ABSTRACT:
This a model from the article:
Influence of delayed viral production on viral dynamics in HIV-1 infected
patients.
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 immunodeficiency
virus type 1 (HIV-1) with target cells that includes a time delay between
initial infection and the formation of productively infected cells. Assuming
that the variation among cells with respect to this 'intracellular' delay can be
approximated by a gamma distribution, a high flexible distribution that can
mimic a variety of biologically plausible delays, we provide analytical
solutions for the expected decline in plasma virus concentration after the
initiation of antiretroviral therapy with one or more protease inhibitors. We
then use the model to investigate whether the parameters that characterize viral
dynamics can be identified from biological data. Using non-linear least-squares
regression to fit the model to simulated data in which the delays conform to a
gamma distribution, we show that good estimates for free viral clearance rates,
infected cell death rates, and parameters characterizing the gamma distribution
can be obtained. For simulated data sets in which the delays were generated
using other biologically plausible distributions, reasonably good estimates for
viral clearance rates, infected cell death rates, and mean delay times can be
obtained using the gamma-delay model. For simulated data sets that include added
simulated noise, viral clearance rate estimates are not as reliable. If the mean
intracellular delay is known, however, we show that reasonable estimates for the
viral clearance rate can be obtained by taking the harmonic mean of viral
clearance rate estimates from a group of patients. These results demonstrate
that it is possible to incorporate distributed intracellular delays into
existing models for HIV dynamics and to use these refined models to estimate the
half-life of free virus from data on the decline in HIV-1 RNA following
treatment.
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
c.lloyd@auckland.ac.nz
The University of Auckland
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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.
Camille Laibe 
