No Arabic abstract
Public health services are constantly searching for new ways to reduce the spread of infectious diseases, such as public vaccination of asymptomatic individuals, quarantine (isolation) and treatment of symptomatic individuals. Epidemic models have a long history of assisting in public health planning and policy making. In this paper, we introduce epidemic models including variable population size, degree-related imperfect vaccination and quarantine on scale-free networks. More specifically, the models are formulated both on the population with and without permanent natural immunity to infection, which corresponds respectively to the susceptible-vaccinated-infected-quarantined-recovered (SVIQR) model and the susceptible-vaccinated-infected-quarantined (SVIQS) model. We develop different mathematical methods and techniques to study the dynamics of two models, including the basic reproduction number, the global stability of disease-free and endemic equilibria. For the SVIQR model, we show that the system exhibits a forward bifurcation. Meanwhile, the disease-free and unique endemic equilibria are shown to be globally asymptotically stable by constructing suitable Lyapunov functions. For the SVIQS model, conditions ensuring the occurrence of multiple endemic equilibria are derived. Under certain conditions, this system cannot undergo a backward bifurcation. The global asymptotical stability of disease-free equilibrium, and the persistence of the disease are proved. The endemic equilibrium is shown to be globally attractive by using monotone iterative technique. Finally, stochastic network simulations yield quantitative agreement with the deterministic mean-field approach.
We study the relative importance of two key control measures for epidemic spreading: endogenous social self-distancing and exogenous imposed quarantine. We use the framework of adaptive networks, moment-closure, and ordinary differential equations (ODEs) to introduce several novel models based upon susceptible-infected-recovered (SIR) dynamics. First, we compare computationally expensive, adaptive network simulations with their corresponding computationally highly efficient ODE equivalents and find excellent agreement. Second, we discover that there exists a relatively simple critical curve in parameter space for the epidemic threshold, which strongly suggests that there is a mutual compensation effect between the two mitigation strategies: as long as social distancing and quarantine measures are both sufficiently strong, large outbreaks are prevented. Third, we study the total number of infected and the maximum peak during large outbreaks using a combination of analytical estimates and numerical simulations. Also for large outbreaks we find a similar compensation effect as for the epidemic threshold. This suggests that if there is little incentive for social distancing within a population, drastic quarantining is required, and vice versa. Both pure scenarios are unrealistic in practice. Our models show that only a combination of measures is likely to succeed to control epidemic spreading. Fourth, we analytically compute an upper bound for the total number of infected on adaptive networks, using integral estimates in combination with the moment-closure approximation on the level of an observable. This is a methodological innovation. Our method allows us to elegantly and quickly check and cross-validate various conjectures about the relevance of different network control measures.
The resurgence of measles is largely attributed to the decline in vaccine adoption and the increase in mobility. Although the vaccine for measles is readily available and highly successful, its current adoption is not adequate to prevent epidemics. Vaccine adoption is directly affected by individual vaccination decisions, and has a complex interplay with the spatial spread of disease shaped by an underlying mobility (travelling) network. In this paper, we model the travelling connectivity as a scale-free network, and investigate dependencies between the networks assortativity and the resultant epidemic and vaccination dynamics. In doing so we extend an SIR-network model with game-theoretic components, capturing the imitation dynamics under a voluntary vaccination scheme. Our results show a correlation between the epidemic dynamics and the networks assortativity, highlighting that networks with high assortativity tend to suppress epidemics under certain conditions. In highly assortative networks, the suppression is sustained producing an early convergence to equilibrium. In highly disassortative networks, however, the suppression effect diminishes over time due to scattering of non-vaccinating nodes, and frequent switching between the predominantly vaccinating and non-vaccinating phases of the dynamics.
Evolutionary game theory is employed to study topological conditions of scale-free networks for the evolution of cooperation. We show that Apollonian Networks (ANs) are perfect scale-free networks, on which cooperation can spread to all individuals, even though there are initially only 3 or 4 hubs occupied by cooperators and all the others by defectors. Local topological features such as degree, clustering coefficient, gradient as well as topology potential are adopted to analyze the advantages of ANs in cooperation enhancement. Furthermore, a degree-skeleton underlying ANs is uncovered for understanding the cooperation diffusion. Constructing this kind degree-skeleton for random scale-free networks promotes cooperation level close to that of Barabasi-Albert networks, which gives deeper insights into the origin of the latter on organization and further promotion of cooperation.
Vaccination is an important measure available for preventing or reducing the spread of infectious diseases. In this paper, an epidemic model including susceptible, infected, and imperfectly vaccinated compartments is studied on Watts-Strogatz small-world, Barabasi-Albert scale-free, and random scale-free networks. The epidemic threshold and prevalence are analyzed. For small-world networks, the effective vaccination intervention is suggested and its influence on the threshold and prevalence is analyzed. For scale-free networks, the threshold is found to be strongly dependent both on the effective vaccination rate and on the connectivity distribution. Moreover, so long as vaccination is effective, it can linearly decrease the epidemic prevalence in small-world networks, whereas for scale-free networks it acts exponentially. These results can help in adopting pragmatic treatment upon diseases in structured populations.
The existence of a die-out threshold (different from the classic disease-invasion one) defining a region of slow extinction of an epidemic has been proved elsewhere for susceptible-aware-infectious-susceptible models without awareness decay, through bifurcation analysis. By means of an equivalent mean-field model defined on regular random networks, we interpret the dynamics of the system in this region and prove that the existence of bifurcation for this second epidemic threshold crucially depends on the absence of awareness decay. We show that the continuum of equilibria that characterizes the slow die-out dynamics collapses into a unique equilibrium when a constant rate of awareness decay is assumed, no matter how small, and that the resulting bifurcation from the disease-free equilibrium is equivalent to that of standard epidemic models. We illustrate these findings with continuous-time stochastic simulations on regular random networks with different degrees. Finally, the behaviour of solutions with and without decay in awareness is compared around the second epidemic threshold for a small rate of awareness decay.