Emergence of Blind Areas in Information Spreading

Recently, contagion-based (disease, information, etc.) spreading on social networks has been extensively studied. In this paper, other than traditional full interaction, we propose a partial interaction based spreading model, considering that the informed individuals would transmit information to only a certain fraction of their neighbors due to the transmission ability in real-world social networks. Simulation results on three representative networks (BA, ER, WS) indicate that the spreading efficiency is highly correlated with the network heterogeneity. In addition, a special phenomenon, namely \emph{Information Blind Areas} where the network is separated by several information-unreachable clusters, will emerge from the spreading process. Furthermore, we also find that the size distribution of such information blind areas obeys power-law-like distribution, which has very similar exponent with that of site percolation. Detailed analyses show that the critical value is decreasing along with the network heterogeneity for the spreading process, which is complete the contrary to that of random selection. Moreover, the critical value in the latter process is also larger that of the former for the same network. Those findings might shed some lights in in-depth understanding the effect of network properties on information spreading

Recoverable prevalence in growing scale-free networks and the effective immunization

We study the persistent recoverable prevalence and the extinction of computer viruses via e-mails on a growing scale-free network with new users, which structure is estimated form real data. The typical phenomenon is simulated in a realistic model with the probabilistic execution and detection of viruses. Moreover, the conditions of extinction by random and targeted immunizations for hubs are derived through bifurcation analysis for simpler models by using a mean-field approximation without the connectivity correlations. We can qualitatively understand the mechanisms of the spread in linearly growing scale-free networks.Comment: 9 pages, 9 figures, 1 table. Update version after helpful referee comment

Approximation of epidemic models by diffusion processes and their statistical inference

Multidimensional continuous-time Markov jump processes $(Z(t))$ on $\mathbb{Z}^p$ form a usual set-up for modeling $SIR$-like epidemics. However, when facing incomplete epidemic data, inference based on $(Z(t))$ is not easy to be achieved. Here, we start building a new framework for the estimation of key parameters of epidemic models based on statistics of diffusion processes approximating $(Z(t))$. First, \previous results on the approximation of density-dependent $SIR$-like models by diffusion processes with small diffusion coefficient $\frac{1}{\sqrt{N}}$, where $N$ is the population size, are generalized to non-autonomous systems. Second, our previous inference results on discretely observed diffusion processes with small diffusion coefficient are extended to time-dependent diffusions. Consistent and asymptotically Gaussian estimates are obtained for a fixed number $n$ of observations, which corresponds to the epidemic context, and for $N\rightarrow \infty$. A correction term, which yields better estimates non asymptotically, is also included. Finally, performances and robustness of our estimators with respect to various parameters such as $R_0$ (the basic reproduction number), $N$, $n$ are investigated on simulations. Two models, $SIR$ and $SIRS$, corresponding to single and recurrent outbreaks, respectively, are used to simulate data. The findings indicate that our estimators have good asymptotic properties and behave noticeably well for realistic numbers of observations and population sizes. This study lays the foundations of a generic inference method currently under extension to incompletely observed epidemic data. Indeed, contrary to the majority of current inference techniques for partially observed processes, which necessitates computer intensive simulations, our method being mostly an analytical approach requires only the classical optimization steps.Comment: 30 pages, 10 figure

The role of multiple marks in epigenetic silencing and the emergence of a stable bivalent chromatin state

We introduce and analyze a minimal model of epigenetic silencing in budding yeast, built upon known biomolecular interactions in the system. Doing so, we identify the epigenetic marks essential for the bistability of epigenetic states. The model explicitly incorporates two key chromatin marks, namely H4K16 acetylation and H3K79 methylation, and explores whether the presence of multiple marks lead to a qualitatively different systems behavior. We find that having both modifications is important for the robustness of epigenetic silencing. Besides the silenced and transcriptionally active fate of chromatin, our model leads to a novel state with bivalent (i.e., both active and silencing) marks under certain perturbations (knock-out mutations, inhibition or enhancement of enzymatic activity). The bivalent state appears under several perturbations and is shown to result in patchy silencing. We also show that the titration effect, owing to a limited supply of silencing proteins, can result in counter-intuitive responses. The design principles of the silencing system is systematically investigated and disparate experimental observations are assessed within a single theoretical framework. Specifically, we discuss the behavior of Sir protein recruitment, spreading and stability of silenced regions in commonly-studied mutants (e.g., sas2, dot1) illuminating the controversial role of Dot1 in the systems biology of yeast silencing.Comment: Supplementary Material, 14 page