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Simon Girel

Publications and source records attributed to Simon Girel.

5 recordsLinked to original sources

Competitive exclusion and coexistence in a model with age-structured resource

In this paper, we introduce and analyse a model in which a shared, age-structured resource is exploited by two competing populations through age-dependent interaction kernels. It provides a general framework for studying resource-mediated competition in epidemiology, immunology and ecology. We use integrated semigroups theory to establish the well-posedness of the model and its fundamental properties, including positivity and the existence of a global attractor. Then, by means of Lyapunov functionals, persistence results and generalised LaSalle principle, we fully characterize the asymptotic dynamics in terms of the competitors's basic reproduction numbers and invasive fitnesses. Our results demonstrate that in addition to the classical competitive exclusion, the system can exhibit globally asymptotically stable coexistence, an outcome allowed by a mechanism of age-mediated niche partitioning.

math.AP

On the global asymptotic stability of an infection-age structured competitive model

We investigate an infection-age structured competitive epidemiological model involving multiple strains. While classical results establish competitive exclusion when a unique maximal basic reproduction number exists, we provide here a complete characterization of the asymptotic behavior for an arbitrary number of populations without assuming uniqueness of the maximal reproduction number. By means of integrated semigroups theory, persistence results, and Lyapunov functionals, we establish global asymptotic stability of equilibria and extend previous results obtained for simpler (ODE) models. A key contribution lies in overcoming technical difficulties related to the definition and differentiation of Lyapunov functionals, as well as in refining arguments based on the LaSalle invariance principle.

math.AP

How delay, isolation and vaccination shape epidemic waves: a bifurcation approach in mathematical epidemiology

This research paper introduces an SQIR-V epidemic model to investigate the transmission of infectious diseases. Particular attention is paid to the roles of vaccination and quarantine (incorporating physical distancing interventions) in protecting susceptible individuals. The model features nonlinear transition rates that depend on the history of infection, allowing the emergence of periodic solutions. We calculate the basic reproduction number, R 0 , and analyze the local asymptotic stability of the equilibrium points. Additionally, we demonstrate that the diseasefree equilibrium is globally asymptotically stable when R 0 $\le$ 1. The study further explores the existence of periodic solutions through a Hopf bifurcation, showing the occurrence of epidemic waves. A condition was derived to determine the direction of the crossing of the imaginary axis. We finish by presenting some numerical simulations to illustrate how vaccination and isolation delays influence disease dynamics. Those findings highlight potential areas for further research and validation.

math.DS

Model-based assessment of the Role of Uneven Partitioning of Molecular Content on Heterogeneity and Regulation of Differentiation in CD8 T-cell Immune Responses

Activation of naive CD8 T-cells can lead to the generation of multiple effector and memory subsets. Multiple parameters associated with activation conditions are involved in generating this diversity that is associated with heterogeneous molecular contents of activated cells. Although naive cell polarisation upon antigenic stimulation and the resulting asymmetric division are known to be a major source of heterogeneity and cell fate regulation, the consequences of stochastic uneven partitioning of molecular content upon subsequent divisions remain unclear yet. Here we aim at studying the impact of uneven partitioning on molecular-content heterogeneity and then on the immune response dynamics at the cellular level. To do so, we introduce a multiscale mathematical model of the CD8 T-cell immune response in the lymph node. In the model, cells are described as agents evolving and interacting in a 2D environment while a set of differential equations, embedded in each cell, models the regulation of intra and extracellular proteins involved in cell differentiation. Based on the analysis of in silico data at the single cell level, we 1 show that immune response dynamics can be explained by the molecular-content heterogeneity generated by uneven partitioning at cell division. In particular, uneven partitioning acts as a regulator of cell differentiation and induces the emergence of two coexisting sub-populations of cells exhibiting antagonistic fates. We show that the degree of unevenness of molecular partitioning, along all cell divisions, affects the outcome of the immune response and can promote the generation of memory cells.

q-bio.CB

Existence and stability of periodic solutions of an impulsive differential equation and application to CD8 T-cell differentiation

Unequal partitioning of the molecular content at cell division has been shown to be a source of heterogeneity in a cell population. We propose to model this phenomenon with the help of a scalar, nonlinear impulsive differential equation (IDE). In a first part, we consider a general autonomous IDE with fixed times of impulse and a specific form of impulse function. We establish properties of the solutions of that equation, most of them obtained under the hypothesis that impulses occur periodically. In particular, we show how to investigate the existence of periodic solutions and their stability by studying the flow of an autonomous differential equation. A second part is dedicated to the analysis of the convexity of this flow. Finally, we apply those results to an IDE describing the concentration of the protein Tbet in a CD8 T-cell, where impulses are associated to cell division, to study the effect of molecular partitioning at cell division on the effector/memory cell-fate decision in a CD8 T-cell lineage. We show that the degree of asymmetry in the molecular partitioning can affect the process of cell differentiation and the phenotypical heterogeneity of a cell population.

math.DS