Most previous studies of epidemic dynamics on complex networks suppose that the disease will eventually stabilize at either a disease-free state or an endemic one. In reality, however, some epidemics always exhibit sporadic and recurrent behaviour in
one region because of the invasion from an endemic population elsewhere. In this paper we address this issue and study a susceptible-infected-susceptible epidemiological model on a network consisting of two communities, where the disease is endemic in one community but alternates between outbreaks and extinctions in the other. We provide a detailed characterization of the temporal dynamics of epidemic patterns in the latter community. In particular, we investigate the time duration of both outbreak and extinction, and the time interval between two consecutive inter-community infections, as well as their frequency distributions. Based on the mean-field theory, we theoretically analyze these three timescales and their dependence on the average node degree of each community, the transmission parameters, and the number of intercommunity links, which are in good agreement with simulations, except when the probability of overlaps between successive outbreaks is too large. These findings aid us in better understanding the bursty nature of disease spreading in a local community, and thereby suggesting effective time-dependent control strategies.
Whether a scientific paper is cited is related not only to the influence of its author(s) but also to the journal publishing it. Scientists, either proficient or tender, usually submit their most important work to prestigious journals which receives
higher citations than the ordinary. How to model the role of scientific journals in citation dynamics is of great importance. In this paper we address this issue through two folds. One is the intrinsic heterogeneity of a paper determined by the impact factor of the journal publishing it. The other is the mechanism of a paper being cited which depends on its citations and prestige. We develop a model for citation networks via an intrinsic nodal weight function and an intuitive ageing mechanism. The nodes weight is drawn from the distribution of impact factors of journals and the ageing transition is a function of the citation and the prestige. The node-degree distribution of resulting networks shows nonuniversal scaling: the distribution decays exponentially for small degree and has a power-law tail for large degree, hence the dual behaviour. The higher the impact factor of the journal, the larger the tipping point and the smaller the power exponent that are obtained. With the increase of the journal rank, this phenomenon will fade and evolve to pure power laws.
Vaccination is an important measure available for preventing or reducing the spread of infectious diseases. In this paper, an epidemic model including susceptible, infected, and imperfectly vaccinated compartments is studied on Watts-Strogatz small-w
orld, Barabasi-Albert scale-free, and random scale-free networks. The epidemic threshold and prevalence are analyzed. For small-world networks, the effective vaccination intervention is suggested and its influence on the threshold and prevalence is analyzed. For scale-free networks, the threshold is found to be strongly dependent both on the effective vaccination rate and on the connectivity distribution. Moreover, so long as vaccination is effective, it can linearly decrease the epidemic prevalence in small-world networks, whereas for scale-free networks it acts exponentially. These results can help in adopting pragmatic treatment upon diseases in structured populations.
In citation networks, the activity of papers usually decreases with age and dormant papers may be discovered and become fashionable again. To model this phenomenon, a competition mechanism is suggested which incorporates two factors: vigorousness and
dormancy. Based on this idea, a citation network model is proposed, in which a node has two discrete stage: vigorous and dormant. Vigorous nodes can be deactivated and dormant nodes may be activated and become vigorous. The evolution of the network couples addition of new nodes and state transitions of old ones. Both analytical calculation and numerical simulation show that the degree distribution of nodes in generated networks displays a good right-skewed behavior. Particularly, scale-free networks are obtained as the deactivated vertex is target selected and exponential networks are realized for the random-selected case. Moreover, the measurement of four real-world citation networks achieves a good agreement with the stochastic model.
Individual nodes in evolving real-world networks typically experience growth and decay --- that is, the popularity and influence of individuals peaks and then fades. In this paper, we study this phenomenon via an intrinsic nodal fitness function and
an intuitive aging mechanism. Each node of the network is endowed with a fitness which represents its activity. All the nodes have two discrete stages: active and inactive. The evolution of the network combines the addition of new active nodes randomly connected to existing active ones and the deactivation of old active nodes with possibility inversely proportional to their fitnesses. We obtain a structured exponential network when the fitness distribution of the individuals is homogeneous and a structured scale-free network with heterogeneous fitness distributions. Furthermore, we recover two universal scaling laws of the clustering coefficient for both cases, $C(k) sim k^{-1}$ and $C sim n^{-1}$, where $k$ and $n$ refer to the node degree and the number of active individuals, respectively. These results offer a new simple description of the growth and aging of networks where intrinsic features of individual nodes drive their popularity, and hence degree.
We propose a new mechanism leading to scale-free networks which is based on the presence of an intrinsic character of a vertex called fitness. In our model, a vertex $i$ is assigned a fitness $x_i$, drawn from a given probability distribution functio
n $f(x)$. During network evolution, with rate $p$ we add a vertex $j$ of fitness $x_j$ and connect to an existing vertex $i$ of fitness $x_i$ selected preferentially to a linking probability function $g(x_i,x_j)$ which depends on the fitnesses of the two vertices involved and, with rate $1-p$ we create an edge between two already existed vertices with fitnesses $x_i$ and $x_j$, with a probability also preferential to the connection function $g(x_i,x_j)$. For the proper choice of $g$, the resulting networks have generalized power laws, irrespective of the fitness distribution of vertices.
We study a simple reaction-diffusion population model [proposed by A. Windus and H. J. Jensen, J. Phys. A: Math. Theor. 40, 2287 (2007)] on scale-free networks. In the case of fully random diffusion, the network topology cannot affect the critical de
ath rate, whereas the heterogeneous connectivity can cause smaller steady population density and critical population density. In the case of modified diffusion, we obtain a larger critical death rate and steady population density, at the meanwhile, lower critical population density, which is good for the survival of species. The results were obtained using a mean-field-like framework and were confirmed by computer simulations.
We investigate the standard susceptible-infected-susceptible model on a random network to study the effects of preference and geography on diseases spreading. The network grows by introducing one random node with $m$ links on a Euclidean space at uni
t time. The probability of a new node $i$ linking to a node $j$ with degree $k_j$ at distance $d_{ij}$ from node $i$ is proportional to $k_{j}^{A}/d_{ij}^{B}$, where $A$ and $B$ are positive constants governing preferential attachment and the cost of the node-node distance. In the case of A=0, we recover the usual epidemic behavior with a critical threshold below which diseases eventually die out. Whereas for B=0, the critical behavior is absent only in the condition A=1. While both ingredients are proposed simultaneously, the network becomes robust to infection for larger $A$ and smaller $B$.
