We present a nonlinear and non-Markovian random walk model for stochastic movement and the spatial aggregation of living organisms that have the ability to sense population density. We take into account social crowding effects for which the dispersal
rate is a decreasing function of the population density and residence time. We perform stochastic simulations of random walk and discover the phenomenon of self-organized anomaly (SOA) which leads to a collapse of stationary aggregation pattern. This anomalous regime is self-organized and arises without the need for a heavy tailed waiting time distribution from the inception. Conditions have been found under which the nonlinear random walk evolves into anomalous state when all particles aggregate inside a tiny domain (anomalous aggregation). We obtain power-law stationary density-dependent survival function and define the critical condition for SOA as the divergence of mean residence time. The role of the initial conditions in different SOA scenarios is discussed. We observe phenomenon of transient anomalous bi-modal aggregation.
We propose a model of sub-diffusion in which an external force is acting on a particle at all times not only at the moment of jump. The implication of this assumption is the dependence of the random trapping time on the force with the dramatic change
of particles behavior compared to the standard continuous time random walk model. Constant force leads to the transition from non-ergodic sub-diffusion to seemingly ergodic diffusive behavior. However, we show it remains anomalous in a sense that the diffusion coefficient depends on the force and the anomalous exponent. For the quadratic potential we find that the anomalous exponent defines not only the speed of convergence but also the stationary distribution which is different from standard Boltzmann equilibrium.
We explore the role of cellular life cycles for viruses and host cells in an infection process. For this purpose, we derive a generalized version of the basic model of virus dynamics (Nowak, M.A., Bangham, C.R.M., 1996. Population dynamics of immune
responses to persistent viruses. Science 272, 74-79) from a mesoscopic description. In its final form the model can be written as a set of Volterra integrodifferential equations. We consider the role of age-distributed delays for death times and the intracellular (eclipse) phase. These processes are implemented by means of probability distribution functions. The basic reproductive ratio $R_0$ of the infection is properly defined in terms of such distributions by using an analysis of the equilibrium states and their stability. It is concluded that the introduction of distributed delays can strongly modify both the value of $R_0$ and the predictions for the virus loads, so the effects on the infection dynamics are of major importance. We also show how the model presented here can be applied to some simple situations where direct comparison with experiments is possible. Specifically, phage-bacteria interactions are analysed. The dynamics of the eclipse phase for phages is characterized analytically, which allows us to compare the performance of three different fittings proposed before for the one-step growth curve.
In this paper we reconsider the Mass Action Law (MAL) for the anomalous reversible reaction $Arightleftarrows B$ with diffusion. We provide a mesoscopic description of this reaction when the transitions between two states $A$ and $B$ are governed by
anomalous (heavy-tailed) waiting-time distributions. We derive the set of mesoscopic integro-differential equations for the mean densities of reacting and diffusing particles in both states. We show that the effective reaction rate memory kernels in these equations and the uniform asymptotic states depend on transport characteristics such as jumping rates. This is in contradiction with the classical picture of MAL. We find that transport can even induce an extinction of the particles such that the density of particles $A$ or $B$ tends asymptotically to zero. We verify analytical results by Monte Carlo simulations and show that the mesoscopic densities exhibit a transient growth before decay.
