No Arabic abstract
We investigate a time-delayed epidemic model for multi-strain diseases with temporary immunity. In the absence of cross-immunity between strains, dynamics of each individual strain exhibits emergence and anni- hilation of limit cycles due to a Hopf bifurcation of the endemic equilibrium, and a saddle-node bifurcation of limit cycles depending on the time delay associated with duration of temporary immunity. Effects of all-to-all and non-local coupling topologies are systematically investigated by means of numerical simulations, and they suggest that cross-immunity is able to induce a diverse range of complex dynamical behaviors and synchro- nization patterns, including discrete traveling waves, solitary states, and amplitude chimeras. Interestingly, chimera states are observed for narrower cross-immunity kernels, which can have profound implications for understanding the dynamics of multi-strain diseases.
We study the dynamics of identical leaky integrate-and-fire neurons with symmetric non-local coupling. Upon varying control parameters (coupling strength, coupling range, refractory period) we investigate the systems behaviour and highlight the formation of chimera states. We show that the introduction of a refractory period enlarges the parameter region where chimera states appear and affects the chimera multiplicity.
We find chimera states with respect to amplitude dynamics in a network of Stuart-Landau oscillators. These partially coherent and partially incoherent spatio-temporal patterns appear due to the interplay of nonlocal network topology and symmetry-breaking coupling. As the coupling range is increased, the oscillations are quenched, amplitude chimeras disappear and the network enters a symmetry-breaking stationary state. This particular regime is a novel pattern which we call chimera death. It is characterized by the coexistence of spatially coherent and incoherent inhomogeneous steady states and therefore combines the features of chimera state and oscillation death. Additionally, we show two different transition scenarios from amplitude chimera to chimera death. Moreover, for amplitude chimeras we uncover the mechanism of transition towards in-phase synchronized regime and discuss the role of initial conditions.
We study the dynamics of mobile, locally coupled identical oscillators in the presence of coupling delays. We find different kinds of chimera states, in which coherent in-phase and anti-phase domains coexist with incoherent domains. These chimera states are dynamic and can persist for long times for intermediate mobility values. We discuss the mechanisms leading to the formation of these chimera states in different mobility regimes. This finding could be relevant for natural and technological systems composed of mobile communicating agents.
Formation of diverse patterns in spatially extended reaction-diffusion systems is an important aspect of study which is pertinent to many chemical and biological processes. Of special interest is the peculiar phenomenon of chimera state having spatial coexistence of coherent and incoherent dynamics in a system of identically interacting individuals. In the present article, we report the emergence of various collective dynamical patterns while considering a system of prey-predator dynamics in presence of a two-dimensional diffusive environment. Particularly, we explore the observance of four distinct categories of spatial arrangements among the species, namely spiral wave, spiral chimera, completely synchronized oscillations, and oscillation death states in a broad region of the diffusion-driven parameter space. Emergence of amplitude mediated spiral chimera states displaying drifted amplitudes and phases in the incoherent subpopulation is detected for parameter values beyond both Turing and Hopf bifurcations. Transition scenarios among all these distinguishable patterns are numerically demonstrated for a wide range of the diffusion coefficients which reveal that the chimera states arise during the transition from oscillatory to steady state dynamics. Furthermore, we characterize the occurrence of each of the recognizable patterns by estimating the strength of incoherent subpopulations in the two-dimensional space.
Between pandemics, the influenza virus exhibits periods of incremental evolution via a process known as antigenic drift. This process gives rise to a sequence of strains of the pathogen that are continuously replaced by newer strains, preventing a build up of immunity in the host population. In this paper, a parsimonious epidemic model is defined that attempts to capture the dynamics of evolving strains within a host population. The `evolving strains epidemic model has many properties that lie in-between the Susceptible-Infected-Susceptible and the Susceptible-Infected-Removed epidemic models, due to the fact that individuals can only be infected by each strain once, but remain susceptible to reinfection by newly emerged strains. Coupling results are used to identify key properties, such as the time to extinction. A range of reproduction numbers are explored to characterize the model, including a novel quasi-stationary reproduction number that can be used to describe the re-emergence of the pathogen into a population with `average levels of strain immunity, analogous to the beginning of the winter peak in influenza. Finally the quasi-stationary distribution of the evolving strains model is explored via simulation.