MODEL1006230061
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is described by: http://identifiers.org/pubmed/13678598
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volume units: 290956
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substance units: 178797
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created:
  W3 CDTF: Fri Jun 25 14:23:00 BST 2010
parameter: 579529
parameter: 579525
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units def: 479842
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modified:
  W3 CDTF: Fri Jun 25 14:23:00 BST 2010
parameter: 579519
parameter: 579515
name: Wodarz2003_ImmunologicalMemory
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area units: 291053
type: SBMLModel
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modified:
  W3 CDTF: Fri Jun 25 14:23:00 BST 2010
creator:
  ORG:
    orgname: University of Auckland
  n:
    given: Catherine
    family: Lloyd
parameter: 579531
creator:
  ORG:
    orgname: University of Auckland
  n:
    given: Catherine
    family: Lloyd
parameter: 579532
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time units: 479842
notes: This a model from the article: Evolution of immunological memory and the regulation of competition between pathogens. Wodarz D. Curr Biol 2003 Sep 16;13(18):1648-52 13678598 , Abstract: Memory is a central characteristic of immune responses. It is defined as an elevated number of specific immune cells that remain after resolution of infection and can protect the host against reinfection. The evolution of immunological memory is subject to debate. The advantages of memory discussed so far include protection from reinfection, control of chronic infection, and the transfer of immune function to the next generation. Mathematical models are used to identify a new force that can drive the evolution of immunological memory: the duration of memory can regulate the degree of competition between different pathogens. While a long duration of memory provides lasting protection against reinfection, it may also allow an inferior pathogen species to persist. This can be detrimental for the host if the inferior pathogen is more virulent. On the other hand, a shorter duration of memory ensures that an inferior pathogen species is excluded. This can be beneficial for the host if the inferior pathogen is more virulent. Thus, while in the absence of pathogen diversity memory is always expected to evolve to a long duration, under specific circumstances, memory can evolve toward shorter durations in the presence of pathogen diversity. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Wodarz D. (2003) - version=1.0 The original CellML model was created by: Catherine Lloyd c.lloyd@auckland.ac.nz The University of Auckland This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public…
modified:
  W3 CDTF: Fri Jun 25 14:23:00 BST 2010
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creator:
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    orgname: University of Auckland
  n:
    given: Catherine
    family: Lloyd

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