ArticleJournal of virology2011
Fitness costs and diversity of the cytotoxic T lymphocyte (CTL) response determine the rate of CTL escape during acute and chronic phases of HIV infection.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
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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.
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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.
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Who cites it
103 citing papers in PubMed, 154 citations in OpenAlex.
- MVA.HIVconsvX vaccination-evoked T cell expansion inversely associates with age in people with HIV-1 on antiretroviral therapy.The Journal of clinical investigation · 2026Trial
- Restriction of V3 region sequence divergence in the HIV-1 envelope gene during antiretroviral treatment in a cohort of recent seroconverters.Retrovirology · 2013Trial
- Autologous neutralizing antibodies and polyfunctional T cells contribute to long-term HIV-1 post-intervention control.Nature immunology · 2026Article
- Mechanism for evolution of diverse autologous antibodies upon broadly neutralizing antibody therapy of people with HIV.Cell reports · 2025Article
- Inferring fitness seascapes from evolutionary histories.bioRxiv : the preprint server for biology · 2025Article
- Antiviral capacity of the early CD8 T-cell response is predictive of natural control of SIV infection: Learning in vivo dynamics using ex vivo data.PLoS computational biology · 2024Article
- Modelling HIV-1 control and remission.NPJ systems biology and applications · 2024Review
- CD3 downregulation identifies high-avidity human CD8 T cells.Clinical and experimental immunology · 2024Article
- Human immunodeficiency virus dynamics in secondary lymphoid tissues and the evolution of cytotoxic T lymphocyte escape mutants.Virus evolution · 2024Article
- Cytotoxic T Lymphocytes Control Growth of B16 Tumor Cells in Collagen-Fibrin Gels by Cytolytic and Non-Lytic Mechanisms.Viruses · 2023Article
- Evolutionary implications of SARS-CoV-2 vaccination for the future design of vaccination strategies.Communications medicine · 2023Review
- No Difference in the Prevalence of HIV-1Vaccines · 2023Article
- Mathematical modeling suggests cytotoxic T lymphocytes control growth of B16 tumor cells in collagin-fibrin gels by cytolytic and non-lytic mechanisms.bioRxiv : the preprint server for biology · 2023Article
- Definition of a New HLA B*52-Restricted Rev CTL Epitope Targeted by an HIV-1-Infected Controller.Viruses · 2023Article
- Identification of human progenitors of exhausted CD8Nature communications · 2022Article
- Bispecific antibody-derived molecules to target persistent HIV infection.Journal of virus eradication · 2022Article
- Evolution during primary HIV infection does not require adaptive immune selection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Homologous peptides derived from influenza A, B and C viruses induce variable CD8Clinical & translational immunology · 2022Article
- Emergence and competition of virus variants in respiratory viral infections.Frontiers in immunology · 2022Article
- Intrahost evolution of the HIV-2 capsid correlates with progression to AIDS.Virus evolution · 2022Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
HIV-1 often evades cytotoxic T cell (CTL) responses by generating variants that are not recognized by CTLs. We used single-genome amplification and sequencing of complete HIV genomes to identify longitudinal changes in the transmitted/founder virus from the establishment of infection to the viral set point at 1 year after the infection. We found that the rate of viral escape from CTL responses in a given patient decreases dramatically from acute infection to the viral set point. Using a novel mathematical model that tracks the dynamics of viral escape at multiple epitopes, we show that a number of factors could potentially contribute to a slower escape in the chronic phase of infection, such as a decreased magnitude of epitope-specific CTL responses, an increased fitness cost of escape mutations, or an increased diversity of the CTL response. In the model, an increase in the number of epitope-specific CTL responses can reduce the rate of viral escape from a given epitope-specific CTL response, particularly if CD8+ T cells compete for killing of infected cells or control virus replication nonlytically. Our mathematical framework of viral escape from multiple CTL responses can be used to predict the breadth and magnitude of HIV-specific CTL responses that need to be induced by vaccination to reduce (or even prevent) viral escape following HIV infection.
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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.