Multiple Parameterisation of Human Immune Response in HIV: Many-Cell Models

Mathematical and computational models of the Human Immune Response have gained considerable attention over recent years and a number of approaches have been reported in the literature. One of the most successful relies on modelling, at cell level, the key components of the response using cellular automata/Monte Carlo strategies. However, a core issue remains the parameterisation required to demonstrate realistic evolution. We discuss a model of 8 cell-types, which can represent both T cell-mediated and humoral functions of the immune system, and focus on parameter sets, with values chosen to reflect realistic time-scales, comparable to natural biological processes. Analysis of the influence of the parameters introduced enables comparison of the properties of the 8-cell and basic models. In particular, a slightly reduced critical mutation value is found to lead to immune deficiency while, when a variable mutation growth factor is applied, immune breakdown occurs rapidly. The 8-cell model is susceptible to some reduction and aggregation, but system “fitness” dominates response.

[1]  A S Perelson,et al.  Pattern formation in one- and two-dimensional shape-space models of the immune system. , 1992, Journal of theoretical biology.

[2]  Michele Bezzi,et al.  The transition between immune and disease states in a cellular automaton model of clonal immune response , 1997 .

[3]  Dietrich Stauffer,et al.  Immunologically Motivated Simulations of Cellular Automata , 1992 .

[4]  G. Oster,et al.  Theoretical studies of clonal selection: minimal antibody repertoire size and reliability of self-non-self discrimination. , 1979, Journal of theoretical biology.

[5]  Heather J. Ruskin,et al.  Effect of cellular mobility on immune response , 2000 .

[6]  Heather J. Ruskin,et al.  Viral load and stochastic mutation in a Monte Carlo simulation of HIV , 2002 .

[7]  F Castiglione,et al.  Selection of escape mutants from immune recognition during HIV infection , 2002, Immunology and cell biology.

[8]  Jack Dongarra,et al.  Computational Science — ICCS 2003 , 2003, Lecture Notes in Computer Science.

[9]  Dietrich Stauffer,et al.  Immune response via interacting three dimensional network of cellular automata , 1989 .

[10]  A S Perelson,et al.  Th1/Th2 cross regulation. , 1993, Journal of theoretical biology.

[11]  R Puzone,et al.  A systematic approach to vaccine complexity using an automaton model of the cellular and humoral immune system. I. Viral characteristics and polarized responses. , 2000, Vaccine.

[12]  Ras B. Pandey,et al.  A computer simulation study of cell population in a fuzzy interaction model for mutating HIV , 1998 .

[13]  Ch. F. Kougias,et al.  Simulating the immune response to the HIV-1 virus with cellular automata , 1990 .

[14]  R. M. Zorzenon dos Santos,et al.  Dynamics of HIV infection: a cellular automata approach. , 2001, Physical review letters.

[15]  R.M.C. de Almeida,et al.  A dynamical model for the immune repertoire , 2001 .

[16]  Henri Atlan,et al.  HIV time hierarchy: winning the war while, loosing all the battles , 2000, nlin/0006023.

[17]  P E Seiden,et al.  A model for simulating cognate recognition and response in the immune system. , 1992, Journal of theoretical biology.

[18]  Jack Dongarra,et al.  Computational Science — ICCS 2002 , 2002, Lecture Notes in Computer Science.

[19]  M Kaufman,et al.  Towards a logical analysis of the immune response. , 1985, Journal of theoretical biology.

[20]  Growth and decay of a cellular population in a multicell immune network , 1990 .