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Getts, D.R., Matsumoto, I., Muller, M., Getts, M.T., Radford, J., Shrestha, B., Campbell, I.L. and King, N.J.C. (2007) Role of IFN-γ in an Experimental Murine Model of West Nile Virus-Induced Seizures. Journal of Neurochemistry, 103, 1019-1030.
http://dx.doi.org/10.1111/j.1471-4159.2007.04798.x

has been cited by the following article:

• TITLE: A Simulation for Flavivirus Infection Decoy Responses

  AUTHORS: James K. Peterson, Alison M. Kesson, Nicholas J. C. King

  KEYWORDS: West Nile Virus, Decoy Model, MHC-I Upregulation, G0 vs G1 Cell State Upregulation Differences

  JOURNAL NAME: Advances in Microbiology, Vol.5 No.2, February 12, 2015

  ABSTRACT: In this work, we discuss the development of simulation code for a model of the cross-reactive adaptive immune response seen in flavivirus infections. The model specifically addresses flavivirus pathogen virulence in G0vs G1cell states. The MHC-I upregulation of resting cells (G0 state) allows the T-cells generated for flavivirus peptide antigens to attack healthy cells also. The cells in G1state are not upregulated as much and so virus hides in them and hence is propagated upon rupture. Hence, this type of model is referred to as a decoy model because the immune system is decoyed into preferentially recognizing the upregulated cells while the virus actively propagates in another small, but important, cell population. We show that the generic assumption of upregulation via a model which includes theG0/G1differential upregulation leads to immunopathological consequences. We outline the details behind the simulation code decisions and provide some theoretical justification for our model of collateral damage and upregulation.