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 AiM  Vol.6 No.4 , April 2016
Using a Collateral Damage Model to Explain Survival Data in West Nile Virus Infections
Abstract: Simulation code for a model of the adaptive immune response seen in flavivirus infections is used to explain the immunopathological consequences seen in West Nile Virus virus (WNV) infections. We use a model that specifically handles the differences in how the virus infects resting cells, the G0 state, versus dividing cells, the G1 state, which includes vastly increased MHC-I upregulation for resting cells over dividing cells. The simulation suggests how the infection progresses in a one host model and the results shed insight into the unusual survival curve data obtained for this infection: there is an increase in health even though viral load has increased.
Cite this paper: Peterson, J. , Kesson, A. , King, N. (2016) Using a Collateral Damage Model to Explain Survival Data in West Nile Virus Infections. Advances in Microbiology, 6, 251-262. doi: 10.4236/aim.2016.64025.
References

[1]   Douglas, D.W., Kesson, A.M. and King, N.J.C. (1994) CTL Recognition of West Nile Virus-Infected Fibroblasts Is Cell Cycle Dependent and Is Associated with Virus-Induced Increases in Class I MHC Antigen Expression. Immunology, 82, 561-570.

[2]   Kesson, A.M., Cheng, Y. and King, N.J.C. (2002) Regulation of Immune Recognition Molecules by Flavivirus, West Nile. Viral Immunology, 15, 273-283. http://dx.doi.org/10.1089/08828240260066224

[3]   King, N.J.C., Getts, D.R., Getts, M.T., Rana, S., Shrestha, B. and Kesson, A.M. (2007) Immunopathology of Flavivirus Infections. Immunology & Cell Biology, 85, 33-42.
http://dx.doi.org/10.1038/sj.icb.7100012

[4]   King, N.J.C. and Kesson, A.M. (2003) Interaction of Flaviviruses with Cells of the Vertebrate Host and Decoy of the Immune Response. Immunology & Cell Biology, 81, 207-216.
http://dx.doi.org/10.1046/j.1440-1711.2003.01167.x

[5]   King, N.J.C. and Kesson, A.M. (1988) Interferon-Independent Increases in Class I Major Histocompatibility Complex Antigen Expression Follow Flavivirus Infection. The Journal of General Virology, 69, 2535-2543.
http://dx.doi.org/10.1099/0022-1317-69-10-2535

[6]   King, N.J.C., Müllbacher, A., Tian, L., Rodger, J.C., Lidbury, B. and Hla, R.T. (1993) West Nile Virus Infection Induces Susceptibility of in Vitro Outgrown Murine Blastocysts to Specific Lysis by Paternally Directed Allo-Immune and Virus-Immune Cytotoxic T Cells. Journal of Reproductive Immunology, 23, 131-144.
http://dx.doi.org/10.1016/0165-0378(93)90003-Z

[7]   King, N.J.K., Davison, A., Getts, D., Lu, D.P., Getts, M., Yeung, A., Peterson, J. and Kesson, A.M. (2008) Enhanced Antigen Processing or Immune Evasion? West Nile Virus and the Induction of Immune Recognition Molecules. In: Diamond, M.S., Ed., West Nile Encephalitis Virus Infection: Viral Pathogenesis and the Host Immune Response, Springer-Verlag, New York, 309-339.

[8]   Peterson, J.K., King, N.J.C. and Kesson, A.M. (2014) Modeling West Nile Virus One Host Infections. Technical Report, Clemson University, Clemson.

[9]   Peterson, J., Kesson, A.M. and King, N.J.C. (2016) A Model of Auto Immune Response. BMC Immunology, 1-40. (Draft Submitted)

[10]   Peterson, J., Kesson, A.M. and King, N.J.C. (2015) A Simulation for Flavivirus Infection Decoy Responses. Advances in Microbiology, 5, 123-142. http://dx.doi.org/10.4236/aim.2015.52013

[11]   Peterson, J., Kesson, A.M. and King, N.J.C. (2016) A Theoretical Model of the West Nile Virus Survival Data. BMC Immunology, 1-34. (Draft Submitted)

[12]   Peterson, J., Kesson, A.M. and King, N.J.C. (2016) Viral Infections and the Central Nervous System Infection Models. 1-40. (Draft)

[13]   Shen, J., T-To, S.S., Schrieber, L. and King, N.J.C. (1997) Early E-Selectin and VCAM-1 and ICAM-1 and Late Major Histocompatibility Complex Antigen Induction on Human Endothelial Cells by Flavivirus and Comodulation of Adhesion Molecule Expression by Immune Cytokines. Journal of Virology, 71, 9323-9332.

 
 
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