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Apoptosis in virus infection dynamics models

In this paper, on the basis of the simplified two-dimensional virus infection dynamics model, we propose two extended models that aim at incorporating the influence of activation-induced apoptosis which directly affects the population of uninfected cells. The theoretical analysis shows that increasi...

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Detalles Bibliográficos
Autores principales: Fan, Ruili, Dong, Yueping, Huang, Gang, Takeuchi, Yasuhiro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220821/
https://www.ncbi.nlm.nih.gov/pubmed/24963975
http://dx.doi.org/10.1080/17513758.2014.895433
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author Fan, Ruili
Dong, Yueping
Huang, Gang
Takeuchi, Yasuhiro
author_facet Fan, Ruili
Dong, Yueping
Huang, Gang
Takeuchi, Yasuhiro
author_sort Fan, Ruili
collection PubMed
description In this paper, on the basis of the simplified two-dimensional virus infection dynamics model, we propose two extended models that aim at incorporating the influence of activation-induced apoptosis which directly affects the population of uninfected cells. The theoretical analysis shows that increasing apoptosis plays a positive role in control of virus infection. However, after being included the third population of cytotoxic T lymphocytes immune response in HIV-infected patients, it shows that depending on intensity of the apoptosis of healthy cells, the apoptosis can either promote or comfort the long-term evolution of HIV infection. Further, the discrete-time delay of apoptosis is incorporated into the pervious model. Stability switching occurs as the time delay in apoptosis increases. Numerical simulations are performed to illustrate the theoretical results and display the different impacts of a delay in apoptosis.
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spelling pubmed-42208212014-11-17 Apoptosis in virus infection dynamics models Fan, Ruili Dong, Yueping Huang, Gang Takeuchi, Yasuhiro J Biol Dyn Original Articles In this paper, on the basis of the simplified two-dimensional virus infection dynamics model, we propose two extended models that aim at incorporating the influence of activation-induced apoptosis which directly affects the population of uninfected cells. The theoretical analysis shows that increasing apoptosis plays a positive role in control of virus infection. However, after being included the third population of cytotoxic T lymphocytes immune response in HIV-infected patients, it shows that depending on intensity of the apoptosis of healthy cells, the apoptosis can either promote or comfort the long-term evolution of HIV infection. Further, the discrete-time delay of apoptosis is incorporated into the pervious model. Stability switching occurs as the time delay in apoptosis increases. Numerical simulations are performed to illustrate the theoretical results and display the different impacts of a delay in apoptosis. Taylor & Francis 2014-01-01 2014-03-13 /pmc/articles/PMC4220821/ /pubmed/24963975 http://dx.doi.org/10.1080/17513758.2014.895433 Text en © 2014 The Author(s). Published by Taylor & Francis. http://creativecommons.org/licenses/by/3.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Original Articles
Fan, Ruili
Dong, Yueping
Huang, Gang
Takeuchi, Yasuhiro
Apoptosis in virus infection dynamics models
title Apoptosis in virus infection dynamics models
title_full Apoptosis in virus infection dynamics models
title_fullStr Apoptosis in virus infection dynamics models
title_full_unstemmed Apoptosis in virus infection dynamics models
title_short Apoptosis in virus infection dynamics models
title_sort apoptosis in virus infection dynamics models
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4220821/
https://www.ncbi.nlm.nih.gov/pubmed/24963975
http://dx.doi.org/10.1080/17513758.2014.895433
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