MODEL1302180002#
type: KineticLaw
name: muw8
name: muw48
constant: true
name: THa
spatial dimensions: 3.0
name: cost
initial amount: 1000000.0
name: _Evolution_D48
boundary condition: false
name: TCPr1
name: rhoD
name: rhoC
size: 1.0
name: CC0
name: rho4
name: C8
name: _Evolution_D8
value: 1000000.0
name: a8
initial amount: 0.0
name: CDr0
name: C48
has only substance units: true
name: alphaD
name: TCPr2
value: 3000000.0
name: _Evolution_V8
value: 0.05
name: gamma4r
value: 0.005
fast: false
name: TCa
name: TCr
name: _Evolution_TCr
name: murevw4
name: gamma8a
value: 5000.0
initial amount: 1.0
type: FunctionDef
name: murevw48
name: k
name: gammaDr
value: 1.0
value: 0.1
type: Species
name: D48
value: 15.0
name: gammaDa
name: C4r0
name: _Evolution_Dw
name: _Evolution_Cw
name: THr
name: C
name: b8
name: gamma4a
reversible: false
name: muw4
type: Parameter
name: rho8
name: _Evolution_TCPr1
type: Compartment
name: gamma8pr
name: sigmaD
name: sigma
name: b
initial amount: 100000.0
name: a8D
name: gamma8r
name: V48
initial amount: 3000000.0
value: 0.0
stoichiometry: NaN
name: _Evolution_V48
value: 100000.0
value: 0.001
name: body
type: Reaction
name: C4
value: 0.01

MODEL1302180002
type: SBMLModel
function def: MODEL1302180002#
name: Sanjuan2013 - Evolution of HIV T-cell epitope, control model
notes: Sanjuan2013 - Evolution of HIV T-cell epitope, control model Control model in which the virus targets a nonimmune cell type C (e.g., hepatocytes, epithelial cells, etc.), instead of T H cells. This model is described in the article: Immune activation promotes evolutionary conservation of T-cell epitopes in HIV-1. Sanjuán R, Nebot MR, Peris JB, Alcamí J. PLoS Biol. 2013 Apr;11(4):e1001523 Abstract: The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (TH cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when TH cell infection is concomitant to epitope recognition (trans-infection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved TH epitopes may be counterproductive. This model is hosted on BioModels Database and identified by: MODEL1302180002 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright a…
reaction: MODEL1302180002#
name: Interaction term
compartment: MODEL1302180002#
parameter: MODEL1302180002#
species: MODEL1302180002#
curated: false