We revisit well-established concepts of epidemiology, the Ising-model, and percolation theory. Also, we employ a spin $S$ = 1/2 Ising-like model and a (logistic) Fermi-Dirac-like function to describe the spread of Covid-19. Our analysis reinforces well-established literature results, namely: \emph{i}) that the epidemic curves can be described by a Gaussian-type function; \emph{ii}) that the temporal evolution of the accumulative number of infections and fatalities follow a logistic function, which has some resemblance with a distorted Fermi-Dirac-like function; \emph{iii}) the key role played by the quarantine to block the spread of Covid-19 in terms of an \emph{interacting} parameter, which emulates the contact between infected and non-infected people. Furthermore, in the frame of elementary percolation theory, we show that: \emph{i}) the percolation probability can be associated with the probability of a person being infected with Covid-19; \emph{ii}) the concepts of blocked and non-blocked connections can be associated, respectively, with a person respecting or not the social distancing, impacting thus in the probability of an infected person to infect other people. Increasing the number of infected people leads to an increase in the number of net connections, giving rise thus to a higher probability of new infections (percolation). We demonstrate the importance of social distancing in preventing the spread of Covid-19 in a pedagogical way. Given the impossibility of making a precise forecast of the disease spread, we highlight the importance of taking into account additional factors, such as climate changes and urbanization, in the mathematical description of epidemics. Yet, we make a connection between the standard mathematical models employed in epidemics and well-established concepts in condensed matter Physics, such as the Fermi gas and the Landau Fermi-liquid picture.
Spatial models for spread of an epidemic may be mapped onto bond percolation. We point out that with disorder in the strength of contacts between individuals patchiness in the spread of the epidemic is very likely, and the criterion for epidemic outbreak depends strongly on the disorder because the critical region of the corresponding percolation model is broadened. In some networks the percolation threshold is zero if another kind of disorder is present, namely divergent fluctuations in the number of contacts. We give an example, a network with a well defined geography, where this is not nece…
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 disorder, 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 disorder. These results are qualitatively different from those of standard models in epidemiology, but correspond to real effects.
The Susceptible-Infected-Recovered (SIR) model is studied in multilayer networks with arbitrary number of links across the layers. By following the mapping to bond percolation we give the analytical expression for the epidemic threshold and the fraction of the infected individuals in arbitrary number of layers. These results provide an exact prediction of the epidemic threshold for infinite locally tree-like multilayer networks, and an lower bound of the epidemic threshold for more general multilayer networks. The case of a multilayer network formed by two interconnected networks is specifical…
The renowned general epidemic process describes the stochastic evolution of a population of individuals which are either susceptible, infected or dead. A second order phase transition belonging to the universality class of dynamic isotropic percolation lies between endemic or pandemic behavior of the process. We generalize the general epidemic process by introducing a fourth kind of individuals, viz. individuals which are weakened by the process but not yet infected. This sensibilization gives rise to a mechanism that introduces a global instability in the spreading of the process and therefor…
In this paper we study the interplay between epidemic spreading and risk perception on multiplex networks. The basic idea is that the effective infection probability is affected by the perception of the risk of being infected, which we assume to be related to the fraction of infected neighbours, as introduced by Bagnoli et al., PRE 76:061904 (2007). We re-derive previous results using a self-organized method, that automatically gives the percolation threshold in just one simulation. We then extend the model to multiplex networks considering that people get infected by contacts in real life but…
Considerable attention has been paid, in recent years, to the use of networks in modeling complex real-world systems. Among the many dynamical processes involving networks, propagation processes -- in which final state can be obtained by studying the underlying network percolation properties -- have raised formidable interest. In this paper, we present a bond percolation model of multitype networks with an arbitrary joint degree distribution that allows heterogeneity in the edge occupation probability. As previously demonstrated, the multitype approach allows many non-trivial mixing patterns s…
We introduce a new percolation model to describe and analyze the spread of an epidemic on a general directed and locally finite graph. We assign a two-dimensional random weight vector to each vertex of the graph in such a way that the weights of different vertices are i.i.d., but the two entries of the vector assigned to a vertex need not be independent. The probability for an edge to be open depends on the weights of its end vertices, but conditionally on the weights, the states of the edges are independent of each other. In an epidemiological setting, the vertices of a graph represent the in…
The recurrent infectious diseases and their increasing impact on the society has promoted the study of strategies to slow down the epidemic spreading. In this review we outline the applications of percolation theory to describe strategies against epidemic spreading on complex networks. We give a general outlook of the relation between link percolation and the susceptible-infected-recovered model, and introduce the node void percolation process to describe the dilution of the network composed by healthy individual, $i.e$, the network that sustain the functionality of a society. Then, we survey …
We study the statistical properties of the SIR epidemics in heterogeneous networks, when an epidemic is defined as only those SIR propagations that reach or exceed a minimum size s_c. Using percolation theory to calculate the average fractional size <M_SIR> of an epidemic, we find that the strength of the spanning link percolation cluster $P_{\infty}$ is an upper bound to <M_SIR>. For small values of s_c, $P_{\infty}$ is no longer a good approximation, and the average fractional size has to be computed directly. The value of s_c for which $P_{\infty}$ is a good approximation is found to depend…
It has been known that epidemic outbreaks in the SIR model on networks are described by phase transitions. Despite the similarity with percolation transitions, whether an epidemic outbreak occurs or not cannot be predicted with probability one in the thermodynamic limit. We elucidate its mechanism by deriving a simple Langevin equation that captures an essential aspect of the phenomenon. We also calculate the probability of epidemic outbreaks near the transition point.
Human to human transmissible infectious diseases spread in a population using human interactions as its transmission vector. The early stages of such an outbreak can be modeled by a graph whose edges encode these interactions between individuals, the vertices. This article attempts to account for the case when each individual entails in different kinds of interactions which have therefore different probabilities of transmitting the disease. The majority of these results can be also stated in the language of percolation theory. The main contributions of the article are: (1) Extend to this setti…
In this work we study a modified Susceptible-Infected-Susceptible (SIS) model in which the infection rate $λ$ decays exponentially with the number of reinfections $n$, saturating after $n=l$. We find a critical decaying rate $ε_{c}(l)$ above which a finite fraction of the population becomes permanently infected. From the mean-field solution and computer simulations on hypercubic lattices we find evidences that the upper critical dimension is 6 like in the SIR model, which can be mapped in ordinary percolation.
We introduce an epidemic spreading model on a network using concepts from percolation theory. The model is motivated by discussing the standard SIR model, with extensions to describe effects of lockdowns within a population. The underlying ideas and behavior of the lattice model, implemented using the same lockdown scheme as for the SIR scheme, are discussed in detail and illustrated with extensive simulations. A comparison between both models is presented for the case of COVID-19 data from the USA. Both fits to the empirical data are very good, but some differences emerge between the two appr…
In contrast to the conventional wisdom that scale-free networks are prone to epidemic propagation, in the paper we present that disease spreading is inhibited in fractal scale-free networks. We first propose a novel network model and show that it simultaneously has the following rich topological properties: scale-free degree distribution, tunable clustering coefficient, "large-world" behavior, and fractal scaling. Existing network models do not display these characteristics. Then, we investigate the susceptible-infected-removed (SIR) model of the propagation of diseases in our fractal scale-fr…
Using digitized images of the three-dimensional, branching structures for root systems of bean seedlings, together with analytical and numerical methods that map a common 'SIR' epidemiological model onto the bond percolation problem, we show how the spatially-correlated branching structures of plant roots affect transmission efficiencies, and hence the invasion criterion, for a soil-borne pathogen as it spreads through ensembles of morphologically complex hosts. We conclude that the inherent heterogeneities in transmissibilities arising from correlations in the degrees of overlap between neigh…
In this work, we study the critical behavior of an epidemic propagation model that considers individuals that can develop drug resistance. In our lattice model, each site can be found in one of four states: empty, healthy, normally infected (not drug resistant) and strain infected (drug resistant) states. The most relevant parameters in our model are related to the mortality, cure and mutation rates. This model presents two distinct stationary active phases: a phase with co-existing normal and drug resistant infected individuals and an intermediate active phase with only drug resistant individ…
Many pathogens spread primarily via direct contact between infected and susceptible hosts. Thus, the patterns of contacts or contact network of a population fundamentally shapes the course of epidemics. While there is a robust and growing theory for the dynamics of single epidemics in networks, we know little about the impacts of network structure on long term epidemic or endemic transmission. For seasonal diseases like influenza, pathogens repeatedly return to populations with complex and changing patterns of susceptibility and immunity acquired through prior infection. Here, we develop two m…
In the past few decades, the frequency of pandemics has been increased due to the growth of urbanization and mobility among countries. Since a disease spreading in one country could become a pandemic with a potential worldwide humanitarian and economic impact, it is important to develop models to estimate the probability of a worldwide pandemic. In this paper, we propose a model of disease spreading in a structural modular complex network (having communities) and study how the number of bridge nodes $n$ that connect communities affects disease spread. We find that our model can be described at…
Chase-escape percolation is a variation of the standard epidemic spread models. In this model, each site can be in one of three states: unoccupied, occupied by a single prey, or occupied by a single predator. Prey particles spread to neighboring empty sites at rate $p$, and predator particles spread only to neighboring sites occupied by prey particles at rate $1$, killing the prey particle that existed at that site. It was found that the prey can survive with non-zero probability, if $p>p_c$ with $p_c<1$. Using Monte Carlo simulations on the square lattice, we estimate the value of $p_c = 0.49…