Recombinant viruses and early global HIV-1 epidemic.
Ontology highlight
ABSTRACT:
SUBMITTER: Kalish ML
PROVIDER: S-EPMC3323344 | biostudies-literature | 2004 Jul
REPOSITORIES: biostudies-literature
Publications
Recombinant viruses and early global HIV-1 epidemic.
Kalish Marcia L ML Robbins Kenneth E KE Pieniazek Danuta D Schaefer Amanda A Nzilambi Nzila N Quinn Thomas C TC St Louis Michael E ME Youngpairoj Ae S AS Phillips Jonathan J Jaffe Harold W HW Folks Thomas M TM
Emerging infectious diseases 20040701 7
Central Africa was the epicenter of the HIV type 1 (HIV-1) pandemic. Understanding the early epidemic in the Democratic Republic of the Congo, formerly Zaire, could provide insight into how HIV evolved and assist vaccine design and intervention efforts. Using enzyme immunosorbent assays, we tested 3,988 serum samples collected in Kinshasa in the mid-1980s and confirmed seroreactivity by Western blot. Polymerase chain reaction of gag p17, env C2V3C3, and/or gp41; DNA sequencing; and genetic analy ...[more]
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Project description:This a model from the article:
Fighting a virus with a virus: a dynamic model for HIV-1 therapy.
Revilla T, Garcia-Ramos G. Math Biosci
2003 Oct;185(2):191-203 12941536
,
Abstract:
A mathematical model examined a potential therapy for controlling viral
infections using genetically modified viruses. The control of the infection is
an indirect effect of the selective elimination by an engineered virus of
infected cells that are the source of the pathogens. Therefore, this engineered
virus could greatly compensate for a dysfunctional immune system compromised by
AIDS. In vitro studies using engineered viruses have been shown to decrease the
HIV-1 load about 1000-fold. However, the efficacy of this potential treatment
for reducing the viral load in AIDS patients is unknown. The present model
studied the interactions among the HIV-1 virus, its main host cell (activated
CD4+ T cells), and a therapeutic engineered virus in an in vivo context; and it
examined the conditions for controlling the pathogen. This model predicted a
significant drop in the HIV-1 load, but the treatment does not eradicate HIV. A
basic estimation using a currently engineered virus indicated an HIV-1 load
reduction of 92% and a recovery of host cells to 17% of their normal level.
Greater success (98% HIV reduction, 44% host cells recovery) is expected as more
competent engineered viruses are designed. These results suggest that therapy
using viruses could be an alternative to extend the survival of AIDS patients.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Revilla T, Garcia-Ramos G. (2003) - 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.
2024-09-02 | BIOMD0000000707 | BioModels
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