Generalized epidemic model incorporating non-Markovian infection processes and waning immunity.

The Markovian approach, which assumes exponentially distributed interinfection times, is dominant in epidemic modeling. However, this assumption is unrealistic as an individual's infectiousness depends on its viral load and varies over time. In this paper, we present a Susceptible-Infected-Recovered-Vaccinated-Susceptible epidemic model incorporating non-Markovian infection processes. The model can be easily adapted to accurately capture the generation time distributions of emerging infectious diseases, which is essential for accurate epidemic prediction. We observe noticeable variations in the transient behavior under different infectiousness profiles and the same basic reproduction number R_{0}. The theoretical analyses show that only R_{0} and the mean immunity period of the vaccinated individuals have an impact on the critical vaccination rate needed to achieve herd immunity. A vaccination level at the critical vaccination rate can ensure a very low incidence among the population in the case of future epidemics, regardless of the infectiousness profiles.

Influence of heterogeneous age-group contact patterns on critical vaccination rates for herd immunity to SARS-CoV-2.

Currently, several western countries have more than half of their population fully vaccinated against COVID-19. At the same time, some of them are experiencing a fourth or even a fifth wave of cases, most of them concentrated in sectors of the populations whose vaccination coverage is lower than the average. So, the initial scenario of vaccine prioritization has given way to a new one where achieving herd immunity is the primary concern. Using an age-structured vaccination model with waning immunity, we show that, under a limited supply of vaccines, a vaccination strategy based on minimizing the basic reproduction number allows for the deployment of a number of vaccine doses lower than the one required for maximizing the vaccination coverage. Such minimization is achieved by giving greater protection to those age groups that, for a given social contact pattern, have smaller fractions of susceptible individuals at the endemic equilibrium without vaccination, that is, to those groups that are more vulnerable to infection.

Robustness of behaviorally induced oscillations in epidemic models under a low rate of imported cases.

This paper is concerned with the robustness of the sustained oscillations predicted by an epidemic ODE model defined on contact networks. The model incorporates the spread of awareness among individuals and, moreover, a small inflow of imported cases. These cases prevent stochastic extinctions when we simulate the epidemics and, hence, they allow to check whether the average dynamics for the fraction of infected individuals are accurately predicted by the ODE model. Stochastic simulations confirm the existence of sustained oscillations for different types of random networks, with a sharp transition from a nonoscillatory asymptotic regime to a periodic one as the alerting rate of susceptible individuals increases from very small values. This abrupt transition to periodic epidemics of high amplitude is quite accurately predicted by the Hopf-bifurcation curve computed from the ODE model using the alerting rate and the infection transmission rate for aware individuals as tuning parameters.

A multilayer temporal network model for STD spreading accounting for permanent and casual partners.

Sexually transmitted diseases (STD) modeling has used contact networks to study the spreading of pathogens. Recent findings have stressed the increasing role of casual partners, often enabled by online dating applications. We study the Susceptible-Infected-Susceptible (SIS) epidemic model -appropriate for STDs- over a two-layer network aimed to account for the effect of casual partners in the spreading of STDs. In this novel model, individuals have a set of steady partnerships (links in layer 1). At certain rates, every individual can switch between active and inactive states and, while active, it establishes casual partnerships with some probability with active neighbors in layer 2 (whose links can be thought as potential casual partnerships). Individuals that are not engaged in casual partnerships are classified as inactive, and the transitions between active and inactive states are independent of their infectious state. We use mean-field equations as well as stochastic simulations to derive the epidemic threshold, which decreases substantially with the addition of the second layer. Interestingly, for a given expected number of casual partnerships, which depends on the probabilities of being active, this threshold turns out to depend on the duration of casual partnerships: the longer they are, the lower the threshold.

Tuning the overlap and the cross-layer correlations in two-layer networks: Application to a susceptible-infectious-recovered model with awareness dissemination.

We study the properties of the potential overlap between two networks A,B sharing the same set of N nodes (a two-layer network) whose respective degree distributions p_{A}(k),p_{B}(k) are given. Defining the overlap coefficient α as the Jaccard index, we prove that α is very close to 0 when A and B are random and independently generated. We derive an upper bound α_{M} for the maximum overlap coefficient permitted in terms of p_{A}(k), p_{B}(k), and N. Then we present an algorithm based on cross rewiring of links to obtain a two-layer network with any prescribed α inside the range (0,α_{M}). A refined version of the algorithm allows us to minimize the cross-layer correlations that unavoidably appear for values of α beyond a critical overlap α_{c}<α_{M}. Finally, we present a very simple example of a susceptible-infectious-recovered epidemic model with information dissemination and use the algorithms to determine the impact of the overlap on the final outbreak size predicted by the model.

Oscillations in epidemic models with spread of awareness.

We study ODE models of epidemic spreading with a preventive behavioral response that is triggered by awareness of the infection. Previous studies of such models have mostly focused on the impact of the response on the initial growth of an outbreak and the existence and location of endemic equilibria. Here we study the question whether this type of response is sufficient to prevent future flare-ups from low endemic levels if awareness is assumed to decay over time. In the ODE context, such flare-ups would translate into sustained oscillations with significant amplitudes. Our results show that such oscillations are ruled out in Susceptible-Aware-Infectious-Susceptible models with a single compartment of aware hosts, but can occur if we consider two distinct compartments of aware hosts who differ in their willingness to alert other susceptible hosts.

Network-Centric Interventions to Contain the Syphilis Epidemic in San Francisco.

The number of reported early syphilis cases in San Francisco has increased steadily since 2005. It is not yet clear what factors are responsible for such an increase. A recent analysis of the sexual contact network of men who have sex with men with syphilis in San Francisco has discovered a large connected component, members of which have a significantly higher chance of syphilis and HIV compared to non-member individuals. This study investigates whether it is possible to exploit the existence of the largest connected component to design new notification strategies that can potentially contribute to reducing the number of cases. We develop a model capable of incorporating multiple types of notification strategies and compare the corresponding incidence of syphilis. Through extensive simulations, we show that notifying the community of the infection state of few central nodes appears to be the most effective approach, balancing the cost of notification and the reduction of syphilis incidence. Additionally, among the different measures of centrality, the eigenvector centrality reveals to be the best to reduce the incidence in the long term as long as the number of missing links (non-disclosed contacts) is not very large.

A Network Epidemic Model with Preventive Rewiring: Comparative Analysis of the Initial Phase.

This paper is concerned with stochastic SIR and SEIR epidemic models on random networks in which individuals may rewire away from infected neighbors at some rate [Formula: see text] (and reconnect to non-infectious individuals with probability [Formula: see text] or else simply drop the edge if [Formula: see text]), so-called preventive rewiring. The models are denoted SIR-[Formula: see text] and SEIR-[Formula: see text], and we focus attention on the early stages of an outbreak, where we derive the expressions for the basic reproduction number [Formula: see text] and the expected degree of the infectious nodes [Formula: see text] using two different approximation approaches. The first approach approximates the early spread of an epidemic by a branching process, whereas the second one uses pair approximation. The expressions are compared with the corresponding empirical means obtained from stochastic simulations of SIR-[Formula: see text] and SEIR-[Formula: see text] epidemics on Poisson and scale-free networks. Without rewiring of exposed nodes, the two approaches predict the same epidemic threshold and the same [Formula: see text] for both types of epidemics, the latter being very close to the mean degree obtained from simulated epidemics over Poisson networks. Above the epidemic threshold, pairwise models overestimate the value of [Formula: see text] computed from simulations, which turns out to be very close to the one predicted by the branching process approximation. When exposed individuals also rewire with [Formula: see text] (perhaps unaware of being infected), the two approaches give different epidemic thresholds, with the branching process approximation being more in agreement with simulations.

Analysis of an epidemic model with awareness decay on regular random networks.

The existence of a die-out threshold (different from the classic disease-invasion one) defining a region of slow extinction of an epidemic has been proved elsewhere for susceptible-aware-infectious-susceptible models without awareness decay, through bifurcation analysis. By means of an equivalent mean-field model defined on regular random networks, we interpret the dynamics of the system in this region and prove that the existence of bifurcation for this second epidemic threshold crucially depends on the absence of awareness decay. We show that the continuum of equilibria that characterizes the slow die-out dynamics collapses into a unique equilibrium when a constant rate of awareness decay is assumed, no matter how small, and that the resulting bifurcation from the disease-free equilibrium is equivalent to that of standard epidemic models. We illustrate these findings with continuous-time stochastic simulations on regular random networks with different degrees. Finally, the behaviour of solutions with and without decay in awareness is compared around the second epidemic threshold for a small rate of awareness decay.

On the early epidemic dynamics for pairwise models.

The relationship between the basic reproduction number R0 and the exponential growth rate, specific to pair approximation models, is derived for the SIS, SIR and SEIR deterministic models without demography. These models are extended by including a random rewiring of susceptible individuals from infectious (and exposed) neighbours. The derived relationship between the exponential growth rate and R0 appears as formally consistent with those derived from homogeneous mixing models, enabling us to measure the transmission potential using the early growth rate of cases. On the other hand, the algebraic expression of R0 for the SEIR pairwise model shows that its value is affected by the average duration of the latent period, in contrast to what happens for the homogeneous mixing SEIR model. Numerical simulations on complex contact networks are performed to check the analytical assumptions and predictions.

Outbreak analysis of an SIS epidemic model with rewiring.

This paper is devoted to the analysis of the early dynamics of an SIS epidemic model defined on networks. The model, introduced by Gross et al. (Phys Rev Lett 96:208701, 2006), is based on the pair-approximation formalism and assumes that, at a given rewiring rate, susceptible nodes replace an infected neighbour by a new susceptible neighbour randomly selected among the pool of susceptible nodes in the population. The analysis uses a triple closure that improves the widely assumed in epidemic models defined on regular and homogeneous networks, and applies it to better understand the early epidemic spread on Poisson, exponential, and scale-free networks. Two extinction scenarios, one dominated by transmission and the other one by rewiring, are characterized by considering the limit system of the model equations close to the beginning of the epidemic. Moreover, an analytical condition for the occurrence of a bistability region is obtained.

Uncorrelatedness in growing networks with preferential survival of nodes.

The emergence of uncorrelated growing networks is proved when nodes are removed either uniformly or under the preferential survival rule recently observed in the World Wide Web evolution. To this aim, the rate equation for the joint probability of degrees is derived, and stationary symmetrical solutions are obtained, by passing to the continuum limit. When a uniformly random removal of extant nodes and linear preferential attachment of new nodes are at work, we prove that the only stationary solution corresponds to uncorrelated networks for any removal rate r∈(0,1). In the more general case of preferential survival of nodes, uncorrelated solutions are also obtained. These results generalize the uncorrelatedness displayed by the (undirected) Barabási-Albert network model to models with uniformly random and selective (against low degrees) removal of nodes.

Extinction threshold for spatial forest dynamics with height structure.

We present a pair-approximation model for spatial forest dynamics defined on a regular lattice. The model assumes three possible states for a lattice site: empty (gap site), occupied by an immature tree, and occupied by a mature tree, and considers three nonlinearities in the dynamics associated to the processes of light interference, gap expansion, and recruitment. We obtain an expression of the basic reproduction number R(0) which, in contrast to the one obtained under the mean-field approach, uses information about the spatial arrangement of individuals close to extinction. Moreover, we analyze the corresponding survival-extinction transition of the forest and the spatial correlations among gaps, immature and mature trees close to this critical point. Predictions of the pair-approximation model are compared with those of a cellular automaton.

Simple model of recovery dynamics after mass extinction.

Biotic recoveries following mass extinctions are characterized by a complex set of dynamics, including the rebuilding of whole ecologies from low-diversity assemblages of survivors and opportunistic species. Three broad classes of diversity dynamics during recovery have been suggested: an immediate linear response, a logistic recovery, and a simple positive feedback pattern of species interaction. Here we present a simple model of recovery which generates these three scenarios via differences in the extent of species interactions, thus capturing the dynamical logic of the recovery pattern. The model results indicate that the lag time to biotic recovery increases significantly as biotic interactions become more important in the recovery process.

Analysis and Monte Carlo simulations of a model for the spread of infectious diseases in heterogeneous metapopulations.

We present a study of the continuous-time equations governing the dynamics of a susceptible-infected-susceptible model on heterogeneous metapopulations. These equations have been recently proposed as an alternative formulation for the spread of infectious diseases in metapopulations in a continuous-time framework. Individual-based Monte Carlo simulations of epidemic spread in uncorrelated networks are also performed revealing a good agreement with analytical predictions under the assumption of simultaneous transmission or recovery and migration processes.

Continuous-time formulation of reaction-diffusion processes on heterogeneous metapopulations.

We present the derivation of the continuous-time equations governing the limit dynamics of discrete-time reaction-diffusion processes defined on heterogeneous metapopulations. We show that, when a rigorous time limit is performed, the lack of an epidemic threshold in the spread of infections is not limited to metapopulations with a scale-free architecture, as it has been predicted from dynamical equations in which reaction and diffusion occur sequentially in time.

Cancer stem cells as the engine of unstable tumor progression.

Genomic instability is considered by many authors the key engine of tumorigenesis. However, mounting evidence indicates that a small population of drug resistant cancer cells can also be a key component of tumor progression. Such cancer stem cells would define a compartment effectively acting as the source of most tumor cells. Here we study the interplay between these two conflicting components of cancer dynamics using two types of tissue architecture. Both mean field and multicompartment models are studied. It is shown that tissue architecture affects the pattern of cancer dynamics and that unstable cancers spontaneously organize into a heterogeneous population of highly unstable cells. This dominant population is in fact separated from the low-mutation compartment by an instability gap, where almost no cancer cells are observed. The possible implications of this prediction are discussed.

Food-web complexity emerging from ecological dynamics on adaptive networks.

Food webs are complex networks describing trophic interactions in ecological communities. Since Robert May's seminal work on random structured food webs, the complexity-stability debate is a central issue in ecology: does network complexity increase or decrease food-web persistence? A multi-species predator-prey model incorporating adaptive predation shows that the action of ecological dynamics on the topology of a food web (whose initial configuration is generated either by the cascade model or by the niche model) render, when a significant fraction of adaptive predators is present, similar hyperbolic complexity-persistence relationships as those observed in empirical food webs. It is also shown that the apparent positive relation between complexity and persistence in food webs generated under the cascade model, which has been pointed out in previous papers, disappears when the final connection is used instead of the initial one to explain species persistence.

Continuum formalism for modeling growing networks with deletion of nodes.

We present a continuum formalism for modeling growing random networks under addition and deletion of nodes based on a differential mass balance equation. As examples of its applicability, we obtain new results on the degree distribution for growing networks with a uniform attachment and deletion of nodes, and complete some recent results on growing networks with preferential attachment and uniform removal.