شبيه سازي عددي برهم كنش ويروس و سيستم ايمني با كمك مدل ماشين هاي سلولي

چكيده انگليسي :

Simulation of the Virus Dynamics Interacting with Immune System using Cellular Automata Student name Fatemeh Heydari Email address f heydari@ph iut ac ir Date of submission 2011 8 28 Department of Physics Isfahan University of Technology Isfahan 84156 83111 Iran Degree M Sc Language Farsi Supervisor Dr Farhad Fazileh Fazileh@cc iut ac ir Abstract Acquired immunodeficiency syndrome AIDS has rapidly emerged as one of the main global healthproblems It is a widely accepted fact that HIV causes AIDS a condition in which the normal human immunesystem becomes suppressed rendering the affected individual unable to fight serious or fatal infections Infectionby HIV 1 has many unusual quantitative features An example is the average 10 year lag from the start ofinfection till HIV totally dominates the immune system In recent decades the infection caused by HIV whichleads to AIDS has been the subject of many researches Although many progresses have happened inunderstanding different aspects of virus host interaction mechanisms through which HIV causes AIDS are stillunder question Nowadays mathematical modeling has become an integral part of the research on the HIVinfection Elaborate mathematical models cannot only help further understanding of HIV dynamics but alsoprovide useful predictions that can be used as the basis for assessing the effects of chemotherapy orimmunotherapy and for the design of optimum therapies and effective vaccines The time scale to develop aspecific immune response may vary from days to weeks In the case of HIV the entire course of infectioninvolves two different time scales The primary infection exhibits the same characteristics as any other viralinfection a dramatic increase of the virus population during the first 2 6 weeks followed by a sharp decline dueto the action of the immune system However instead of being completely eliminated after the primary infection as many other viruses a low HIV concentration is detected for a long asymptomatic time the clinical latencyperiod This period may vary from one to ten years Besides the low virus burden detected during this period agradual deterioration of the immune system is manifested by the reduction of CD4 T cell populations in theperipheral blood The third phase of the disease is achieved when the concentration of the T cells is lower than acritical value leading to the development of AIDS So in this research first basic concepts of immunology andvirology are explained After that the structure and history of HIV virus which is the aim of this project isdiscussed Then the simplest model of dynamic and demography is studied In following steps quasispeciesmodel some concepts of Evoluionary Games Prisoner s Dilemma game and tit for tat strategy and cellularautomata model which is a discontinuous model in time and space are introduced and investigated respectively Finally the results obtained applying above models to HIV virus are discussed The goal of this thesis is to use acombination of cellular automata and quasispecies model in order to investigate the dynamic interaction whichproduces AIDS between HIV viruses and immune system Changing virus concentration applying cellular andhomoral immune separately and removing the RNA mutation of viruses are studied Additionally throughoutchanging the length of Antigen epitope on virus variable a threshold for genetic variety that immune system canbear until the infection caused by HIV doesn t lead to AIDS is obtained Key words immune system Human Immunodeficiency Virus AIDS quasispecies model cellular automata

حيدري، فاطمه

شبيه سازي عددي برهم كنش ويروس و سيستم ايمني با كمك مدل ماشين هاي سلولي

ايدز , بدل شبه گونه