We introduce a new model of competition on growing networks. This extends the preferential attachment model, with the key property that node choices evolve simultaneously with the network. When a new node joins the network, it chooses neighbours by preferential attachment, and selects its type based on the number of initial neighbours of each type. The model is analysed in detail, and in particular, we determine the possible proportions of the various types in the limit of large networks. An important qualitative feature we find is that, in contrast to many current theoretical models, often several competitors will coexist. This matches empirical observations in many real-world networks.
Another large area of epidemiology studies conditions under which multiple strains of a pathogen can coexist (see, e.g., @cite_7 and references therein), while the physics community has been studying the effects of the underlying network on competing epidemics @cite_43 @cite_40 @cite_9 .
@cite_43 @cite_40 @cite_9 @cite_7
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In recent years the research community has accumulated overwhelming evidence for the emergence of complex and heterogeneous connectivity patterns in a wide range of biological and sociotechnical systems. The complex properties of real-world networks have a profound impact on the behavior of equilibrium and nonequilibrium phenomena occurring in various systems, and the study of epidemic spreading is central to our understanding of the unfolding of dynamical processes in complex networks. The theoretical analysis of epidemic spreading in heterogeneous networks requires the development of novel analytical frameworks, and it has produced results of conceptual and practical relevance. A coherent and comprehensive review of the vast research activity concerning epidemic processes is presented, detailing the successful theoretical approaches as well as making their limits and assumptions clear. Physicists, mathematicians, epidemiologists, computer, and social scientists share a common interest in studying epidemic spreading and rely on similar models for the description of the diffusion of pathogens, knowledge, and innovation. For this reason, while focusing on the main results and the paradigmatic models in infectious disease modeling, the major results concerning generalized social contagion processes are also presented. Finally, the research activity at the forefront in the study of epidemic spreading in coevolving, coupled, and time-varying networks is reported. We consider a spatial model related to bond percolation for the spread of a disease that includes variation in the susceptibility to infection. We work on a lattice with random bond strengths and show that with strong heterogeneity, i.e. a wide range of variation of susceptibility, patchiness in the spread of the epidemic is very likely, and the criterion for epidemic outbreak depends strongly on the heterogeneity. These results are qualitatively different from those of standard models in epidemiology, but correspond to real effects. We suggest that heterogeneity in the epidemic will affect the phylogenetic distance distribution of the disease-causing organisms. We also investigate small world lattices, and show that the effects mentioned above are even stronger. Many real networks are not isolated from each other but form networks of networks, often interrelated in non trivial ways. Here, we analyze an epidemic spreading process taking place on top of two interconnected complex networks. We develop a heterogeneous mean field approach that allows us to calculate the conditions for the emergence of an endemic state. Interestingly, a global endemic state may arise in the coupled system even though the epidemics is not able to propagate on each network separately, and even when the number of coupling connections is small. Our analytic results are successfully confronted against large-scale numerical simulations. The strong analogy between biological viruses and their computational counterparts has motivated the authors to adapt the techniques of mathematical epidemiology to the study of computer virus propagation. In order to allow for the most general patterns of program sharing, a standard epidemiological model is extended by placing it on a directed graph and a combination of analysis and simulation is used to study its behavior. The conditions under which epidemics are likely to occur are determined, and, in cases where they do, the dynamics of the expected number of infected individuals are examined as a function of time. It is concluded that an imperfect defense against computer viruses can still be highly effective in preventing their widespread proliferation, provided that the infection rate does not exceed a well-defined critical epidemic threshold. >