Effects of measures on phase transitions in two cooperative susceptible-infectious-recovered dynamics.

In recent studies, it has been shown that a cooperative interaction in a co-infection spread can lead to a discontinuous transition at a decreased threshold. Here, we investigate the effects of immunization with a rate proportional to the extent of the infection on phase transitions of a cooperative co-infection. We use the mean-field approximation to illustrate how measures that remove a portion of the susceptible compartment, like vaccination, with high enough rates can change discontinuous transitions in two coupled susceptible-infectious-recovered dynamics into continuous ones while increasing the threshold of transitions. First, we introduce vaccination with a fixed rate into a symmetric spread of two diseases and investigate the numerical results. Second, we set the rate of measures proportional to the size of the infectious compartment and scrutinize the dynamics. We solve the equations numerically and analytically and probe the transitions for a wide range of parameters. We also determine transition points from the analytical solutions. Third, we adopt a heterogeneous mean-field approach to include heterogeneity and asymmetry in the dynamics and see if the results corresponding to homogeneous symmetric case stand.

Emergence of Hopf bifurcation in an extended SIR dynamic.

In this paper, the original SIR model is improved by considering a new compartment, representing the hospitalization of critical cases. A system of differential equations with four blocks is developed to analyze the treatment of severe cases in an Intensive Care Unit (ICU). The outgoing rate of the infected individuals who survive is divided into nI and [Formula: see text] where the second term represents the transition rate of critical cases that are hospitalized in ICU. The findings demonstrate the existence of forward, backward and Hopf bifurcations in various ranges of parameters.

Emergence of synergistic and competitive pathogens in a coevolutionary spreading model.

Cooperation and competition between pathogens can alter the amount of individuals affected by a coinfection. Nonetheless, the evolution of the pathogens' behavior has been overlooked. Here, we consider a coevolutionary model where the simultaneous spreading is described by a two-pathogen susceptible-infected-recovered model in an either synergistic or competitive manner. At the end of each epidemic season, the pathogens species reproduce according to their fitness that, in turn, depends on the payoff accumulated during the spreading season in a hawk-and-dove game. This coevolutionary model displays a rich set of features. Specifically, the evolution of the pathogens' strategy induces abrupt transitions in the epidemic prevalence. Furthermore, we observe that the long-term dynamics results in a single, surviving pathogen species, and that the cooperative behavior of pathogens can emerge even under unfavorable conditions.

Stability of Boolean and continuous dynamics.

Regulatory dynamics in biology is often described by continuous rate equations for continuously varying chemical concentrations. Binary discretization of state space and time leads to Boolean dynamics. In the latter, the dynamics has been called unstable if flip perturbations lead to damage spreading. Here, we find that this stability classification strongly differs from the stability properties of the original continuous dynamics under small perturbations of the state vector. In particular, random networks of nodes with large sensitivity yield stable dynamics under small perturbations.

Impact of temporal correlations on high risk outbreaks of independent and cooperative SIR dynamics.

We first propose a quantitative approach to detect high risk outbreaks of independent and coinfective SIR dynamics on three empirical networks: a school, a conference and a hospital contact network. This measurement is based on the k-means clustering method and identifies proper samples for calculating the mean outbreak size and the outbreak probability. Then we systematically study the impact of different temporal correlations on high risk outbreaks over the original and differently shuffled counterparts of each network. We observe that, on the one hand, in the coinfection process, randomization of the sequence of the events increases the mean outbreak size of high-risk cases. On the other hand, these correlations do not have a consistent effect on the independent infection dynamics, and can either decrease or increase this mean. Randomization of the daily pattern correlations has no strong impact on the size of the outbreak in either the coinfection or the independent spreading cases. We also observe that an increase in the mean outbreak size does not always coincide with an increase in the outbreak probability; therefore, we argue that merely considering the mean outbreak size of all realizations may lead us into falsely estimating the outbreak risks. Our results suggest that some sort of contact randomization in the organizational level in schools, events or hospitals might help to suppress the spreading dynamics while the risk of an outbreak is high.

Social distancing in pedestrian dynamics and its effect on disease spreading.

Nonpharmaceutical measures such as social distancing can play an important role in controlling the spread of an epidemic. In this paper, we use a mathematical model combining human mobility and disease spreading. For the mobility dynamics, we design an agent-based model consisting of pedestrian dynamics with a novel type of force to resemble social distancing in crowded sites. For the spreading dynamics, we consider the compartmental susceptible-exposed-infective (SEI) dynamics plus an indirect transmission with the footprints of the infectious pedestrians being the contagion factor. We show that the increase in the intensity of social distancing has a significant effect on the exposure risk. By classifying the population into social distancing abiders and nonabiders, we conclude that the practice of social distancing, even by a minority of potentially infectious agents, results in a drastic change in the population exposure risk, but it reduces the effectiveness of the protocols when practiced by the rest of the population. Furthermore, we observe that for contagions for which the indirect transmission is more significant, the effectiveness of social distancing would be reduced. This study can help to provide a quantitative guideline for policy-making on exposure risk reduction.

Interplay between competitive and cooperative interactions in a three-player pathogen system.

In ecological systems, heterogeneous interactions between pathogens take place simultaneously. This occurs, for instance, when two pathogens cooperate, while at the same time, multiple strains of these pathogens co-circulate and compete. Notable examples include the cooperation of human immunodeficiency virus with antibiotic-resistant and susceptible strains of tuberculosis or some respiratory infections with Streptococcus pneumoniae strains. Models focusing on competition or cooperation separately fail to describe how these concurrent interactions shape the epidemiology of such diseases. We studied this problem considering two cooperating pathogens, where one pathogen is further structured in two strains. The spreading follows a susceptible-infected-susceptible process and the strains differ in transmissibility and extent of cooperation with the other pathogen. We combined a mean-field stability analysis with stochastic simulations on networks considering both well-mixed and structured populations. We observed the emergence of a complex phase diagram, where the conditions for the less transmissible, but more cooperative strain to dominate are non-trivial, e.g. non-monotonic boundaries and bistability. Coupled with community structure, the presence of the cooperative pathogen enables the coexistence between strains by breaking the spatial symmetry and dynamically creating different ecological niches. These results shed light on ecological mechanisms that may impact the epidemiology of diseases of public health concern.

Exact solution of generalized cooperative susceptible-infected-removed (SIR) dynamics.

In this paper, we introduce a general framework for coinfection as cooperative susceptible-infected-removed (SIR) dynamics. We first solve the SIR model analytically for two symmetric cooperative contagions [L. Chen et al., Europhys. Lett. 104, 50001 (2013)10.1209/0295-5075/104/50001] and then generalize and solve the model exactly in the symmetric scenarios for three and more cooperative contagions. We calculate the transition points and order parameters, i.e., the total number of infected hosts. We show that the behavior of the system does not change qualitatively with the inclusion of more diseases. We also show analytically that there is a saddle-node-like bifurcation for two cooperative SIR dynamics and that the transition is hybrid. Moreover, we investigate where the symmetric solution is stable for initial fluctuations. We finally explore sets of parameters which give rise to asymmetric cases, namely, the asymmetric cases of primary and secondary infection rates of one pathogen with respect to another. This setting can lead to fewer infected hosts, a higher epidemic threshold, and also continuous transitions. These results open the road to a better understanding of disease ecology.

Particle velocity controls phase transitions in contagion dynamics.

Interactions often require the proximity between particles. The movement of particles, thus, drives the change of the neighbors which are located in their proximity, leading to a sequence of interactions. In pathogenic contagion, infections occur through proximal interactions, but at the same time, the movement facilitates the co-location of different strains. We analyze how the particle velocity impacts on the phase transitions on the contagion process of both a single infection and two cooperative infections. First, we identify an optimal velocity (close to half of the interaction range normalized by the recovery time) associated with the largest epidemic threshold, such that decreasing the velocity below the optimal value leads to larger outbreaks. Second, in the cooperative case, the system displays a continuous transition for low velocities, which becomes discontinuous for velocities of the order of three times the optimal velocity. Finally, we describe these characteristic regimes and explain the mechanisms driving the dynamics.

Phase transitions in cooperative coinfections: Simulation results for networks and lattices.

We study the spreading of two mutually cooperative diseases on different network topologies, and with two microscopic realizations, both of which are stochastic versions of a susceptible-infected-removed type model studied by us recently in mean field approximation. There it had been found that cooperativity can lead to first order transitions from spreading to extinction. However, due to the rapid mixing implied by the mean field assumption, first order transitions required nonzero initial densities of sick individuals. For the stochastic model studied here the results depend strongly on the underlying network. First order transitions are found when there are few short but many long loops: (i) No first order transitions exist on trees and on 2-d lattices with local contacts. (ii) They do exist on Erdos-Rényi (ER) networks, on d-dimensional lattices with d≥4, and on 2-d lattices with sufficiently long-ranged contacts. (iii) On 3-d lattices with local contacts the results depend on the microscopic details of the implementation. (iv) While single infected seeds can always lead to infinite epidemics on regular lattices, on ER networks one sometimes needs finite initial densities of infected nodes. (v) In all cases the first order transitions are actually "hybrid"; i.e., they display also power law scaling usually associated with second order transitions. On regular lattices, our model can also be interpreted as the growth of an interface due to cooperative attachment of two species of particles. Critically pinned interfaces in this model seem to be in different universality classes than standard critically pinned interfaces in models with forbidden overhangs. Finally, the detailed results mentioned above hold only when both diseases propagate along the same network of links. If they use different links, results can be rather different in detail, but are similar overall.

Extracting information from S-curves of language change.

It is well accepted that adoption of innovations are described by S-curves (slow start, accelerating period and slow end). In this paper, we analyse how much information on the dynamics of innovation spreading can be obtained from a quantitative description of S-curves. We focus on the adoption of linguistic innovations for which detailed databases of written texts from the last 200 years allow for an unprecedented statistical precision. Combining data analysis with simulations of simple models (e.g. the Bass dynamics on complex networks), we identify signatures of endogenous and exogenous factors in the S-curves of adoption. We propose a measure to quantify the strength of these factors and three different methods to estimate it from S-curves. We obtain cases in which the exogenous factors are dominant (in the adoption of German orthographic reforms and of one irregular verb) and cases in which endogenous factors are dominant (in the adoption of conventions for romanization of Russian names and in the regularization of most studied verbs). These results show that the shape of S-curve is not universal and contains information on the adoption mechanism.