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We propose a generalization of the adaptive N-Intertwined Mean-Field Approximation (aNIMFA) model studied in \emph{Achterberg and Sensi} \cite{achterbergsensi2022adaptive} to a heterogeneous network of communities. In particular, the multigroup aNIMFA model describes the impact of both local and global disease awareness on the spread of a disease in a network. We obtain results on existence and stability of the equilibria of the system, in terms of the basic reproduction number~$R_0$. Under light constraints, we show that the basic reproduction number~$R_0$ is equivalent to the basic reproduction number of the NIMFA model on static networks. Based on numerical simulations, we demonstrate that with just two communities periodic behaviour can occur, which contrasts the case with only a single community, in which periodicity was ruled out analytically. We also find that breaking connections between communities is more fruitful compared to breaking connections within communities to reduce the disease outbreak on dense networks, but both strategies are viable to networks with fewer links. Finally, we emphasise that our method of modelling adaptivity is not limited to SIS models, but has huge potential to be applied in other compartmental models in epidemiology., Comment: 19 pages, 10 figures

We propose a novel slow-fast SIRS compartmental model with demography, by coupling a slow disease spreading model and a fast information and misinformation spreading model. Beside the classes of susceptible, infected and recovered individuals of a common SIRS model, here we define three new classes related to the information spreading model, e.g. unaware individuals, misinformed individuals and individuals who are skeptical to disease-related misinformation. Under our assumptions, the system evolves on two time scales. We completely characterize its asymptotic behaviour with techniques of Geometric Singular Perturbation Theory (GSPT). We exploit the time scale separation to analyse two lower dimensional subsystem separately. First, we focus on the analysis of the fast dynamics and we find three equilibrium point which are feasible and stable under specific conditions. We perform a theoretical bifurcation analysis of the fast system to understand the relations between these three equilibria when varying specific parameters of the fast system. Secondly, we focus on the evolution of the slow variables and we identify three branches of the critical manifold, which are described by the three equilibria of the fast system. We fully characterize the slow dynamics on each branch. Moreover, we show how the inclusion of (mis)information spread may negatively or positively affect the evolution of the epidemic, depending on whether the slow dynamics evolves on the second branch of the critical manifold, related to the skeptical-free equilibrium or on the third one, related to misinformed-free equilibrium, respectively. We conclude with numerical simulations which showcase our analytical results., Comment: 28 pages, 8 figures, 1 table

We propose a compartmental model for a disease with temporary immunity and secondary infections. From our assumptions on the parameters involved in the model, the system naturally evolves in three time scales. We characterize the equilibria of the system and analyze their stability. We find conditions for the existence of two endemic equilibria, for some cases in which $\mathcal{R}_0 < 1$. Then, we unravel the interplay of the three time scales, providing conditions to foresee whether the system evolves in all three scales, or only in the fast and the intermediate ones. We conclude with numerical simulations and bifurcation analysis, to complement our analytical results., Comment: 31 pages, 9 figures

In contemporary society, social networks accelerate decision dynamics causing a rapid switch of opinions in a number of fields, including the prevention of infectious diseases by means of vaccines. This means that opinion dynamics can nowadays be much faster than the spread of epidemics. Hence, we propose a Susceptible-Infectious-Removed epidemic model coupled with an evolutionary vaccination game embedding the public health system efforts to increase vaccine uptake. This results in a global system ``epidemic model + evolutionary game''. The epidemiological novelty of this work is that we assume that the switching to the strategy ``pro vaccine'' depends on the incidence of the disease. As a consequence of the above-mentioned accelerated decisions, the dynamics of the system acts on two different scales: a fast scale for the vaccine decisions and a slower scale for the spread of the disease. Another, and more methodological, element of novelty is that we apply Geometrical Singular Perturbation Theory (GSPT) to such a two-scale model and we then compare the geometric analysis with the Quasi-Steady-State Approximation (QSSA) approach, showing a criticality in the latter. Later, we apply the GSPT approach to the disease prevalence-based model already studied in (Della Marca and d'Onofrio, Comm Nonl Sci Num Sim, 2021) via the QSSA approach by considering medium-large values of the strategy switching parameter., Comment: 26 pages, 6 figures

In this survey, we propose an overview on Lyapunov functions for a variety of compartmental models in epidemiology. We exhibit the most widely employed functions, together with a commentary on their use. Our aim is to provide a comprehensive starting point to readers who are attempting to prove global stability of systems of ODEs. The focus is on mathematical epidemiology, however some of the functions and strategies presented in this paper can be adapted to a wider variety of models, such as prey-predator or rumor spreading., Comment: 18 pages, 4 figures

We study a multi-group SAIRS-type epidemic model with vaccination. The role of asymptomatic and symptomatic infectious individuals is explicitly considered in the transmission pattern of the disease among the groups in which the population is divided. This is a natural extension of the homogeneous mixing SAIRS model with vaccination studied in Ottaviano et. al (2021) to a network of communities. We provide a global stability analysis for the model. We determine the value of the basic reproduction number $\mathcal{R}_0$ and prove that the disease-free equilibrium is globally asymptotically stable if $\mathcal{R}_0 < 1$. In the case of the SAIRS model without vaccination, we prove the global asymptotic stability of the disease-free equilibrium also when $\mathcal{R}_0=1$. Moreover, if $\mathcal{R}_0 > 1$, the disease-free equilibrium is unstable and a unique endemic equilibrium exists. First, we investigate the local asymptotic stability of the endemic equilibrium and subsequently its global stability, for two variations of the original model. Last, we provide numerical simulations to compare the epidemic spreading on different networks topologies., Comment: 36 pages, 8 figures

We study an SAIRS-type epidemic model with vaccination, where the role of asymptomatic and symptomatic infectious individuals are explicitly considered in the transmission patterns of the disease. We provide a global stability analysis for the model. We determine the value of the basic reproduction number $\mathcal{R}_0$ and prove that the disease-free equilibrium is globally asymptotically stable if $\mathcal{R}_0<1$ and unstable if $\mathcal{R}_0>1$, condition under which a positive endemic equilibrium exists. We investigate the global stability of the endemic equilibrium for some variations of the original model under study and answer to an open problem proposed in Ansumali et al. \cite{ansumali2020modelling}. In the case of the SAIRS model without vaccination, we prove the global asymptotic stability of the disease-free equilibrium also when $\mathcal{R}_0=1$. We provide a thorough numerical exploration of our model, to validate our analytical results., Comment: 29 page, 7 figures

With the premise that social interactions are described by power-law distributions, we study a SIR stochastic dynamic on a static scale-free random network generated via configuration model. We verify our model with respect to deterministic considerations and provide a theoretical result on the probability of the extinction of the disease. Based on this calibration, we explore the variability in disease spread by stochastic simulations. In particular, we demonstrate how important epidemic indices change as a function of the contagiousness of the disease and the connectivity of the network. Our results quantify the role of starting node degree in determining these indices, commonly used to describe epidemic spread., Comment: 22 pages, 9 figures

Aim of this manuscript is to show a simple method to infer the time-course of new COVID-19 infections (the most important information in order to establish the effect of containment strategies) from available aggregated data, such as number of deaths and hospitalizations. The method, that was used for HIV-AIDS and was named `back-calculation', relies on good estimates of the distribution of the delays between infection and the observed events; assuming that the epidemic follows a simple SIR model with a known generation interval, we can then estimate the parameters that define the time-varying contact rate through maximum likelihood. We show the application of the method to data from Italy and several of its region; it is found that $R_0$ had decreased consistently below 1 around March 20, and in the beginning of April it was between 0.5 and 0.8 in the whole Italy and in most regions.