Killer Cell Dynamics: Mathematical and Computational by Dominik Wodarz

By Dominik Wodarz

This booklet experiences how arithmetic can be utilized together with organic facts in an effort to enhance figuring out of ways the immune method works. this is often illustrated mostly within the context of viral infections. Mathematical versions enable scientists to catch advanced organic interactions in a transparent mathematical language and to stick to them to their certain logical conclusions. this may provide upward thrust to counter-intuitive insights which might now not be attained by way of experiments on my own, and will be used for the layout of additional experiments with a view to tackle the mathematical results.This ebook offers either an creation to the sphere of mathematical immunology, and an outline of many issues that are the topic of present study, overlaying a wide number of immunological themes. It begins with simple rules of immunology and covers the dynamical interactions among the immune method and particular viral infections, together with very important human pathogens comparable to HIV. basic organic and mathematical history fabric to either virus an infection and immune procedure dynamics is supplied, and every bankruptcy starts with an easy creation to the organic questions examined.This booklet is meant for an interdisciplinary viewers. It explains the concept that of mathematical modeling in immunology and exhibits how modeling has been used to handle particular questions. it's meant either for the mathematical biologists who're drawn to immunology, and for the organic readership that's attracted to using mathematical types in immunology.

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Extra resources for Killer Cell Dynamics: Mathematical and Computational Approaches to Immunology

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This culminates in the differentiation into CTL effectors that fight the virus. Memory CTL are again precursor CTL without antiviral activity. In order to attain antiviral activity, the memory CTL need to be stimulated again. Mathematical models have been constructed that take into account this subdivision of the CTL [Wodarz et al. (1998); Wodarz et al. (2000b); Wodarz et al. (2000c)]. Denoting the population of CTL precursors by w and the population of CTL effectors by z, the model is given by the following set of differential equations.

Central memory cells express certain surface receptors that allow homing of the cells to the lymph nodes. Central memory cells seem to have the greatest capacity to persist in the absence of antigenic stimulation and to react against secondary challenges. Effector memory cells lack these homing receptors and are located primarily in the blood, spleen, and nonlymphoid tissues. It is thought that effector memory cells are an intermediate stage, and that they differentiate into central memory cells when the infection is cleared.

Therefore, in order to eradicate HIV from patients, drug therapy would have to be applied for a duration of time that is longer than the life span of patients. These different phases of virus decay are explained by the fact that HIV can infect a variety of different cell types. The first and fast phase of virus decay reflects the death of infected CD4 T helper cells. The second and longer phase of virus decay reflects the death of infected antigen presenting cells. HIV can infect a variety of such cells, most importantly dendritic cells and macrophages.

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