Impact of random and targeted disruptions on information diffusion during outbreaks.

Outbreaks are complex multi-scale processes that are impacted not only by cellular dynamics and the ability of pathogens to effectively reproduce and spread, but also by population-level dynamics and the effectiveness of mitigation measures. A timely exchange of information related to the spread of novel pathogens, stay-at-home orders, and other measures can be effective at containing an infectious disease, particularly during the early stages when testing infrastructure, vaccines, and other medical interventions may not be available at scale. Using a multiplex epidemic model that consists of an information layer (modeling information exchange between individuals) and a spatially embedded epidemic layer (representing a human contact network), we study how random and targeted disruptions in the information layer (e.g., errors and intentional attacks on communication infrastructure) impact the total proportion of infections, peak prevalence (i.e., the maximum proportion of infections), and the time to reach peak prevalence. We calibrate our model to the early outbreak stages of the SARS-CoV-2 pandemic in 2020. Mitigation campaigns can still be effective under random disruptions, such as failure of information channels between a few individuals. However, targeted disruptions or sabotage of hub nodes that exchange information with a large number of individuals can abruptly change outbreak characteristics, such as the time to reach the peak of infection. Our results emphasize the importance of the availability of a robust communication infrastructure during an outbreak that can withstand both random and targeted disruptions.

Topological analysis of interaction patterns in cancer-specific gene regulatory network: persistent homology approach.

In this study, we investigated cancer cellular networks in the context of gene interactions and their associated patterns in order to recognize the structural features underlying this disease. We aim to propose that the quest of understanding cancer takes us beyond pairwise interactions between genes to a higher-order construction. We characterize the most prominent network deviations in the gene interaction patterns between cancer and normal samples that contribute to the complexity of this disease. What we hope is that through understanding these interaction patterns we will notice a deeper structure in the cancer network. This study uncovers the significant deviations that topological features in cancerous cells show from the healthy one, where the last stage of filtration confirms the importance of one-dimensional holes (topological loops) in cancerous cells and two-dimensional holes (topological voids) in healthy cells. In the small threshold region, the drop in the number of connected components of the cancer network, along with the rise in the number of loops and voids, all occurring at some smaller weight values compared to the normal case, reveals the cancerous network tendency to certain pathways.