Human mobility networks and persistence of rapidly mutating pathogens

Rapidly mutating pathogens may be able to persist in the population and reach an endemic equilibrium by escaping hosts' acquired immunity. For such diseases, multiple biological, environmental and population-level mechanisms determine the dynamics of the outbreak, including pathogen's epidemiological traits (e.g. transmissibility, infectious period and duration of immunity), seasonality, interaction with other circulating strains and hosts' mixing and spatial fragmentation. Here, we study a susceptible-infected-recovered-susceptible model on a metapopulation where individuals are distributed in subpopulations connected via a network of mobility flows. Through extensive numerical simulations, we explore the phase space of pathogen's persistence and map the dynamical regimes of the pathogen following emergence. Our results show that spatial fragmentation and mobility play a key role in the persistence of the disease whose maximum is reached at intermediate mobility values. We describe the occurrence of different phenomena including local extinction and emergence of epidemic waves, and assess the conditions for large scale spreading. Findings are highlighted in reference to previous works and to real scenarios. Our work uncovers the crucial role of hosts' mobility on the ecological dynamics of rapidly mutating pathogens, opening the path for further studies on disease ecology in the presence of a complex and heterogeneous environment.Comment: 29 pages, 7 figures. Submitted for publicatio

A Polarized Temporal Network Model to Study the Spread of Recurrent Epidemic Diseases in a Partially Vaccinated Population

Motivated by massive outbreaks of COVID-19 that occurred even in populations with high vaccine uptake, we propose a novel multi-population temporal network model for the spread of recurrent epidemic diseases. We study the effect of human behavior, testing, and vaccination campaigns on the control of local outbreaks and infection prevalence. Our modeling framework decouples the vaccine effectiveness in protecting against transmission and the development of severe symptoms. Furthermore, the framework accounts for the polarizing effect of the decision to vaccinate and captures homophily, i.e., the tendency of people to interact with like-minded individuals. By means of a mean-field approach, we analytically derive the epidemic threshold. Our theoretical results suggest that, while vaccination campaigns reduce pressure on hospitals, they might facilitate resurgent outbreaks, highlighting the key role that testing campaigns may have in eradicating the disease. Numerical simulations are then employed to confirm and extend our theoretical findings to more realistic scenarios. Our numerical and analytical results agree that vaccination is not sufficient to achieve full eradication, without employing massive testing campaigns or relying on the population's responsibility. Furthermore, we show that homophily plays a critical role in the control of local outbreaks, highlighting the peril of a polarized network structure.Comment: Submitted to IEEE Transactions on Network Science and Engineerin

Virus spread over networks: Modeling, analysis, and control

The spread of viruses in biological networks, computer networks, and human contact networks can have devastating effects; developing and analyzing mathematical models of these systems can provide insights that lead to long-term societal benefits. Basic virus models have been studied for over three centuries; however, as the world continues to become connected and networked in more complex ways, previous models no longer are sufficient. Therefore virus spread over networks is a newer research topic, which provides a compelling modeling technique to capture real world behavior, and interest from the control field has provided an exciting new outlook on the area. Prior research has focused mainly on network models with static graph structures; however, the systems being modeled typically have dynamic graph structures and have not been validated with real spread data over a network. In this dissertation, we consider virus spread models over networks with dynamic graph structures, and we investigate the behavior of these systems. We perform stability analyses of epidemic processes over time-varying networks, providing sufficient conditions for convergence to the disease free equilibrium (the origin, or healthy state), in both the deterministic and stochastic cases. We also explore the scenario of multiple viruses, in the case of competing viruses, including human awareness, and coupled competing viruses. We analyze the healthy state and the endemic states of these models over static and dynamic graph structures. Various control techniques are also proposed to mitigate virus spread in networks. Illustrative figures and simulations are presented throughout. No previous work has explored identification and validation of network dependent virus spread models, which is considered herein using two datasets: 1) John Snow's fundamental 1854 cholera dataset and 2) a 2009-2012 USDA farm subsidy dataset. We conclude by discussing current work and future research directions

A review of wildland fire spread modelling, 1990-present 3: Mathematical analogues and simulation models

In recent years, advances in computational power and spatial data analysis (GIS, remote sensing, etc) have led to an increase in attempts to model the spread and behvaiour of wildland fires across the landscape. This series of review papers endeavours to critically and comprehensively review all types of surface fire spread models developed since 1990. This paper reviews models of a simulation or mathematical analogue nature. Most simulation models are implementations of existing empirical or quasi-empirical models and their primary function is to convert these generally one dimensional models to two dimensions and then propagate a fire perimeter across a modelled landscape. Mathematical analogue models are those that are based on some mathematical conceit (rather than a physical representation of fire spread) that coincidentally simulates the spread of fire. Other papers in the series review models of an physical or quasi-physical nature and empirical or quasi-empirical nature. Many models are extensions or refinements of models developed before 1990. Where this is the case, these models are also discussed but much less comprehensively.Comment: 20 pages + 9 pages references + 1 page figures. Submitted to the International Journal of Wildland Fir

Forward simulation MCMC with applications to stochastic epidemic models

For many stochastic models, it is difficult to make inference about the model parameters because it is impossible to write down a tractable likelihood given the observed data. A common solution is data augmentation in a Markov chain Monte Carlo (MCMC) framework. However, there are statistical problems where this approach has proved infeasible but where simulation from the model is straightforward leading to the popularity of the approximate Bayesian computation algorithm. We introduce a forward simulation MCMC (fsMCMC) algorithm, which is primarily based upon simulation from the model. The fsMCMC algorithm formulates the simulation of the process explicitly as a data augmentation problem. By exploiting non-centred parameterizations, an efficient MCMC updating schema for the parameters and augmented data is introduced, whilst maintaining straightforward simulation from the model. The fsMCMC algorithm is successfully applied to two distinct epidemic models including a birth–death–mutation model that has only previously been analysed using approximate Bayesian computation methods

Risk factors for the evolutionary emergence of pathogens

Recent outbreaks of novel infectious diseases (e.g. SARS, influenza H1N1) have highlighted the threat of cross-species pathogen transmission. When first introduced to a population, a pathogen is often poorly adapted to its new host and must evolve in order to escape extinction. Theoretical arguments and empirical studies have suggested various factors to explain why some pathogens emerge and others do not, including host contact structure, pathogen adaptive pathways and mutation rates. Using a multi-type branching process, we model the spread of an introduced pathogen evolving through several strains. Extending previous models, we use a network-based approach to separate host contact patterns from pathogen transmissibility. We also allow for arbitrary adaptive pathways. These generalizations lead to novel predictions regarding the impact of hypothesized risk factors. Pathogen fitness depends on the host population in which it circulates, and the ‘riskiest’ contact distribution and adaptive pathway depend on initial transmissibility. Emergence probability is sensitive to mutation probabilities and number of adaptive steps required, with the possibility of large adaptive steps (e.g. simultaneous point mutations or recombination) having a dramatic effect. In most situations, increasing overall mutation probability increases the risk of emergence; however, notable exceptions arise when deleterious mutations are available