A probability cellular automaton model for hepatitis B viral infections.

The existing models of hepatitis B virus (HBV) infection dynamics are based on the assumption that the populations of viruses and cells are uniformly mixed. However, the real virus infection system is actually not homogeneous and some spatial factors might play a nontrivial role in governing the development of HBV infection and its outcome. For instance, the localized populations of dead cells might adversely affect the spread of infection. To consider this kind of inhomogeneous feature, a simple 2D (dimensional) probability Cellular Automaton model was introduced to study the dynamic process of HBV infection. The model took into account the existence of different types of HBV infectious and non-infectious particles. The simulation results thus obtained showed that the Cellular Automaton model could successfully account for some important features of the disease, such as its wide variety in manifestation and its age dependency. Meanwhile, the effects of the model's parameters on the dynamical process of the infection were also investigated. It is anticipated that the Cellular Automaton model may be extended to serve as a useful vehicle for studying, among many other complicated dynamic biological systems, various persistent infections with replicating parasites.

[1]  C. Gibbs,et al.  Combination therapy with lamivudine and famciclovir for chronic hepatitis B–infected Chinese patients: A viral dynamics study , 2000, Hepatology.

[2]  Yongsheng Ding,et al.  An application of gene comparative image for predicting the effect on replication ratio by HBV virus gene missense mutation. , 2005, Journal of theoretical biology.

[3]  Gert Lubec,et al.  Searching for hypothetical proteins: Theory and practice based upon original data and literature , 2005, Progress in Neurobiology.

[4]  F. Salvatore,et al.  Hepatitis B virus reactivation after fludarabine-based regimens for indolent non-Hodgkin's lymphomas: high prevalence of acquired viral genomic mutations. , 2003, Haematologica.

[5]  G. Alexander.  Immunology of hepatitis B virus infection. , 1990, British medical bulletin.

[6]  L. Resnick,et al.  The quinoline U-78036 is a potent inhibitor of HIV-1 reverse transcriptase. , 1993, The Journal of biological chemistry.

[7]  Z. Huang,et al.  Using cellular automata images and pseudo amino acid composition to predict protein subcellular location , 2005, Amino Acids.

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

[9]  J. Chou,et al.  Kinetic studies with the non-nucleoside HIV-1 reverse transcriptase inhibitor U-88204E. , 1993, Biochemistry.

[10]  G. Marchuk,et al.  Mathematical model of antiviral immune response. II. Parameters identification for acute viral hepatitis B. , 1991, Journal of theoretical biology.

[11]  G. Marchuk,et al.  Mathematical model of antiviral immune response. I. Data analysis, generalized picture construction and parameters evaluation for hepatitis B. , 1991, Journal of theoretical biology.

[12]  A S Perelson,et al.  Hepatitis C viral dynamics in vivo and the antiviral efficacy of interferon-alpha therapy. , 1998, Science.

[13]  K. Chou,et al.  Role of the protein outside active site on the diffusion-controlled reaction of enzymes , 1982 .

[14]  C Kuo-Chen.  The kinetics of the combination reaction between enzyme and substrate. , 1976, Scientia Sinica.

[15]  F. Chisari,et al.  Hepatitis B virus immunopathogenesis. , 1995, Annual review of immunology.

[16]  W. London,et al.  A Cellular Model of the Role of Hepatitis B Virus in the Pathogenesis of Primary Hepatocellular Carcinoma , 2000 .

[17]  Diffusion-controlled reactions of enzymes. A comparison between Chou's model and Alberty-Hammes-Eigen's model. , 1982, European journal of biochemistry.

[18]  C. Gibbs,et al.  Biphasic clearance kinetics of hepatitis B virus from patients during adefovir dipivoxil therapy , 1999, Hepatology.

[19]  Alan S. Perelson,et al.  Kinetics of Acute Hepatitis B Virus Infection in Humans , 2000, The Journal of experimental medicine.

[20]  S. Thorgeirsson,et al.  Origin and fate of oval cells in dipin-induced hepatocarcinogenesis in the mouse. , 1994, The American journal of pathology.

[21]  M. Shapiro,et al.  Viral clearance without destruction of infected cells during acute HBV infection. , 1999, Science.

[22]  John Samuel,et al.  A simple cellular automaton model for influenza A viral infections. , 2004, Journal of theoretical biology.

[23]  Meng Wang,et al.  A new nucleotide-composition based fingerprint of SARS-CoV with visualization analysis. , 2005, Medicinal chemistry (Shariqah (United Arab Emirates)).

[24]  K C Chou,et al.  Kinetics of processive nucleic acid polymerases and nucleases. , 1994, Analytical biochemistry.

[25]  C. Seeger,et al.  Hepatitis B Virus Biology , 2000, Microbiology and Molecular Biology Reviews.

[26]  K.-C. Chou,et al.  Using cellular automata to generate image representation for biological sequences , 2005, Amino Acids.

[27]  A. Perelson.  Modelling viral and immune system dynamics , 2002, Nature Reviews Immunology.

[28]  A. Neumann,et al.  The influence of baseline characteristics on viral dynamic parameters in chronic hepatitis B patients treated with lamivudine. , 2002, Journal of hepatology.

[29]  C. Kuo-chen,et al.  Studies on the rate of diffusion-controlled reactions of enzymes. Spatial factor and force field factor. , 1974, Scientia Sinica.

[30]  J. Chou,et al.  Steady-state kinetic studies with the non-nucleoside HIV-1 reverse transcriptase inhibitor U-87201E. , 1993, The Journal of biological chemistry.

[31]  E. Schiff,et al.  Durability of serologic response after lamivudine treatment of chronic hepatitis B , 2003, Hepatology.

[32]  Pei-shan Wu,et al.  Biochemical and Biophysical Research Communications , 1960, Nature.

[33]  M A Nowak,et al.  Viral dynamics in hepatitis B virus infection. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[34]  H. Will,et al.  Precore mutant hepatitis B virus infection and liver disease. , 1992, Gastroenterology.

[35]  Alan S. Perelson,et al.  Hepatitis C Viral Dynamics in Vivo and the Antiviral Efficacy of Interferon-α Therapy , 1998 .

[36]  K. Chou,et al.  The flexibility during the juxtaposition of reacting groups and the upper limits of enzyme reactions. , 1981, Biophysical chemistry.

[37]  Stephen Wolfram,et al.  A New Kind of Science , 2003, Artificial Life.

[38]  W. Zhong,et al.  Diffusion‐Controlled Reactions of Enzymes , 2005 .

[39]  Stephen Wolfram,et al.  Cellular automata as models of complexity , 1984, Nature.

[40]  M A Nowak,et al.  The dynamics of hepatitis B virus infection. , 1996, Proceedings of the National Academy of Sciences of the United States of America.