BioModelsapplication/xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.pdfhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683-biopax3.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683-biopax2.owlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=MODEL1006230062.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683_urn.xmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.vcmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.xpphttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.scihttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=MODEL1006230062.cpshttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=MODEL1006230062.sedmlhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.mhttps://www.ebi.ac.uk/biomodels/model/download/BIOMD0000000683?filename=BIOMD0000000683.pngprimaryOK200Camille LaibeManually curatedL2V4https://www.ebi.ac.uk/biomodels/BIOMD000000068310588728falseBioModelsSBMLModelsWodarz1999 CTL memory response HIV1999MODEL1006230062Wodarz D, Nowak MAWodarz D10588728,
We use mathematical models to study the relationship between HIV and the immune system during the natural course of infection and in the context of different antiviral treatment regimes. The models suggest that an efficient cytotoxic T lymphocyte (CTL) memory response is required to control the virus. We define CTL memory as long-term persistence of CTL precursors in the absence of antigen. Infection and depletion of CD4(+) T helper cells interfere with CTL memory generation, resulting in persistent viral replication and disease progression. We find that antiviral drug therapy during primary infection can enable the development of CTL memory. In chronically infected patients, specific treatment schedules, either including deliberate drug holidays or antigenic boosts of the immune system, can lead to a re-establishment of CTL memory. Whether such treatment regimes would lead to long-term immunologic control deserves investigation under carefully controlled conditions.. 25, 96.
Institute for Advanced Study, Olden Lane, Princeton, NJ 08540, USA. wodarz@ias.edulaibe@ebi.ac.ukEMBL-EBIBIOMD0000000683We use mathematical models to study the relationship between HIV and the immune system during the natural course of infection and in the context of different antiviral treatment regimes. The models suggest that an efficient cytotoxic T lymphocyte (CTL) memory response is required to control the virus. We define CTL memory as long-term persistence of CTL precursors in the absence of antigen. Infection and depletion of CD4(+) T helper cells interfere with CTL memory generation, resulting in persistent viral replication and disease progression. We find that antiviral drug therapy during primary infection can enable the development of CTL memory. In chronically infected patients, specific treatment schedules, either including deliberate drug holidays or antigenic boosts of the immune system, can lead to a re-establishment of CTL memory. Whether such treatment regimes would lead to long-term immunologic control deserves investigation under carefully controlled conditions.Specific therapy regimes could lead to long-term immunological control of HIV.Wodarz D D, Nowak M A MAAcquired Immune Deficiency Syndrome Virus, reactivity, Human T-Cell Lymphotropic Virus Type III, Human T-Lymphotropic Virus Type III, Human Immunodeficiency Virus, Human T Lymphotropic Virus Type III, killer T-lymphocyte, Lymphadenopathy-Associated, Viruses, AIDS Viruses, DmelCG33122, AIDS Virus, HTLV-III, killer T-cell, Immunodeficiency Viruses, Lymphadenopathy-Associated Virus., CG10030, ctl, cytotoxic T-cell, Human T Cell Leukemia Virus Type III, LAV-HTLV-III, Human Immunodeficiency, cytolytic T-cell, Human, Lymphadenopathy Associated Virus, AIDS, Immunodeficiency Virus, responsivity, Acquired Immunodeficiency Syndrome Virus, Virus, Lymphadenopathy-Associated Viruses, HIV, response, Human T-Cell Leukemia Virus Type III, Human Immunodeficiency Viruses, CTL, Human T Cell Lymphotropic Virus Type III, CG33122, AIDS virus, cytolytic T-lymphocyteHuman T-Cell Lymphotropic Virus Type III, viral infectious cycle, Concept Relationship, Immune Systems, T-cell surface antigen T4/Leu-3, single-organism developmental process, Math, Different, CDISC Relationship Class, cytotoxic T cell, Suggestion, AIDS Virus, HTLV-III, Infestations and Infections, Nurture, killer T lymphocyte, CG10030, Antiviral, Antiviral Agent, model, ctl, Human Immunodeficiency, Antiviral Drug, Long Term, Human, Agent, Lymphadenopathy Associated Virus, L3T4, Relations, responsivity, Virus, Antigen, Ly-4, viral replication, Clinical Progression, Requirement, Festivals, Related, alpha-beta cytotoxic T-cell, Human T-Cell Leukemia Virus Type III, Persistent Embryonic Structure, Models, Conditions., primary, Object Relationship, Drugs, Progression, study, reactivity, Project ENABLE, Modeling System, Human T-Lymphotropic Virus Type III, {Course}, killer T-lymphocyte, Clinical, Viruses, reference sample, Natural, Suggest, absent from organism, egress, Association, Immunodeficiency Viruses, killer T-cell, Long-Term, course, cytotoxic T-cell, Human T Cell Leukemia Virus Type III, Employ, Immunology (NCI Program), Context, Usage, Infestation and Infection, Application Context, drugs, Use, Immune, Clinical Course, Mathematical, medicine, Clients, Exacerbation, Lymphadenopathy-Associated Viruses, HIV, Infections and Infestations, Holiday, Relationship, Model, Human Immunodeficiency Viruses, alpha-beta cytotoxic T lymphocyte, Including, cytolytic T-lymphocyte, Controlled, Lymphadenopathy-Associated Virus, Human Immunodeficiency Virus, Controlling, Disease, Primary Tumor, Human T Lymphotropic Virus Type III, Protocol Treatment Course, alpha-beta cytotoxic T-lymphocyte, Interfere, T-cell surface antigen T4|Leu-3, Difference, killer T cell, DmelCG33122, drug, Disease Exacerbation, maturation, Primary, rel, Antiviral Drugs, Course, Client, immunology, sigma virus replication, Festival, development, and release, Interference, AIDS, T-cell differentiation antigen L3T4, Primary Neoplasm, Immunodeficiency Virus, ENABLE, Immunology (Including BRMP), Systems, Infection, PRCDTH, cytotoxic T lymphocyte, Educate, Conflict, Interfered, RELATIONSHIP, AIDS virus, CG33122, Mandatory, viral assembly, Acquired Immune Deficiency Syndrome Virus, absence, Lymphadenopathy-Associated, Model System, AIDS Viruses, Mathematics, System, COURSE, T-cell surface glycoprotein CD4, Relationships, Immunology, Required, Infection and Infestation, CD4mut, lytic viral life cycle, Immunologic, cytotoxic T-lymphocyte, rela, LAV-HTLV-III, Requisite, Drug, cytolytic T-cell, Specified, Condition, PERSISTENT, Differential, CD8-positive, Agents, Patient, Persistent, primary tumor, Primary Cause of Death, Specific, Acquired Immunodeficiency Syndrome Virus, CD4, Inclusive, response, Antivirals, CTL, Human T Cell Lymphotropic Virus Type III, Advise Before Life Endsextent, activated cell autonomous cell death, fs(1)A384, dec, Human T-Cell Lymphotropic Virus Type III, viral infectious cycle, Public Sectors, Immune Systems, T-cell surface antigen T4/Leu-3, single-organism developmental process, NetrinA, AUTSX5, AIDS Virus, D430049E23Rik, Infestations and Infections, E-Cadherin, killer T lymphocyte, CG10030, Antiviral, Antiviral Agent, ctl, CCN3, QM, Human Immunodeficiency, Lymphadenopathy Associated Virus, dmTAF[[II]]230, fs(1)A257, L3T4, responsivity, Virus, Antigen, Ly-4, Festivals, alpha-beta cytotoxic T-cell, TEP1, fs(1)5, Public Enterprise, fs(1)M104, fs(1)M102, Progression, treatment, dec1, Elkh, fs(1)14-963, killer T-lymphocyte, reference sample, TFIID TAF250, cel, fs(1)11-549, DCAD2, long, DCad2, Public Domains, EK6, killer T-cell, Sap-2, cytotoxic T-cell, activated T-lymphocyte autonomous cell death, DECad, CG3722, DmelCG4063, IBP-9, DE Cad, neuroendocrine tumour, Immune, activated T cell apoptosis, DE-CAD2, dEcad, Solute carrier family 6 member 2, medicine, disease management, CT27014, Exacerbation, NET1, SLC6A5, fs(1)M1021, TBL1, Tbl1, Infections and Infestations, Holiday, DECadh, netA, NOVh, DEcad, fs(1)12-3907, alpha-beta cytotoxic T lymphocyte, activated T-cell autonomous cell death, cytolytic T-lymphocyte, DE, dTAF[[II]]230, Elk, ELK, alpha-beta cytotoxic T-lymphocyte, T-cell surface antigen T4|Leu-3, completeness, Neuronally-expressed EPH-related tyrosine kinase, DmelCG33122, Disease Exacerbation, TAF200, Shg, SAP2, 9330129L11, DE-Cad2, TAFII-250, TAF250/230, activated T lymphocyte autonomous cell death, neuroendocrine neoplasm, DE-cadh, fs(1)12-1873, sigma virus replication, Festival, fs(1)1501, fs(1)12-365, TAFII250, and release, AIDS, PTEN1, Norepinephrine transporter, ECadh, DE-Cadherin, Public Domain, Domains, DE-cadherin, EPH-like kinase 6, University, NOV, PlexA1, Domain, Acquired Immune Deficiency Syndrome Virus, shg/DE-Cad, Plxn1, absence, D E-cad, Lymphadenopathy-Associated, CG4063, E-cadherin, MMAC1, System, T-cell surface glycoprotein CD4, nov, Infection and Infestation, CD4mut, lytic viral life cycle, hEK6, CG17603, TAF[[II]], gp150, cytotoxic T-lymphocyte, E-2f, mKIAA4053, Fc, E-2g, fs(1)Y[b], cytolytic T-cell, DmelCG18657, Sector, Agents, Taf250, Patient, DmelCG3722, SR3-5, C130088N23Rik, Acquired Immunodeficiency Syndrome Virus, Fc1, Antivirals, DXS648E, CT12481, com5, BZS, DCad, ECad2, TAF230, AW488255, fs(1)12-2514, d230, Sectors, DE Cadh, Tb11, YB, GLM2, fs(1)14A-114, fs(1)384, cytotoxic T cell, number, HTLV-III, dTAFII250, Copyrights, EfW1, presence, Antiviral Drug, Human, l(2)10469, l(2)k03401, DmelCG2175, FBXW4, netrin, Agent, MHAM, Yb, dmTAF1, Hek6, Taf230, viral replication, Clinical Progression, Cek6, Human T-Cell Leukemia Virus Type III, Enterprises, CG2706, ENSMUSG00000074119, TAF250, CadE, Drugs, Ecad, study, reactivity, Erp, APUDoma, ERP, Human T-Lymphotropic Virus Type III, Taf200, dTAF[[II]]250, Clinical, Viruses, cadh, cell, EBI, Ebi, absent from organism, egress, Tyrosine-protein kinase receptor EPH-2, Immunodeficiency Viruses, Taf1p, Fcp7C, IGFBP9, Public Enterprises, Human T Cell Leukemia Virus Type III, ECAD, ECad, fs(1)12-3512, dTAF250, Infestation and Infection, drugs, Abstract, 2.7.10.1, Clinical Course, D-cad, L10, Clients, Etrp, Lymphadenopathy-Associated Viruses, HIV, NAT1, Human Immunodeficiency Viruses, TAF, Enterprise, Net, NET, CADH, Controlled, Lymphadenopathy-Associated Virus, DE[cyto], Controlling, Human Immunodeficiency Virus, Disease, TAF[[II]]250, C130099E04Rik, Human T Lymphotropic Virus Type III, dec[[1]], fs(1)13C-73, killer T cell, DmelCG2706, drug, DE-cad, EPH tyrosine kinase 2, maturation, DXS648, l(3)84Ab, CG2175, BG:DS00004.13, SMAP55, Antiviral Drugs, neuroendocrine tumor, Client, net, Cadh, Cell, dTAF230, fs(1)C1, development, fs(1)12-403, count in organism, N-cad, Cad, fs(1)12-4860, T-cell differentiation antigen L3T4, IGFBP-9, Immunodeficiency Virus, Public, p230, CWS1, Systems, Infection, DE-CAD, DE-Cad, TAF[[II]]250/230, TFIID, fs(1)14E19, cytotoxic T lymphocyte, AIDS virus, CG33122, Data Base, viral assembly, Taf[[II]]250, cad, TAF[[II]]230, AIDS Viruses, 10q23del, TAF[II]250, ACAD, CG18657, E-cad, LAV-HTLV-III, l(2)k16213, Drug, DEC, presence or absence in organism., DmelCG17603, CD8-positive, EPHT2, EG:95B7.8, fs(1)13-453, CD4, fs(1)13C-57, 2600013D04Rik, response, quantitative, CTL, e-cad, netrin A, Human T Cell Lymphotropic Virus Type III, E-CAD, E-Cad, l(2)k10220, TAF1treatment, Acquired Immune Deficiency Syndrome Virus, Controlling, Human T-Cell Lymphotropic Virus Type III, Human T-Lymphotropic Virus Type III, Human Immunodeficiency Virus, Human T Lymphotropic Virus Type III, Lymphadenopathy-Associated, reference sample, Viruses, AIDS Viruses, AIDS Virus, HTLV-III, Immunodeficiency Viruses, Immunotherapy, immunotherapy, Lymphadenopathy-Associated Virus., Long-Term, Human T Cell Leukemia Virus Type III, LAV-HTLV-III, Long Term, Immunological, Human Immunodeficiency, Specified, Human, Lymphadenopathy Associated Virus, AIDS, Specific, Immunodeficiency Virus, Immunologically Directed Therapy, Acquired Immunodeficiency Syndrome Virus, disease management, Virus, Lymphadenopathy-Associated Viruses, HIV, IMMUNOTHERAPY, Human T-Cell Leukemia Virus Type III, Human Immunodeficiency Viruses, Human T Cell Lymphotropic Virus Type III, AIDS virus, Immunological Therapy, ControlledfalseWodarz1999 CTL memory response HIV
This a model from the article:
Specific therapy regimes could lead to long-term immunological control of HIV.
Wodarz D, Nowak MA. Proc Natl Acad Sci U S A
1999 Dec 7;96(25):14464-9 10588728
,
Abstract:
We use mathematical models to study the relationship between HIV and the immune
system during the natural course of infection and in the context of different
antiviral treatment regimes. The models suggest that an efficient cytotoxic T
lymphocyte (CTL) memory response is required to control the virus. We define CTL
memory as long-term persistence of CTL precursors in the absence of antigen.
Infection and depletion of CD4(+) T helper cells interfere with CTL memory
generation, resulting in persistent viral replication and disease progression.
We find that antiviral drug therapy during primary infection can enable the
development of CTL memory. In chronically infected patients, specific treatment
schedules, either including deliberate drug holidays or antigenic boosts of the
immune system, can lead to a re-establishment of CTL memory. Whether such
treatment regimes would lead to long-term immunologic control deserves
investigation under carefully controlled conditions.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Nowak MA. (1999) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
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.
2019-08-222019-08-222010-06-23BIOMD0000000683SBO:0000610SBO:000017910588728C12537MODEL1006230062BIOMD0000000683GO:0046718GO:0008219GO:0001909GO:0045065GO:0046651GO:0042493CL:00009119606BTO:0000289BTO:00024170000764000165100014600000544