Long Term and Short Term Effects of Perturbations in a Immune Network Model

In this paper we review the trajectory of a model proposed by Stauffer and Weisbuch in 1992 to describe the evolution of the immune repertoire and present new results about its dynamical behavior. Ten years later this model, which is based on the ideas of the immune network as proposed by Jerne, has been able to describe a multi-connected network and could be used to reproduce immunization and aging experiments performed with mice. Besides its biological implications, the physical aspects of the complex dynamics of this network is very interesting {\it per se}. The immunization protocol is simulated by introducing small and large perturbations (damages), and in this work we discuss the role of both. In a very recent paper we studied the aging effects by using auto-correlation functions, and the results obtained apparently indicated that the small perturbations would be more important than the large ones, since their cumulative effects may change the attractor of the dynamics. However our new results indicate that both types of perturbations are important. It is the cooperative effects between both that lead to the complex behavior which allows to reproduce experimental results.Comment: 15 pages, 5 figure

On the Aging Dynamics in an Immune Network Model

Recently we have used a cellular automata model which describes the dynamics of a multi-connected network to reproduce the refractory behavior and aging effects obtained in immunization experiments performed with mice when subjected to multiple perturbations. In this paper we investigate the similarities between the aging dynamics observed in this multi-connected network and the one observed in glassy systems, by using the usual tools applied to analyze the latter. An interesting feature we show here is that the model reproduces the biological aspects observed in the experiments during the long transient time it takes to reach the stationary state. Depending on the initial conditions, and without any perturbation, the system may reach one of a family of long-period attractors. The pertrubations may drive the system from its natural attractor to other attractors of the same family. We discuss the different roles played by the small random perturbations (noise) and by the large periodic perturbations (immunizations)

Immunization and Aging: a Learning Process in the Immune Network

The immune system can be thought as a complex network of different interacting elements. A cellular automaton, defined in shape-space, was recently shown to exhibit self-regulation and complex behavior and is, therefore, a good candidate to model the immune system. Using this model to simulate a real immune system we find good agreement with recent experiments on mice. The model exhibits the experimentally observed refractory behavior of the immune system under multiple antigen presentations as well as loss of its plasticity caused by aging.Comment: 4 latex pages, 3 postscript figures attached. To be published in Physical Review Letters (Tentatively scheduled for 5th Oct. issue

A Simple Cellular Automaton Model for Influenza A Viral Infections

Viral kinetics have been extensively studied in the past through the use of spatially homogeneous ordinary differential equations describing the time evolution of the diseased state. However, spatial characteristics such as localized populations of dead cells might adversely affect the spread of infection, similar to the manner in which a counter-fire can stop a forest fire from spreading. In order to investigate the influence of spatial heterogeneities on viral spread, a simple 2-D cellular automaton (CA) model of a viral infection has been developed. In this initial phase of the investigation, the CA model is validated against clinical immunological data for uncomplicated influenza A infections. Our results will be shown and discussed.Comment: LaTeX, 12 pages, 18 EPS figures, uses document class ReTeX4, and packages amsmath and SIunit

Emergence of Hierarchy on a Network of Complementary Agents

Complementarity is one of the main features underlying the interactions in biological and biochemical systems. Inspired by those systems we propose a model for the dynamical evolution of a system composed by agents that interact due to their complementary attributes rather than their similarities. Each agent is represented by a bit-string and has an activity associated to it; the coupling among complementary peers depends on their activity. The connectivity of the system changes in time respecting the constraint of complementarity. We observe the formation of a network of active agents whose stability depends on the rate at which activity diffuses in the system. The model exhibits a non-equilibrium phase transition between the ordered phase, where a stable network is generated, and a disordered phase characterized by the absence of correlation among the agents. The ordered phase exhibits multi-modal distributions of connectivity and activity, indicating a hierarchy of interaction among different populations characterized by different degrees of activity. This model may be used to study the hierarchy observed in social organizations as well as in business and other networks.Comment: 13 pages, 4 figures, submitte

Robustness of a Cellular Automata Model for the HIV Infection

An investigation was conducted to study the robustness of the results obtained from the cellular automata model which describes the spread of the HIV infection within lymphoid tissues [R. M. Zorzenon dos Santos and S. Coutinho, Phys. Rev. Lett. 87, 168102 (2001)]. The analysis focussed on the dynamic behavior of the model when defined in lattices with different symmetries and dimensionalities. The results illustrated that the three-phase dynamics of the planar models suffered minor changes in relation to lattice symmetry variations and, while differences were observed regarding dimensionality changes, qualitative behavior was preserved. A further investigation was conducted into primary infection and sensitiveness of the latency period to variations of the model's stochastic parameters over wide ranging values. The variables characterizing primary infection and the latency period exhibited power-law behavior when the stochastic parameters varied over a few orders of magnitude. The power-law exponents were approximately the same when lattice symmetry varied, but there was a significant variation when dimensionality changed from two to three. The dynamics of the three-dimensional model was also shown to be insensitive to variations of the deterministic parameters related to cell resistance to the infection, and the necessary time lag to mount the specific immune response to HIV variants. The robustness of the model demonstrated in this work reinforce that its basic hypothesis are consistent with the three-stage dynamic of the HIV infection observed in patients.Comment: 14 pages, 6 figures, 21 references, Latex style Elsar