Abstract. We give a survey of results on global stability for deterministic compartmental epidemiological models. Using Lyapunov techniques we revisit a classical result, and give a simple proof. By the same methods we also give a new result on differential susceptibility and infectivity models with mass action and an arbitrary number of compartments. These models encompass the so-called differential infectivity and staged progression models. In the two cases we prove that if the basic reproduction ratio R 0 ≤ 1, then the disease free equilibrium is globally asymptotically stable. If R 0 > 1, there exists an unique endemic equilibrium which is asymptotically stable on the positive orthant.

International audienceIn this paper we propose a malaria within-host model with k classes of age for the parasitized red blood cells and n strains for the parasite. We provide a global analysis for this model. A competitive exclusion principle holds. If R0, the basic reproduction number, satisfies R0 ≤ 1, then the disease-free equilibrium is globally asymptotically stable. On the contrary if R0 > 1, then generically there is a unique endemic equilibrium which corresponds to the endemic stabilization of the most virulent parasite strain and to the extinction of all the other parasites strains. We prove that this equilibrium is globally asymptotically stable on the positive orthant if a mild sufficient condition is satisfied

International audienceWe consider SIS, SIR and MSIR models with standard mass action and varying population, with $n$ different pathogen strains of an infectious disease. We also consider the same models with vertical transmission. We prove that under generic conditions a competitive exclusion principle holds. To each strain a basic reproduction ratio can be associated. It corresponds to the case where only this strain exists. The basic reproduction ratio of the complete system is the maximum of each individual basic reproduction ratio. Actually we also define an equivalent threshold for each strain. The winner of the competition is the strain with the maximum threshold. It turns out that this strain is the most virulent, i.e., this is the strain for which the endemic equilibrium gives the minimum population for the susceptible host population. This can be interpreted as a pessimization principle.On considère les modèles SIS, SIR et MSIR avec la loi de l'action de masse standard et une population non constante, avec n différentes souches de pathogènes. Nous considérons aussi les même modèles avec transmission verticale. On prouve que sous une condition générique, le principe de compétition exclusive est vérifié. Pour chaque souche, un nombre de reproduction de base est associé. Il correspond au cas où seule cette souche existe. Le nombre de reproduction de base du système complet est le maximum de tous les nombres de reproduction de base pris individuellement. Nous définissons aussi un seuil équivalent pour chaque souche. La souche qui gagne la compétition est celle qui maximise le nombre de reproduction de base. C'est aussi la souche la plus virulente, i.e., c'est la souche pour laquelle l'équilibre endémique donne le minimum des individus susceptibles dans la population hôte. C'est le principe de pessimisation

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An extension of the backstepping approach is proposed. It allows to globally asymptotically stabilize by bounded feedbacks families of nonlinear control systems. Explicit expressions of control laws and Lyapunov functions are given.

We develop a multi-patch and multi-group model that captures the dynamics of an infectious disease when the host is structured into an arbitrary number of groups and interacts into an arbitrary number of patches where the infection takes place. In this framework, we model host mobility that depends on its epidemiological status, by a Lagrangian approach. This framework is applied to a general SEIRS model and the basic reproduction number [Formula: see text] is derived. The effects of heterogeneity in groups, patches and mobility patterns on [Formula: see text] and disease prevalence are explored. Our results show that for a fixed number of groups, the basic reproduction number increases with respect to the number of patches and the host mobility patterns. Moreover, when the mobility matrix of susceptible individuals is of rank one, the basic reproduction number is explicitly determined and was found to be independent of the latter if the matrix is also stochastic. The cases where mobility matrices are of rank one capture important modeling scenarios. Additionally, we study the global analysis of equilibria for some special cases. Numerical simulations are carried out to showcase the ramifications of mobility pattern matrices on disease prevalence and basic reproduction number.

We introduce classes of differential susceptibility and infectivity epidemic models. These models address the problem of flows between the different susceptible, infectious and infected compartments and differential death rates as well. We prove the global stability of the disease free equilibrium when the basic reproduction ratio R0≤1 and the existence and uniqueness of an endemic equilibrium when R0>1. We also prove the global asymptotic stability of the endemic equilibrium for a differential susceptibility and staged progression infectivity model, when R0>1. Our results encompass and generalize those of Hyman and Li (J Math Biol 50:626-644, 2005; Math Biosci Eng 3:89-100, 2006).

Abstract. The resurgence of vector-borne diseases is an increasing public health concern, and there is a need for a better understanding of their dynamics. For a number of diseases, e.g. dengue and chikungunya, this resurgence occurs mostly in urban environments, which are naturally very heterogeneous, particularly due to population circulation. In this scenario, there is an increasing interest in both multi-patch and multigroup models for such diseases. In this work, we study the dynamics of a vector borne disease within a class of multi-group models that extends the classical Bailey-Dietz model. This class includes many of the proposed models in the literature, and it can accommodate various functional forms of the infection force. For such models, the vector-host/host-vector contact network topology gives rise to a bipartite graph which has different properties from the ones usually found in directly transmitted diseases. Under the assumption that the contact network is strongly connected, we can define the basic reproductive number R 0 and show that this system has only two equilibria: the so called disease free equilibrium (DFE); and a unique interior equilibrium-usually termed the endemic equilibrium (EE)-that exists if, and only if, R 0 > 1. We also show that, if R 0 ≤ 1, then the DFE equilibrium is globally asymptotically stable, while when R 0 > 1, we have that the EE is globally asymptotically stable.