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Using a Collateral Damage Model to Explain Survival Data in West Nile Virus Infections
Department of Mathematical and Biological Sciences, Clemson University, Clemson, SC, USA
Department of Infectious Diseases and Microbiology, The Children’s Hospital, Sydney, Australia
Discipline of Pathology, University of Sydney, Sydney, Australia
Discipline of Pediatrics and Child Health, The Marie Bashir Institute for Emerging Infectious Diseases and Biosecurity, University of Sydney, Sydney, Australia
- 1 Department of Mathematical and Biological Sciences, Clemson University, Clemson, SC, USA
- 2 Department of Infectious Diseases and Microbiology, The Children’s Hospital, Sydney, Australia
- 3 Discipline of Pathology, University of Sydney, Sydney, Australia
- 4 Discipline of Pediatrics and Child Health, The Marie Bashir Institute for Emerging Infectious Diseases and Biosecurity, University of Sydney, Sydney, Australia
Advances in Microbiology·Volume 06 (2016)·Pages 251–262·Published 7 April 2016·DOI10.4236/aim.2016.64025
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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.
KeywordsAuto Immune ResponsesWest Nile VirusHost Survival ModelsMHC-I UpregulationIFN-γ UpregulationFree Antigen Levels
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