ArticlePLoS medicine2007
Understanding the slow depletion of memory CD4+ T cells in HIV infection.
Article in PLoS medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 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
35 citing papers in PubMed, 71 citations in OpenAlex.
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- TRAIL (DR5) receptor and the modulation of TRAIL pathway in PLWHIV: key mechanisms in the progression of HIV disease.BMC molecular and cell biology · 2025Article
- Review
- Modeling dynamics of acute HIV infection incorporating density-dependent cell death and multiplicity of infection.PLoS computational biology · 2024Article
- Review
- Modeling T Cell Fate.Annual review of immunology · 2023Review
- Microfluidic Devices for HIV Diagnosis and Monitoring at Point-of-Care (POC) Settings.Biosensors · 2022Review
- Impact of HIV-1 CRF55_01B infection on the evolution of CD4 count and plasma HIV RNA load in men who have sex with men prior to antiretroviral therapy.Retrovirology · 2021Article
- Dual Antiretroviral Therapy-All Quiet Beneath the Surface?Frontiers in immunology · 2021Review
- The Rules of Human T Cell FateFrontiers in immunology · 2020Article
- Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System.Frontiers in immunology · 2020Review
- Salp15, a Multifunctional Protein From Tick Saliva With Potential Pharmaceutical Effects.Frontiers in immunology · 2019Review
- Insight into treatment of HIV infection from viral dynamics models.Immunological reviews · 2018Review
- Modeling Kick-Kill Strategies toward HIV Cure.Frontiers in immunology · 2017Review
- Pathophysiology of CD4+ T-Cell Depletion in HIV-1 and HIV-2 Infections.Frontiers in immunology · 2017Review
- Kynurenine Reduces Memory CD4 T-Cell Survival by Interfering with Interleukin-2 Signaling Early during HIV-1 Infection.Journal of virology · 2016Article
- Article
- Modeling the Slow CD4+ T Cell Decline in HIV-Infected Individuals.PLoS computational biology · 2015Article
- A non-synonymous polymorphism in IL-23R Gene (rs1884444) is associated with reduced risk to schistosomiasis-associated Immune Reconstitution Inflammatory Syndrome in a Kenyan population.BMC infectious diseases · 2014Article
- Computational study to determine when to initiate and alternate therapy in HIV infection.BioMed research international · 2014Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe asymptomatic phase of HIV infection is characterised by a slow decline of peripheral blood CD4(+) T cells. Why this decline is slow is not understood. One potential explanation is that the low average rate of homeostatic proliferation or immune activation dictates the pace of a "runaway" decline of memory CD4(+) T cells, in which activation drives infection, higher viral loads, more recruitment of cells into an activated state, and further infection events. We explore this hypothesis using mathematical models. METHODS AND
findingsUsing simple mathematical models of the dynamics of T cell homeostasis and proliferation, we find that this mechanism fails to explain the time scale of CD4(+) memory T cell loss. Instead it predicts the rapid attainment of a stable set point, so other mechanisms must be invoked to explain the slow decline in CD4(+) cells.
conclusionsA runaway cycle in which elevated CD4(+) T cell activation and proliferation drive HIV production and vice versa cannot explain the pace of depletion during chronic HIV infection. We summarize some alternative mechanisms by which the CD4(+) memory T cell homeostatic set point might slowly diminish. While none are mutually exclusive, the phenomenon of viral rebound, in which interruption of antiretroviral therapy causes a rapid return to pretreatment viral load and T cell counts, supports the model of virus adaptation as a major force driving depletion.
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.