Nelson2000- HIV-1 general model 1

This is the general model without delay described by the equation system (1) in: A model of HIV-1 pathogenesis that includes an intracellular delay.
Nelson PW, Murray JD, Perelson AS; Math Biosci.
2000 Feb;163(2):201-15. PMID: 10701304
; doi: 10.1016/S0025-5564(99)00055-3
Abstract:
Mathematical modeling combined with experimental measurements have yielded important insights into HIV-1 pathogenesis. For example, data from experiments in which HIV-infected patients are given potent antiretroviral drugs that perturb the infection process have been used to estimate kinetic parameters underlying HIV infection. Many of the models used to analyze data have assumed drug treatments to be completely efficacious and that upon infection a cell instantly begins producing virus. We consider a model that allows for less then perfect drug effects and which includes a delay in the initiation of virus production. We present detailed analysis of this delay differential equation model and compare the results to a model without delay. Our analysis shows that when drug efficacy is less than 100%, as may be the case in vivo, the predicted rate of decline in plasma virus concentration depends on three factors: the death rate of virus producing cells, the efficacy of therapy, and the length of the delay. Thus, previous estimates of infected cell loss rates can be improved upon by considering more realistic models of viral infection.
Author Keywords:
HIV; Delay; Viral life cycle; T-cells
As there are no results given for this model in the article it cannot be checked for MIRIAM compliance. The SBML file should be equivalent to the described ODE file though.
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A model of HIV-1 pathogenesis that includes an intracellular delay.
- Nelson PW, Murray JD, Perelson AS
- Mathematical biosciences , 2/ 2000 , Volume 163 , pages: 201-215 , PubMed ID: 10701304
- Department of Mathematics, Duke University, Durham, NC 27708, USA.
- Mathematical modeling combined with experimental measurements have yielded important insights into HIV-1 pathogenesis. For example, data from experiments in which HIV-infected patients are given potent antiretroviral drugs that perturb the infection process have been used to estimate kinetic parameters underlying HIV infection. Many of the models used to analyze data have assumed drug treatments to be completely efficacious and that upon infection a cell instantly begins producing virus. We consider a model that allows for less then perfect drug effects and which includes a delay in the initiation of virus production. We present detailed analysis of this delay differential equation model and compare the results to a model without delay. Our analysis shows that when drug efficacy is less than 100%, as may be the case in vivo, the predicted rate of decline in plasma virus concentration depends on three factors: the death rate of virus producing cells, the efficacy of therapy, and the length of the delay. Thus, previous estimates of infected cell loss rates can be improved upon by considering more realistic models of viral infection.
Submitter of this revision: Mohammad Umer Sharif Shohan
Modellers: Lukas Endler, Mohammad Umer Sharif Shohan
Metadata information
isDescribedBy (1 statement)
hasTaxon (1 statement)
isVersionOf (2 statements)
Gene Ontology response to drug
hasProperty (1 statement)
Connected external resources
Name | Description | Size | Actions |
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Model files |
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Nelson2000.xml | SBML L2V4 representation of Nelson2000 HIV-1_general_model | 26.71 KB | Preview | Download |
Additional files |
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MODEL8268650277-biopax2.owl | Auto-generated BioPAX (Level 2) | 7.25 KB | Preview | Download |
MODEL8268650277-biopax3.owl | Auto-generated BioPAX (Level 3) | 12.77 KB | Preview | Download |
MODEL8268650277.m | Auto-generated Octave file | 3.60 KB | Preview | Download |
MODEL8268650277.pdf | Auto-generated PDF file | 162.37 KB | Preview | Download |
MODEL8268650277.png | Auto-generated Reaction graph (PNG) | 30.94 KB | Preview | Download |
MODEL8268650277.sci | Auto-generated Scilab file | 226.00 Bytes | Preview | Download |
MODEL8268650277.svg | Auto-generated Reaction graph (SVG) | 15.39 KB | Preview | Download |
MODEL8268650277.vcml | Auto-generated VCML file | 19.40 KB | Preview | Download |
MODEL8268650277.xpp | Auto-generated XPP file | 2.42 KB | Preview | Download |
MODEL8268650277_url.xml | old xml file | 13.24 KB | Preview | Download |
MODEL8268650277_urn.xml | Auto-generated SBML file with URNs | 14.13 KB | Preview | Download |
Nelson2000.cps | COPASI version 4.24 (Build 197) representation of Nelson2000 HIV-1_general_model | 59.34 KB | Preview | Download |
Nelson2000.sedml | SEDML L1V2 representation of Nelson2000 HIV-1_general_model | 3.70 KB | Preview | Download |
- Model originally submitted by : Lukas Endler
- Submitted: Jul 22, 2009 3:17:34 PM
- Last Modified: Nov 26, 2019 1:39:42 PM
Revisions
-
Version: 5
- Submitted on: Nov 26, 2019 1:39:42 PM
- Submitted by: Mohammad Umer Sharif Shohan
- With comment: Automatically added model identifier BIOMD0000000875
-
Version: 2
- Submitted on: Sep 23, 2009 4:52:15 PM
- Submitted by: Lukas Endler
- With comment: Current version of Nelson2000_HIV-1_general_model
-
Version: 1
- Submitted on: Jul 22, 2009 3:17:34 PM
- Submitted by: Lukas Endler
- With comment: Original import of Nelson 2000 HIV-1 general model
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: Variable used inside SBML models
Species | Initial Concentration/Amount |
---|---|
V I C14283 |
134000.0 item |
T uninfected |
180000.0 item |
V NI | 0.0 item |
T i infected cell |
1675.0 item |
Reactions | Rate | Parameters |
---|---|---|
V_I => | plasma*c*V_I | c = 3.0 1/ms |
T => T_i; V_I | plasma*k*V_I*T | k = 3.43E-8 l/(s*#) |
=> V_NI; T_i | plasma*np*N*delta*T_i | np = 0.5 1; N = 480.0 1; delta = 0.5 1/ms |
=> V_I; T_i | plasma*(1-np)*N*delta*T_i | np = 0.5 1; N = 480.0 1; delta = 0.5 1/ms |
T => | plasma*delta1*T | delta1 = 0.03 1/ms |
=> T | plasma*lambda | lambda = 10.0 #/(l*s) |
T_i => | plasma*delta*T_i | delta = 0.5 1/ms |
V_NI => | plasma*c*V_NI | c = 3.0 1/ms |
(added: 26 Nov 2019, 13:38:47, updated: 26 Nov 2019, 13:38:47)