ArticleAntimicrobial agents and chemotherapy2010
Stage-dependent inhibition of HIV-1 replication by antiretroviral drugs in cell culture.
Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- HIV viral kinetics and T cell dynamics in antiretroviral naïve persons starting an integrase strand transfer inhibitor and protease inhibitor regimen.HIV clinical trials · 2017Trial
- Modelling the impact of initiation delay, duration and prior PrEP on the efficacy of post-exposure prophylaxis containing a tenofovir/emtricitabine backbone.Journal of the International AIDS Society · 2025Article
- HIV-1 Integrase T218I/S Polymorphisms Do Not Reduce HIV-1 Integrase Inhibitors' Phenotypic Susceptibility.AIDS research and human retroviruses · 2025Article
- Two Disaccharide-Bearing Polyethers, K-41B and K-41Bm, Potently Inhibit HIV-1 via Mechanisms Different from That of Their Precursor Polyether, K-41A.Current issues in molecular biology · 2024Article
- Direct translation of incoming retroviral genomes.Nature communications · 2024Article
- TraFo-CRISPR: Enhanced Genome Engineering by Transient Foamy Virus Vector-Mediated Delivery of CRISPR/Cas9 Components.Molecular therapy. Nucleic acids · 2019Article
- The R263K Dolutegravir Resistance-Associated Substitution Progressively Decreases HIV-1 Integration.mBio · 2017Article
- Efficient Inhibition of Hepatitis B Virus Infection by a preS1-binding Peptide.Scientific reports · 2016Article
- SUN2 Overexpression Deforms Nuclear Shape and Inhibits HIV.Journal of virology · 2016Article
- Kinetics of lentiviral vector transduction in human CD34(+) cells.Experimental hematology · 2016Article
- Single-Cell and Single-Cycle Analysis of HIV-1 Replication.PLoS pathogens · 2015Article
- A cell-based strategy to assess intrinsic inhibition efficiencies of HIV-1 reverse transcriptase inhibitors.Antimicrobial agents and chemotherapy · 2015Article
- A comparison of elasticities of viral levels to specific immune response mechanisms in human immunodeficiency virus infection.BMC research notes · 2014Article
- Latent HIV-1 can be reactivated by cellular superinfection in a Tat-dependent manner, which can lead to the emergence of multidrug-resistant recombinant viruses.Journal of virology · 2013Article
- Automethylation of protein arginine methyltransferase 6 (PRMT6) regulates its stability and its anti-HIV-1 activity.Retrovirology · 2013Article
- HIV Drug Resistance and the Advent of Integrase Inhibitors.Current infectious disease reports · 2013Article
- Explaining the determinants of first phase HIV decay dynamics through the effects of stage-dependent drug action.PLoS computational biology · 2013Article
- Article
- Maraviroc and other HIV-1 entry inhibitors exhibit a class-specific redistribution effect that results in increased extracellular viral load.Antimicrobial agents and chemotherapy · 2012Article
- Saquinavir inhibits early events associated with establishment of HIV-1 infection: potential role for protease inhibitors in prevention.Antimicrobial agents and chemotherapy · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recent clinical trials have shown that the use of the HIV-1 integrase (IN) inhibitor raltegravir (RAL) results in drops in the viral load that are more rapid than those achieved by use of the reverse transcriptase (RT) inhibitor efavirenz. Previously, mathematical modeling of viral load decay that takes into account the stage of viral replication targeted by a drug has yielded data that closely approximate the clinical trial results. This model predicts greater inhibition of viral replication by drugs that act later in the viral replication cycle. In the present study, we have added drugs that target entry, reverse transcription, integration, or proteolytic processing to acutely infected cells and have shown modest viral inhibition by entry inhibitors, intermediate levels of inhibition by RT and IN inhibitors, and high levels of inhibition by protease inhibitors relative to the levels of growth for the no-drug controls. When dual or triple combinations of these drugs were added to acutely infected cells, we found that the levels of inhibition achieved by any given combination were comparable to those achieved by the latest-acting drug in the combination. In single-round infections in which the kinetics of reverse transcription and integration had been determined by quantitative PCR, addition of IN inhibitors at various times postinfection resulted in levels of inhibition equal to or greater than those achieved by addition of RT inhibitors. Collectively, our data provide in vitro evidence of the stage-dependent inhibition of HIV-1 by clinically relevant drugs. We discuss how stage-dependent inhibition helps to explain the unique viral load decay dynamics observed clinically with RAL.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.