- Author:
- pmr2.import <nobody@models.cellml.org>
- Date:
- 2009-06-17 16:08:36+12:00
- Desc:
- committing version01 of stilianakis_dietz_schenzle_1997
- Permanent Source URI:
- http://models.cellml.org/workspace/stilianakis_dietz_schenzle_1997/rawfile/c0b586fcfe35e7296bb40be5809fd948f1d6c582/stilianakis_dietz_schenzle_1997.cellml
<?xml version='1.0' encoding='utf-8'?>
<!-- FILE : stilianakis_model_1997.xml
CREATED : 25th August 2004
LAST MODIFIED : 25th August 2004
AUTHOR : Catherine Lloyd
Bioengineering Institute
The University of Auckland
MODEL STATUS : This model conforms to the CellML 1.0 Specification released on
10th August 2001, and the 16/01/2002 CellML Metadata 1.0 Specification.
DESCRIPTION : This file contains a CellML description of Stilianakis et al's 1997 mathematical model for the pathogenesis of AIDS.
CHANGES:
--><model xmlns="http://www.cellml.org/cellml/1.0#" xmlns:cmeta="http://www.cellml.org/metadata/1.0#" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bqs="http://www.cellml.org/bqs/1.0#" xmlns:cellml="http://www.cellml.org/cellml/1.0#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:vCard="http://www.w3.org/2001/vcard-rdf/3.0#" cmeta:id="stilianakis_dietz_schenzle_1997_version01" name="stilianakis_dietz_schenzle_1997_version01">
<documentation xmlns="http://cellml.org/tmp-documentation">
<article>
<articleinfo>
<title>Modelling the Pathogenesis of AIDS</title>
<author>
<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
</affiliation>
</author>
</articleinfo>
<section id="sec_status">
<title>Model Status</title>
<para>
This is the original unchecked version of the model imported from the previous
CellML model repository, 24-Jan-2006.
</para>
</section>
<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
Mathematical modelling provides a method for describing the dynamical mechanisms underlying the course of infection and the progression of the disease, including a consideration of the complex interactions which occur between the immune system and the virus. Mathematical models of HIV help to improve our understanding of the pathogenesis of the disease, which in turn leads to better patient treatment.
</para>
<para>
Although HIV can infect several types of cell, it preferentially infects T cells which express the surface marker CD4. HIV attaches to this receptor molecule with high affinity. The AIDS model which is considered here includes five variables which change with time (see the figure below). These variables include:
</para>
<itemizedlist>
<listitem>
<para>X: The number of susceptible (non-infected) CD4+ T cells;</para>
</listitem>
<listitem>
<para>Y: The number of HIV-infected CD4+ T cells;</para>
</listitem>
<listitem>
<para>V: The number of free HIV particles;</para>
</listitem>
<listitem>
<para>Z: The anti-HIV activity of the immune system towards removing infected CD4+ T cells and HIV; and</para>
</listitem>
<listitem>
<para>K: The rate at which HIV infects susceptible CD4+ T cells.</para>
</listitem>
</itemizedlist>
<para>
Following the primary infection with the virus, a patient's viral load will slowly increase over time, while destruction of the virus-infected T cells leads to a slow decrease in the numbers of CD4+ T cells. In the final stages of the disease immunocompetence, due to low T cell numbers, is combined with a relatively large viral load. Depending on the parameters entered into the mathematical model, the model predicts very different patterns of T cell decline following the primary viral infection.
</para>
<para>
The complete original paper reference is cited below:
</para>
<para>
<ulink url="http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VHX-3X2B6XV-1G&_user=140507&_coverDate=10%2F01%2F1997&_alid=195920268&_rdoc=1&_fmt=summary&_orig=search&_qd=1&_cdi=6078&_sort=d&_docanchor=&view=c&_acct=C000011498&_version=1&_urlVersion=0&_userid=140507&md5=a6090c0469da1308d33b01f23ef205b2">Analysis of a model for the pathogenesis of AIDS</ulink>, Stilianakis NI, Dietz K, and Schenzle D, 1997, <ulink url="http://www.molbiolcell.org/">
<emphasis>Mathematical Biosciences</emphasis>
</ulink>, 145, 27-46. (A PDF version of the article is available to subscribers on the <emphasis>Mathematical Biosciences</emphasis> website.) <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9271894&dopt=Abstract">PubMed ID: 9271894</ulink>
</para>
<informalfigure float="0" id="fig_reaction_diagram">
<mediaobject>
<imageobject>
<objectinfo>
<title>reaction diagram</title>
</objectinfo>
<imagedata fileref="stiliankis_1997.png"/>
</imageobject>
</mediaobject>
<caption>A schematic diagram showing how susceptible T cells are infected by free HIV particles at a rate K to become infected T cells. This process is influenced by the anti-HIV activity of the immune system against infected T cells and HIV.</caption>
</informalfigure>
</sect1>
</article>
</documentation>
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<rdf:li>viral dynamics</rdf:li>
<rdf:li>aids</rdf:li>
<rdf:li>hiv-1</rdf:li>
<rdf:li>immunology</rdf:li>
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The University of Auckland, Bioengineering Institute
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<vCard:FN>Catherine Lloyd</vCard:FN>
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<rdf:value>
This is the CellML description of Stilianakis et al's 1997 mathematical model for the pathogenesis of AIDS.
</rdf:value>
</rdf:Description>
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<dc:title>Mathematical Biosciences</dc:title>
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<bqs:Pubmed_id>9271894</bqs:Pubmed_id>
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<dcterms:alternative>CD4+ T cell infection rate</dcterms:alternative>
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<vCard:Given>Catherine</vCard:Given>
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<vCard:Other>May</vCard:Other>
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<dcterms:alternative>free HIV particles</dcterms:alternative>
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<rdf:value>c.lloyd@auckland.ac.nz</rdf:value>
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<dc:title>
Stilianakis et al's 1997 mathematical model for the pathogenesis of AIDS.
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<cmeta:bio_entity>T-cells</cmeta:bio_entity>
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<dcterms:W3CDTF>1997-10-01</dcterms:W3CDTF>
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<dcterms:alternative>anti-HIV activity</dcterms:alternative>
<dc:title>Z</dc:title>
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<dcterms:alternative>susceptible CD4+ T cells</dcterms:alternative>
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<dcterms:alternative>infected CD4+ T cells</dcterms:alternative>
<dc:title>Y</dc:title>
</rdf:Description>
<rdf:Description rdf:about="rdf:#c2508f07-44e6-4f6e-ae7a-bb891412fcfc">
<dcterms:W3CDTF>2004-08-25</dcterms:W3CDTF>
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<vCard:Given>Klaus</vCard:Given>
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<vCard:Given>Dieter</vCard:Given>
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<dcterms:W3CDTF>2007-06-15T10:45:47+12:00</dcterms:W3CDTF>
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<vCard:Given>Catherine</vCard:Given>
<vCard:Family>Lloyd</vCard:Family>
<vCard:Other>May</vCard:Other>
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<rdf:Description rdf:about="rdf:#255a1fb1-ed75-4ddc-927d-3d60cd80b9ba">
<vCard:Given>Nikolaos</vCard:Given>
<vCard:Family>Stilianakis</vCard:Family>
<vCard:Other>I</vCard:Other>
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<dc:creator rdf:resource="rdf:#fb51f8ad-3ee6-4e38-b08e-2b63b590f490"/>
<dc:title>
Analysis of a Model for the Pathogenesis of AIDS
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