ArticleMathematical biosciences2009
Asymmetric division of activated latently infected cells may explain the decay kinetics of the HIV-1 latent reservoir and intermittent viral blips.
Article in Mathematical biosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Monitoring of HIV type 1 DNA load and drug resistance in peripheral blood mononuclear cells during suppressive antiretroviral therapy does not predict virologic failure.AIDS research and human retroviruses · 2012Trial
- Quantifying the treatment efficacy of reverse transcriptase inhibitors: new analyses of clinical data based on within-host modeling.BMC public health · 2009Trial
- AZD5582 robustly reactivates latently infected cells and clears the majority of those reactivated from the SIV reservoir.bioRxiv : the preprint server for biology · 2026Article
- Modeling the Interplay Between Viral and Immune Dynamics in HIV: A Review and Mrgsolve Implementation and Exploration.Clinical and translational science · 2025Review
- Understanding early HIV-1 rebound dynamics following antiretroviral therapy interruption: The importance of effector cell expansion.PLoS pathogens · 2024Article
- Modeling dynamics of acute HIV infection incorporating density-dependent cell death and multiplicity of infection.PLoS computational biology · 2024Article
- Understanding early HIV-1 rebound dynamics following antiretroviral therapy interruption: The importance of effector cell expansion.bioRxiv : the preprint server for biology · 2024Article
- A delay model for persistent viral infections in replicating cells.Journal of mathematical biology · 2021Article
- Dynamics of a new HIV model with the activation status of infected cells.Journal of mathematical biology · 2021Article
- Modeling the role of macrophages in HIV persistence during antiretroviral therapy.Journal of mathematical biology · 2020Article
- Andronov-Hopf and Neimark-Sacker bifurcations in time-delay differential equations and difference equations with applications to models for diseases and animal populations.Advances in difference equations · 2020Article
- Dynamics of an HIV model with cytotoxic T-lymphocyte memory.Advances in difference equations · 2020Article
- Conflict and accord of optimal treatment strategies for HIV infection within and between hosts.Mathematical biosciences · 2019Article
- Duration of SHIV production by infected cells is not exponentially distributed: Implications for estimates of infection parameters and antiviral efficacy.Scientific reports · 2017Article
- Modeling Kick-Kill Strategies toward HIV Cure.Frontiers in immunology · 2017Review
- Backward bifurcations, turning points and rich dynamics in simple disease models.Journal of mathematical biology · 2016Article
- Residual Viremia in Treated HIV+ Individuals.PLoS computational biology · 2016Article
- Modeling the Slow CD4+ T Cell Decline in HIV-Infected Individuals.PLoS computational biology · 2015Article
- Modeling the Effects of Vorinostat In Vivo Reveals both Transient and Delayed HIV Transcriptional Activation and Minimal Killing of Latently Infected Cells.PLoS pathogens · 2015Article
- Global stability of infection-free state and endemic infection state of a modified human immunodeficiency virus infection model.IET systems biology · 2015Article
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2 authors.
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Abstract
Most HIV-infected patients when treated with combination antiretroviral therapy achieve viral loads that are below the current limit of detection of standard assays after a few months. Despite this, virus eradication from the host has not been achieved. Latent, replication-competent HIV-1 can generally be identified in resting memory CD4(+) T cells in patients with "undetectable" viral loads. Turnover of these cells is extremely slow but virus can be released from the latent reservoir quickly upon cessation of therapy. In addition, a number of patients experience transient episodes of viremia, or HIV-1 blips, even with suppression of the viral load to below the limit of detection for many years. The mechanisms underlying the slow decay of the latent reservoir and the occurrence of intermittent viral blips have not been fully elucidated. In this study, we address these two issues by developing a mathematical model that explores a hypothesis about latently infected cell activation. We propose that asymmetric division of latently infected cells upon sporadic antigen encounter may both replenish the latent reservoir and generate intermittent viral blips. Interestingly, we show that occasional replenishment of the latent reservoir induced by reactivation of latently infected cells may reconcile the differences between the divergent estimates of the half-life of the latent reservoir in the literature.
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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.