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MODEL8268650277 - Nelson2000_HIV-1_general_model

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 10701304
Nelson PW, Murray JD, Perelson AS.
A model of HIV-1 pathogenesis that includes an intracellular delay.
Math Biosci 2000 Feb; 163(2): 201-215
Department of Mathematics, Duke University, Durham, NC 27708, USA.  [more]
Model
Original Model: MODEL8268650277.origin
Submitter: Lukas Endler
Submission Date: 22 Jul 2009 15:17:34 UTC
Last Modification Date: 23 Sep 2009 16:52:15 UTC
Creation Date: 15 Jul 2009 12:56:50 UTC
Encoders:
bqmodel:isDerivedFrom PubMed 8599114
PubMed 9780612
bqbiol:isVersionOf Gene Ontology response to drug
Human Disease Ontology Human immunodeficiency virus infectious disease
bqbiol:hasTaxon Taxonomy Homo sapiens
Notes

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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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.

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