No Arabic abstract
Metapopulations are models of ecological systems, describing the interactions and the behavior of populations that live in fragmented habitats. In this paper, we present a model of metapopulations based on the multivolume simulation algorithm tau-DPP, a stochastic class of membrane systems, that we utilize to investigate the influence that different habitat topologies can have on the local and global dynamics of metapopulations. In particular, we focus our analysis on the migration rate of individuals among adjacent patches, and on their capability of colonizing the empty patches in the habitat. We compare the simulation results obtained for each habitat topology, and conclude the paper with some proposals for other research issues concerning metapopulations.
We present new empirical evidence, based on millions of interactions on Twitter, confirming that human contacts scale with population sizes. We integrate such observations into a reaction-diffusion metapopulation framework providing an analytical expression for the global invasion threshold of a contagion process. Remarkably, the scaling of human contacts is found to facilitate the spreading dynamics. Our results show that the scaling properties of human interactions can significantly affect dynamical processes mediated by human contacts such as the spread of diseases, and ideas.
Multi-strain competition on networks is observed in many contexts, including infectious disease ecology, information dissemination or behavioral adaptation to epidemics. Despite a substantial body of research has been developed considering static, time-aggregated networks, it remains a challenge to understand the transmission of concurrent strains when links of the network are created and destroyed over time. Here we analyze how network dynamics shapes the outcome of the competition between an initially endemic strain and an emerging one, when both strains follow a susceptible-infected-susceptible dynamics, and spread at time scales comparable with the network evolution one. Using time-resolved data of close-proximity interactions between patients admitted to a hospital and medical health care workers, we analyze the impact of temporal patterns and initial conditions on the dominance diagram and coexistence time. We find that strong variations in activity volume cause the probability that the emerging strain replaces the endemic one to be highly sensitive to the time of emergence. The temporal structure of the network shapes the dominance diagram, with significant variations in the replacement probability (for a given set of epidemiological parameters) observed from the empirical network and a randomized version of it. Our work contributes towards the description of the complex interplay between competing pathogens on temporal networks.
We introduce a 2-layer network model for the study of the immunization dynamics in epidemics. Spreading of an epidemic is modeled as an excitatory process in a small-world network (body layer) while immunization by prevention for the disease as a dynamic process in a scale-free network (head layer). It is shown that prevention indeed turns periodic rages of an epidemic into small fluctuation. The study also reveals that, in a certain situation, prevention actually plays an adverse role and helps the disease survive. We argue that the presence of two different characteristic time scales contributes to the immunization dynamics observed.
We introduce a new dominance concept consisting of three new dominance metrics based on Lloyds (1967) mean crowding index. The new metrics link communities and species, whereas existing ones are applicable only to communities. Our community-level metric is a function of Simpsons diversity index. For species, our metric quantifies the difference between community dominance and the dominance of a virtual community whose mean population size (per species) equals the population size of the focal species. The new metrics have at least two immediate applications: (i) acting as proxies for diversity in diversity-stability modeling (ii) replacing population abundance in reconstructing species dominance networks. The first application is demonstrated here using data from a longitudinal study of the human vaginal microbiome, and provides new insights relevant for microbial community stability and disease etiology.
Under the hypothesis that both influenza and respiratory syncytial virus (RSV) are the two leading causes of acute respiratory infections (ARI), in this paper we have used a standard two-pathogen epidemic model as a regressor to explain, on a yearly basis, high season ARI data in terms of the contact rates and initial conditions of the mathematical model. The rationale is that ARI high season is a transient regime of a noisy system, e.g., the system is driven away from equilibrium every year by fluctuations in variables such as humidity, temperature, viral mutations and human behavior. Using the value of the replacement number as a phenotypic trait associated to fitness, we provide evidence that influenza and RSV coexists throughout the ARI high season through superinfection.