ArticlePLoS computational biology2008
Dynamics of immune escape during HIV/SIV infection.
Article in PLoS computational biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 146 citations in OpenAlex.
- In vivo suppression of HIV by antigen specific T cells derived from engineered hematopoietic stem cells.PLoS pathogens · 2012Trial
- Quantifying the treatment efficacy of reverse transcriptase inhibitors: new analyses of clinical data based on within-host modeling.BMC public health · 2009Trial
- Mechanism for evolution of diverse autologous antibodies upon broadly neutralizing antibody therapy of people with HIV.Cell reports · 2025Article
- Immune-mediated strategies to solving the HIV reservoir problem.Nature reviews. Immunology · 2025Review
- Compartmental structure in the secondary lymphoid tissue can slow downJournal of the Royal Society, Interface · 2025Article
- Review
- 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
- Human immunodeficiency virus dynamics in secondary lymphoid tissues and the evolution of cytotoxic T lymphocyte escape mutants.Virus evolution · 2024Article
- Mathematical modeling of N-803 treatment in SIV-infected non-human primates.PLoS computational biology · 2021Article
- Rise and fall of the new variant ofSexually transmitted infections · 2020Article
- Cancer-induced immunosuppression can enable effectiveness of immunotherapy through bistability generation: A mathematical and computational examination.Journal of theoretical biology · 2020Article
- Genetically barcoded SIV reveals the emergence of escape mutations in multiple viral lineages during immune escape.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Defining Kinetic Properties of HIV-Specific CD8⁺ T-Cell Responses in Acute Infection.Microorganisms · 2019Article
- CD8mSphere · 2019Article
- Dynamics of virus and immune response in multi-epitope network.Journal of mathematical biology · 2018Article
- Modeling the immune response to HIV infection.Current opinion in systems biology · 2018Article
- Inhibitory killer cell immunoglobulin-like receptors strengthen CD8Science immunology · 2018Article
- Insight into treatment of HIV infection from viral dynamics models.Immunological reviews · 2018Review
- Kinetics of HIV-Specific CTL Responses Plays a Minimal Role in Determining HIV Escape Dynamics.Frontiers in immunology · 2018Article
- Global properties of nested network model with application to multi-epitope HIV/CTL dynamics.Journal of mathematical biology · 2017Article
6 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have shown that cytotoxic T lymphocytes (CTLs) play an important role in controlling HIV/SIV infection. Notably, the observation of escape mutants suggests a selective pressure induced by the CTL response. However, it remains difficult to assess the definite role of the cellular immune response. We devise a computational model of HIV/SIV infection having a broad cellular immune response targeting different viral epitopes. The CTL clones are stimulated by viral antigen and interact with the virus population through cytotoxic killing of infected cells. Consequently, the virus population reacts through the acquisition of CTL escape mutations. Our model provides realistic virus dynamics and describes several experimental observations. We postulate that inter-clonal competition and immunodominance may be critical factors determining the sequential emergence of escapes. We show that even though the total killing induced by the CTL response can be high, escape rates against a single CTL clone are often slow and difficult to estimate from infrequent sequence measurements. Finally, our simulations show that a higher degree of immunodominance leads to more frequent escape with a reduced control of viral replication but a substantially impaired replicative capacity of the virus. This result suggests two strategies for vaccine design: Vaccines inducing a broad CTL response should decrease the viral load, whereas vaccines stimulating a narrow but dominant CTL response are likely to induce escape but may dramatically reduce the replicative capacity of the virus.
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.