012Review
- Raltegravir in HIV-1 infection: Safety and Efficacy in Treatment-naïve Patients.Clinical medicine reviews in therapeutics · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The emergence of human immunodeficiency virus type 1 resistance to raltegravir, an integrase strand transfer inhibitor, follows distinct and independent genetic pathways, among which the N155H and Q148HKR pathways are the most frequently encountered in treated patients. After prolonged viral escape, mutants of the N155H pathway are replaced by mutants of the Q148HKR pathway. We have examined the mechanisms driving this evolutionary pattern using an approach that assesses the selective advantage of site-directed mutant viruses as a function of drug concentration. These selective-advantage curves revealed that among single mutants, N155H had the highest and the widest (1 to 500 nM) selective-advantage profile. Despite the higher 50% inhibitory concentration, Q148H displayed a lower and narrower (10 to 100 nM) selective-advantage profile. Among double mutants, the highest and widest selective-advantage profile was seen with G140S+Q148H. This finding likely explains why N155H can be selected early in the course of RAL resistance evolution in vivo but is later replaced by genotypes that include Q148HKR.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.