ArticlePLoS computational biology2010
Treatment-mediated alterations in HIV fitness preserve CD4+ T cell counts but have minimal effects on viral load.
Article in PLoS computational biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 25 citations in OpenAlex.
- Understanding early HIV-1 rebound dynamics following antiretroviral therapy interruption: The importance of effector cell expansion.PLoS pathogens · 2024Article
- Understanding early HIV-1 rebound dynamics following antiretroviral therapy interruption: The importance of effector cell expansion.bioRxiv : the preprint server for biology · 2024Article
- Modeling resistance to the broadly neutralizing antibody PGT121 in people living with HIV-1.PLoS computational biology · 2024Article
- Mechanistic basis of post-treatment control of SIV after anti-α4β7 antibody therapy.PLoS computational biology · 2021Article
- Estimation of the HIV-1 backward mutation rate from transmitted drug-resistant strains.Theoretical population biology · 2016Article
- Residual Viremia in Treated HIV+ Individuals.PLoS computational biology · 2016Article
- Recombination Enhances HIV-1 Envelope Diversity by Facilitating the Survival of Latent Genomic Fragments in the Plasma Virus Population.PLoS computational biology · 2015Article
- Post-treatment control of HIV infection.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Estimating HIV-1 fitness characteristics from cross-sectional genotype data.PLoS computational biology · 2014Article
- The majority of CD4+ T-cell depletion during acute simian-human immunodeficiency virus SHIV89.6P infection occurs in uninfected cells.Journal of virology · 2014Article
- The role of backward mutations on the within-host dynamics of HIV-1.Journal of mathematical biology · 2013Article
- Modeling the within-host dynamics of HIV infection.BMC biology · 2013Review
- Replication-independent expression of anti-apoptosis marker genes in human peripheral blood mononuclear cells infected with the wild-type HIV-1 and reverse transcriptase variants.Viral immunology · 2012Article
- Article
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 5 institutions in 1 country.
Funding
Abstract
For most HIV-infected patients, antiretroviral therapy controls viral replication. However, in some patients drug resistance can cause therapy to fail. Nonetheless, continued therapy with a failing regimen can preserve or even lead to increases in CD4+ T cell counts. To understand the biological basis of these observations, we used mathematical models to explain observations made in patients with drug-resistant HIV treated with enfuvirtide (ENF/T-20), an HIV-1 fusion inhibitor. Due to resistance emergence, ENF was removed from the drug regimen, drug-sensitive virus regrown, and ENF was re-administered. We used our model to study the dynamics of plasma-viral RNA and CD4+ T cell levels, and the competition between drug-sensitive and resistant viruses during therapy interruption and re-administration. Focusing on resistant viruses carrying the V38A mutation in gp41, we found ENF-resistant virus to be 17±3% less fit than ENF-sensitive virus in the absence of the drug, and that the loss of resistant virus during therapy interruption was primarily due to this fitness cost. Using viral dynamic parameters estimated from these patients, we show that although re-administration of ENF cannot suppress viral load, it can, in the presence of resistant virus, increase CD4+ T cell counts, which should yield clinical benefits. This study provides a framework to investigate HIV and T cell dynamics in patients who develop drug resistance to other antiretroviral agents and may help to develop more effective strategies for treatment.
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.