Human mobility and disease prevalence.

We examine the effect of human mobility on disease prevalence by studying the dependence of the total infected population at endemic equilibria with respect to population diffusion rates of a diffusive epidemic model. For small diffusion rates, our results indicate that the total infected population size is strictly decreasing with respect to the ratio of the diffusion rate of the infected population over that of the susceptible population. Moreover, when the disease local reproductive function is spatially heterogeneous, we found that: (i) for large diffusion rate of the infected population, the total infected population size is strictly maximized at large diffusion rate of the susceptible population when the recovery rate is spatially homogeneous, while it is strictly maximized at intermediate diffusion rate of the susceptible population when the difference of the transmission and recovery rates are spatially homogeneous; (ii) for large diffusion rate of the susceptible population, the total infected population size is strictly maximized at intermediate diffusion rate of the infected population when the recovery rate is spatially homogeneous, while it is strictly minimized at large diffusion rate of the infected population when the difference of the transmission and recovery rates is spatially homogeneous. Numerical simulations are provided to complement the theoretical results. Our studies may provide some insight into the impact of human mobility on disease outbreaks and the severity of epidemics.

Impact of population size and movement on the persistence of a two-strain infectious disease.

This article studies the asymptotic profiles of coexistence endemic equilibrium solutions of a two-strain reaction-diffusion epidemic model with mass-action incidence when the diffusion rates are sufficiently small. We address the question of how the population size and environmental heterogeneity impact the persistence and extinction of the disease when the diffusion rates approach zero. In particular, we show that there is a sharp critical number which depends delicately on the infected groups' diffusion rates and each strain's spatially heterogeneous infection and recovery rates. Moreover, if the total size of the population is kept below this critical number, then the disease could be eradicated by restricting the susceptible hosts' movement . However, if the total population exceeds this critical number, the disease may persist no matter how the movement of the susceptible hosts is controlled. Additionally, our results suggest that the disease may persist if the diffusion rates of the infected groups are kept sufficiently smaller than that of the susceptible group.

Control Strategies for a Multi-strain Epidemic Model.

This article studies a multi-strain epidemic model with diffusion and environmental heterogeneity. We address the question of a control strategy for multiple strains of the infectious disease by investigating how the local distributions of the transmission and recovery rates affect the dynamics of the disease. Our study covers both full model (in which case the diffusion rates for all subgroups of the population are positive) and the ODE-PDE case (in which case we require a total lock-down of the susceptible subgroup and allow the infected subgroups to have positive diffusion rates). In each case, a basic reproduction number of the epidemic model is defined and it is shown that if this reproduction number is less than one then the disease will be eradicated in the long run. On the other hand, if the reproduction number is greater than one, then the disease will become permanent. Moreover, we show that when the disease is permanent, creating a common safety area against all strains and lowering the diffusion rate of the susceptible subgroup will result in reducing the number of infected populations. Numerical simulations are presented to support our theoretical findings.

Can chemotaxis speed up or slow down the spatial spreading in parabolic-elliptic Keller-Segel systems with logistic source?

The current paper is concerned with the spatial spreading speed and minimal wave speed of the following Keller-Segel chemoattraction system, [Formula: see text]where [Formula: see text], a, b, [Formula: see text], and [Formula: see text] are positive constants. Assume [Formula: see text] . Then if in addition [Formula: see text] holds, it is proved that [Formula: see text] is the spreading speed of the solutions of (0.1) with nonnegative continuous initial function [Formula: see text] with nonempty compact support, that is, [Formula: see text]and [Formula: see text]where [Formula: see text] is the unique global classical solution of (0.1) with [Formula: see text]. It is also proved that, if [Formula: see text] and [Formula: see text] holds, then [Formula: see text] is the minimal speed of the traveling wave solutions of (0.1) connecting (0, 0) and [Formula: see text], that is, for any [Formula: see text], (0.1) has a traveling wave solution connecting (0, 0) and [Formula: see text] with speed c, and (0.1) has no such traveling wave solutions with speed less than [Formula: see text]. Note that [Formula: see text] is the spatial spreading speed as well as the minimal wave speed of the following Fisher-KPP equation, [Formula: see text]Hence, if [Formula: see text] and [Formula: see text], or [Formula: see text] and [Formula: see text], then the chemotaxis neither speeds up nor slows down the spatial spreading in (0.1).