Role of masks in mitigating viral spread on networks.

Masks have remained an important mitigation strategy in the fight against COVID-19 due to their ability to prevent the transmission of respiratory droplets between individuals. In this work, we provide a comprehensive quantitative analysis of the impact of mask-wearing. To this end, we propose a novel agent-based model of viral spread on networks where agents may either wear no mask or wear one of several types of masks with different properties (e.g., cloth or surgical). We derive analytical expressions for three key epidemiological quantities: The probability of emergence, the epidemic threshold, and the expected epidemic size. In particular, we show how the aforementioned quantities depend on the structure of the contact network, viral transmission dynamics, and the distribution of the different types of masks within the population. Through extensive simulations, we then investigate the impact of different allocations of masks within the population and tradeoffs between the outward efficiency and inward efficiency of the masks. Interestingly, we find that masks with high outward efficiency and low inward efficiency are most useful for controlling the spread in the early stages of an epidemic, while masks with high inward efficiency but low outward efficiency are most useful in reducing the size of an already large spread. Last, we study whether degree-based mask allocation is more effective in reducing the probability of epidemic as well as epidemic size compared to random allocation. The result echoes the previous findings that mitigation strategies should differ based on the stage of the spreading process, focusing on source control before the epidemic emerges and on self-protection after the emergence.

Spreading processes with mutations over multilayer networks.

A key scientific challenge during the outbreak of novel infectious diseases is to predict how the course of the epidemic changes under countermeasures that limit interaction in the population. Most epidemiological models do not consider the role of mutations and heterogeneity in the type of contact events. However, pathogens have the capacity to mutate in response to changing environments, especially caused by the increase in population immunity to existing strains, and the emergence of new pathogen strains poses a continued threat to public health. Further, in the light of differing transmission risks in different congregate settings (e.g., schools and offices), different mitigation strategies may need to be adopted to control the spread of infection. We analyze a multilayer multistrain model by simultaneously accounting for i) pathways for mutations in the pathogen leading to the emergence of new pathogen strains, and ii) differing transmission risks in different settings, modeled as network layers. Assuming complete cross-immunity among strains, namely, recovery from any infection prevents infection with any other (an assumption that will need to be relaxed to deal with COVID-19 or influenza), we derive the key epidemiological parameters for the multilayer multistrain framework. We demonstrate that reductions to existing models that discount heterogeneity in either the strain or the network layers may lead to incorrect predictions. Our results highlight that the impact of imposing/lifting mitigation measures concerning different contact network layers (e.g., school closures or work-from-home policies) should be evaluated in connection with their effect on the likelihood of the emergence of new strains.

The effects of evolutionary adaptations on spreading processes in complex networks.

A common theme among previously proposed models for network epidemics is the assumption that the propagating object (e.g., a pathogen [in the context of infectious disease propagation] or a piece of information [in the context of information propagation]) is transferred across network nodes without going through any modification or evolutionary adaptations. However, in real-life spreading processes, pathogens often evolve in response to changing environments and medical interventions, and information is often modified by individuals before being forwarded. In this article, we investigate the effects of evolutionary adaptations on spreading processes in complex networks with the aim of 1) revealing the role of evolutionary adaptations on the threshold, probability, and final size of epidemics and 2) exploring the interplay between the structural properties of the network and the evolutionary adaptations of the spreading process.

Cascading failures in interdependent systems under a flow redistribution model.

Robustness and cascading failures in interdependent systems has been an active research field in the past decade. However, most existing works use percolation-based models where only the largest component of each network remains functional throughout the cascade. Although suitable for communication networks, this assumption fails to capture the dependencies in systems carrying a flow (e.g., power systems, road transportation networks), where cascading failures are often triggered by redistribution of flows leading to overloading of lines. Here, we consider a model consisting of systems A and B with initial line loads and capacities given by {L_{A,i},C_{A,i}}_{i=1}^{n} and {L_{B,i},C_{B,i}}_{i=1}^{n}, respectively. When a line fails in system A, a fraction of its load is redistributed to alive lines in B, while remaining (1-a) fraction is redistributed equally among all functional lines in A; a line failure in B is treated similarly with b giving the fraction to be redistributed to A. We give a thorough analysis of cascading failures of this model initiated by a random attack targeting p_{1} fraction of lines in A and p_{2} fraction in B. We show that (i) the model captures the real-world phenomenon of unexpected large scale cascades and exhibits interesting transition behavior: the final collapse is always first order, but it can be preceded by a sequence of first- and second-order transitions; (ii) network robustness tightly depends on the coupling coefficients a and b, and robustness is maximized at non-trivial a,b values in general; (iii) unlike most existing models, interdependence has a multifaceted impact on system robustness in that interdependency can lead to an improved robustness for each individual network.

Clustering determines the dynamics of complex contagions in multiplex networks.

We present the mathematical analysis of generalized complex contagions in a class of clustered multiplex networks. The model is intended to understand spread of influence, or any other spreading process implying a threshold dynamics, in setups of interconnected networks with significant clustering. The contagion is assumed to be general enough to account for a content-dependent linear threshold model, where each link type has a different weight (for spreading influence) that may depend on the content (e.g., product, rumor, political view) that is being spread. Using the generating functions formalism, we determine the conditions, probability, and expected size of the emergent global cascades. This analysis provides a generalization of previous approaches and is especially useful in problems related to spreading and percolation. The results present nontrivial dependencies between the clustering coefficient of the networks and its average degree. In particular, several phase transitions are shown to occur depending on these descriptors. Generally speaking, our findings reveal that increasing clustering decreases the probability of having global cascades and their size, however, this tendency changes with the average degree. There exists a certain average degree from which on clustering favors the probability and size of the contagion. By comparing the dynamics of complex contagions over multiplex networks and their monoplex projections, we demonstrate that ignoring link types and aggregating network layers may lead to inaccurate conclusions about contagion dynamics, particularly when the correlation of degrees between layers is high.

Optimizing the robustness of electrical power systems against cascading failures.

Electrical power systems are one of the most important infrastructures that support our society. However, their vulnerabilities have raised great concern recently due to several large-scale blackouts around the world. In this paper, we investigate the robustness of power systems against cascading failures initiated by a random attack. This is done under a simple yet useful model based on global and equal redistribution of load upon failures. We provide a comprehensive understanding of system robustness under this model by (i) deriving an expression for the final system size as a function of the size of initial attacks; (ii) deriving the critical attack size after which system breaks down completely; (iii) showing that complete system breakdown takes place through a first-order (i.e., discontinuous) transition in terms of the attack size; and (iv) establishing the optimal load-capacity distribution that maximizes robustness. In particular, we show that robustness is maximized when the difference between the capacity and initial load is the same for all lines; i.e., when all lines have the same redundant space regardless of their initial load. This is in contrast with the intuitive and commonly used setting where capacity of a line is a fixed factor of its initial load.

Robustness of power systems under a democratic-fiber-bundle-like model.

We consider a power system with N transmission lines whose initial loads (i.e., power flows) L(1),...,L(N) are independent and identically distributed with P(L)(x)=P[L≤x]. The capacity C(i) defines the maximum flow allowed on line i and is assumed to be given by C(i)=(1+α)L(i), with α>0. We study the robustness of this power system against random attacks (or failures) that target a p fraction of the lines, under a democratic fiber-bundle-like model. Namely, when a line fails, the load it was carrying is redistributed equally among the remaining lines. Our contributions are as follows. (i) We show analytically that the final breakdown of the system always takes place through a first-order transition at the critical attack size p(☆)=1-(E[L]/max(x)(P[L>x](αx+E[L|L>x])), where E[·] is the expectation operator; (ii) we derive conditions on the distribution P(L)(x) for which the first-order breakdown of the system occurs abruptly without any preceding diverging rate of failure; (iii) we provide a detailed analysis of the robustness of the system under three specific load distributions-uniform, Pareto, and Weibull-showing that with the minimum load L(min) and mean load E[L] fixed, Pareto distribution is the worst (in terms of robustness) among the three, whereas Weibull distribution is the best with shape parameter selected relatively large; (iv) we provide numerical results that confirm our mean-field analysis; and (v) we show that p(☆) is maximized when the load distribution is a Dirac delta function centered at E[L], i.e., when all lines carry the same load. This last finding is particularly surprising given that heterogeneity is known to lead to high robustness against random failures in many other systems.

Analysis of complex contagions in random multiplex networks.

We study the diffusion of influence in random multiplex networks where links can be of r different types, and, for a given content (e.g., rumor, product, or political view), each link type is associated with a content-dependent parameter ci in [0,∞] that measures the relative bias type i links have in spreading this content. In this setting, we propose a linear threshold model of contagion where nodes switch state if their "perceived" proportion of active neighbors exceeds a threshold τ. Namely a node connected to mi active neighbors and ki-mi inactive neighbors via type i links will turn active if ∑cimi/∑ciki exceeds its threshold τ. Under this model, we obtain the condition, probability and expected size of global spreading events. Our results extend the existing work on complex contagions in several directions by (i) providing solutions for coupled random networks whose vertices are neither identical nor disjoint, (ii) highlighting the effect of content on the dynamics of complex contagions, and (iii) showing that content-dependent propagation over a multiplex network leads to a subtle relation between the giant vulnerable component of the graph and the global cascade condition that is not seen in the existing models in the literature.