摘要
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.
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.
作者
James K. Peterson
Alison M. Kesson
Nicholas J. C. King
James K. Peterson;Alison M. Kesson;Nicholas J. C. King(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 Pediatrics and Child Health, The Marie Bashir Institute for Emerging Infectious Diseases and Biosecurity, University of Sydney, Sydney, Australia;Discipline of Pathology, University of Sydney, Sydney, Australia)
