MODEL1302180001#
type: Parameter
name: C8r0
initial concentration: NaN
value: 0.03
name: THw
name: muw48
value: 1.0
type: Species
name: _Evolution_TCPr1
name: D48
value: 15.0
name: gammaDa
name: C4r0
name: _Evolution_TH8
initial amount: 100000.0
name: d
name: rhoD
reversible: false
initial amount: 3000000.0
initial amount: 1000000.0
name: _Evolution_V48
value: 1000000.0
name: _Evolution_TH48
type: Reaction
name: b
name: _Evolution_V8
size: 1.0
name: alphaD
name: TCPr2
name: rho4
name: _Evolution_Dr
name: TH48
name: _Evolution_D4
name: a4
name: _Evolution_D8
value: 0.0
name: alpha
constant: false
name: CDr0
value: 100000.0
value: 0.001
name: D8
name: TCr
value: 0.05
name: _Evolution_TCPr2
name: gamma8a
value: 0.01
name: Vw
name: V8
name: k
name: TH8
name: _Evolution_TCr
name: murevw4
type: FunctionDef
value: 0.1
name: Dr
name: D4
name: muw4
boundary condition: false
name: THr
name: TCPr1
name: TH4
type: Compartment
name: gamma4a
name: sigma
name: gamma8r
name: a8D
name: THa
name: rho8
spatial dimensions: 3.0
name: cost
name: a8
type: KineticLaw
initial amount: 0.0
name: gamma8pr
name: sigmaD
name: _Evolution_D48
has only substance units: true
name: _Evolution_THw
name: body

MODEL1302180001
type: SBMLModel
reaction: MODEL1302180001#
parameter: MODEL1302180001#
name: Sanjuan2013 - Evolution of HIV T-cell epitope, immune activation model
name: Interaction term
compartment: MODEL1302180001#
notes: Sanjuan2013 - Evolution of HIV T-cell epitope, immune activation model Model of cellular immune response against HIV. 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. Note from the author: this version of the model is more general that the one described in the paper. This is because: (i) it can consider simultaneously Th-epitope escape mutants, CTL-epitope escape mutants and full T-cell (Th and CTL) escape mutants, by setting the mutation rate of Th and CTL escape mutants to zero. (ii) It allows for back mutations…
species: MODEL1302180001#
curated: false
function def: MODEL1302180001#