ArticleJournal of theoretical biology2010
Model with two types of CTL regulation and experiments on CTL dynamics.
Article in Journal of theoretical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- An Evolutionary Model of Progression to AIDS.Microorganisms · 2020Article
- Defining Kinetic Properties of HIV-Specific CD8⁺ T-Cell Responses in Acute Infection.Microorganisms · 2019Article
- Modeling the immune response to HIV infection.Current opinion in systems biology · 2018Article
- Article
- The route of HIV escape from immune response targeting multiple sites is determined by the cost-benefit tradeoff of escape mutations.PLoS computational biology · 2014Article
- Design requirements for interfering particles to maintain coadaptive stability with HIV-1.Journal of virology · 2013Article
- Estimate of effective recombination rate and average selection coefficient for HIV in chronic infection.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Implications of CTL-mediated killing of HIV-infected cells during the non-productive stage of infection.PloS one · 2011Article
- Interpreting the effect of vaccination on steady state infection in animals challenged with Simian immunodeficiency virus.Journal of theoretical biology · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Recently, we developed a mathematical model of interaction between the HIV and the immune system to match various dynamic experiments carried out in HIV-infected humans and SIV-infected macaques. The model includes helper cell-dependent and helper cell-independent cytotoxic lymphocytes (CTLs) and predicts two stable steady states, a state with a high virus load and few helper cells, and another state with a low virus load and many helper cells. Here we upgrade the model to take into account recent reports on the link between the activation status of infected cells and their ability to produce virus, the effect of helper cells at the time of priming on CTL differentiation, and virus dynamics in unvaccinated macaques with a broad genetic background acutely infected with SIVmac251. We also discuss in detail the experimental justification of the CTL block and the robustness of model predictions with respect to the hypothesis of two CTL subtypes.
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