Mittler1998_HIV1_interactingTargetCells

ABSTRACT:

This a model from the article:
Influence of delayed viral production on viral dynamics in HIV-1 infectedpatients.
Mittler JE, Sulzer B, Neumann AU, Perelson AS. Math Biosci 1998 Sep;152(2):143-63 9780612 ,
Abstract:
We present and analyze a model for the interaction of human immunodeficiencyvirus type 1 (HIV-1) with target cells that includes a time delay betweeninitial infection and the formation of productively infected cells. Assumingthat the variation among cells with respect to this 'intracellular' delay can beapproximated by a gamma distribution, a high flexible distribution that canmimic a variety of biologically plausible delays, we provide analyticalsolutions for the expected decline in plasma virus concentration after theinitiation of antiretroviral therapy with one or more protease inhibitors. Wethen use the model to investigate whether the parameters that characterize viraldynamics can be identified from biological data. Using non-linear least-squaresregression to fit the model to simulated data in which the delays conform to agamma distribution, we show that good estimates for free viral clearance rates,infected cell death rates, and parameters characterizing the gamma distributioncan be obtained. For simulated data sets in which the delays were generatedusing other biologically plausible distributions, reasonably good estimates forviral clearance rates, infected cell death rates, and mean delay times can beobtained using the gamma-delay model. For simulated data sets that include addedsimulated noise, viral clearance rate estimates are not as reliable. If the meanintracellular delay is known, however, we show that reasonable estimates for theviral clearance rate can be obtained by taking the harmonic mean of viralclearance rate estimates from a group of patients. These results demonstratethat it is possible to incorporate distributed intracellular delays intoexisting models for HIV dynamics and to use these refined models to estimate thehalf-life of free virus from data on the decline in HIV-1 RNA followingtreatment.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Mittler JE, Sulzer B, Neumann AU, Perelson AS. (1998) - version=1.0
The original CellML model was created by:
Catherine Lloyd
[e-mail]
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 domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..

To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

ORGANISM(S): Homo sapiens

SUBMITTER: Camille Laibe 

PROVIDER: MODEL1006230055 | biostudies-other |

SECONDARY ACCESSION(S): 9780612

REPOSITORIES: biostudies-other