The study of complex networks sheds light on the relation between the structure and function of complex systems. One remarkable result is the absence of an epidemic threshold in infinite-size scale-free networks, which implies that any infection will
perpetually propagate regardless of the spreading rate. The vast majority of current theoretical approaches assumes that infections are transmitted as a reaction process from nodes to all neighbors. Here we adopt a different perspective and show that the epidemic incidence is shaped by traffic flow conditions. Specifically, we consider the scenario in which epidemic pathways are defined and driven by flows. Through extensive numerical simulations and theoretical predictions, it is shown that the value of the epidemic threshold in scale-free networks depends directly on flow conditions, in particular on the first and second moments of the betweenness distribution given a routing protocol. We consider the scenarios in which the delivery capability of the nodes is bounded or unbounded. In both cases, the threshold values depend on the traffic and decrease as flow increases. Bounded delivery provokes the emergence of congestion, slowing down the spreading of the disease and setting a limit for the epidemic incidence. Our results provide a general conceptual framework to understand spreading processes on complex networks.
Many epidemic processes in networks spread by stochastic contacts among their connected vertices. There are two limiting cases widely analyzed in the physics literature, the so-called contact process (CP) where the contagion is expanded at a certain
rate from an infected vertex to one neighbor at a time, and the reactive process (RP) in which an infected individual effectively contacts all its neighbors to expand the epidemics. However, a more realistic scenario is obtained from the interpolation between these two cases, considering a certain number of stochastic contacts per unit time. Here we propose a discrete-time formulation of the problem of contact-based epidemic spreading. We resolve a family of models, parameterized by the number of stochastic contact trials per unit time, that range from the CP to the RP. In contrast to the common heterogeneous mean-field approach, we focus on the probability of infection of individual nodes. Using this formulation, we can construct the whole phase diagram of the different infection models and determine their critical properties.
