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Cellular Automata Model of Drug Therapy for HIV Infection
| Book Series | Lecture Notes in Computer Science |
| Publisher | Springer Berlin / Heidelberg |
| ISSN | 0302-9743 (Print) 1611-3349 (Online) |
| Volume | Volume 2493/2002 |
| Book | Cellular Automata |
| DOI | 10.1007/3-540-45830-1 |
| Copyright | 2002 |
| ISBN | 978-3-540-44304-9 |
| DOI | 10.1007/3-540-45830-1_27 |
| Pages | 282-293 |
| Subject Collection | Computer Science |
| SpringerLink Date | Tuesday, January 01, 2002 |
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Cellular Automata Model of Drug Therapy for HIV Infection
Peter Sloot7 , Fan Chen7 and Charles Boucher8 
| (7) |
Faculty of Sciences, Section Computational Science, University of Amsterdam, The Netherlands |
| (8) |
Department of Virology, University Hospital Utrecht, Utrecht University, The Netherlands |
Abstract
In this study, we employ non-uniform Cellular Automata (CA) to simulate drug treatment of HIV infection, where each computational
domain may contain different CA rules, in contrast to normal uniform CA models. Ordinary (or partial) differential equation
models are insufficient to describe the two extreme time scales involved in HIV infection (days and decades), as well as the
implicit spatial heterogeneity [4,3, 10]. R.M.Zorzenon dos Santose [13] (2001) reported a cellular automata approach to simulate three-phase patterns of human immunodeficiency virus (HIV) infection
consisting of primary response, clinical latency and onset of acquired immunodeficiency syndrome (AIDS), Here we report a
related model. We developed a non-uniform CA model to study the dynamics of drug therapy of HIV infection, which simulates
four-phases (acute, chronic, drug treatment responds and onset of AIDS). Our results indicate that both simulations (with
and without treatments) evolve to the relatively same steady state (characteristic of Wolfram’s class II behaviour). Three
different drug therapies (mono-therapy, combined drug therapy and highly active antiretroviral therapy HAART) can also be
simulated in our model. Our model for prediction of the temporal behaviour of the immune system to drug therapy qualitatively
corresponds to clinical data.
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