Differential equation and complex network approaches for epidemic modelling

This study consists of three parts. The first part focuses on bifurcation analysis of epidemic models with sub-optimal immunity and saturated treatment/recovery rate as well as nonlinear incidence rate. The second part of the research focuses on estimating the domain of attraction for sub-optimal immunity epidemic models. In the third part of the research, we develop a bond percolation model for community clustered networks with an arbitrarily specified joint degree distribution

Computation of the domain of attraction for suboptimal immunity epidemic models using the maximal Lyapunov function method

We are concerned with the estimation of the domain of attraction (DOA) for suboptimal immunity epidemic models. We establish a procedure to determine the maximal Lyapunov function in the form of rational functions. Based on the definition of DOA and the maximal Lyapunov function, a theorem and subsequently a numerical procedure are established to determine the maximal Lyapunov function and the DOA. Determination of the domain of attraction for epidemic models is very important for understanding the dynamic behaviour of the disease transmission as a function of the state of population distribution in different categories of disease states. We focus on suboptimal immunity epidemic models with saturated treatment rate and nonlinear incidence rate. Different from classical models, suboptimal immunity models are more realistic to explain the microparasite infection diseases such as Pertussis and Influenza A. We show that, for certain values of the parameter, larger k value (i.e., the model is more toward the SIR model) leads to a smaller DOA

Seasonality in epidemic models: a literature review

We provide a review of some key literature results on the influence of seasonality and other time heterogeneities of contact rates, and other parameters, such as vaccination rates, on the spread of infectious diseases. This is a classical topic where highly theoretical methodologies have provided new insight on the seemingly random behavior observed in epidemic time-series. We follow the line of providing a highly personal non-systematic review of this topic, mainly based on the history of mathematical epidemiology and on the impact of reviewed articles. Our aim is to stress some issues of increasing interest, such as the public health implications of the biomathematical literature and the impact of seasonality on epidemic extinction or elimination

Localization, epidemic transitions, and unpredictability of multistrain epidemics with an underlying genotype network

Mathematical disease modelling has long operated under the assumption that any one infectious disease is caused by one transmissible pathogen spreading among a population. This paradigm has been useful in simplifying the biological reality of epidemics and has allowed the modelling community to focus on the complexity of other factors such as population structure and interventions. However, there is an increasing amount of evidence that the strain diversity of pathogens, and their interplay with the host immune system, can play a large role in shaping the dynamics of epidemics. Here, we introduce a disease model with an underlying genotype network to account for two important mechanisms. One, the disease can mutate along network pathways as it spreads in a host population. Two, the genotype network allows us to define a genetic distance across strains and therefore to model the transcendence of immunity often observed in real world pathogens. We study the emergence of epidemics in this model, through its epidemic phase transitions, and highlight the role of the genotype network in driving cyclicity of diseases, large scale fluctuations, sequential epidemic transitions, as well as localization around specific strains of the associated pathogen. More generally, our model illustrates the richness of behaviours that are possible even in well-mixed host populations once we consider strain diversity and go beyond the "one disease equals one pathogen" paradigm

Activity‑driven network modeling and control of the spread of two concurrent epidemic strains

The emergency generated by the current COVID-19 pandemic has claimed millions of lives worldwide. There have been multiple waves across the globe that emerged as a result of new variants, due to arising from unavoidable mutations. The existing network toolbox to study epidemic spreading cannot be readily adapted to the study of multiple, coexisting strains. In this context, particularly lacking are models that could elucidate re-infection with the same strain or a different strain—phenomena that we are seeing experiencing more and more with COVID-19. Here, we establish a novel mathematical model to study the simultaneous spreading of two strains over a class of temporal networks. We build on the classical susceptible–exposed–infectious–removed model, by incorporating additional states that account for infections and re-infections with multiple strains. The temporal network is based on the activity-driven network paradigm, which has emerged as a model of choice to study dynamic processes that unfold at a time scale comparable to the network evolution. We draw analytical insight from the dynamics of the stochastic network systems through a mean-field approach, which allows for characterizing the onset of different behavioral phenotypes (non-epidemic, epidemic, and endemic). To demonstrate the practical use of the model, we examine an intermittent stay-at-home containment strategy, in which a fraction of the population is randomly required to isolate for a fixed period of time

An epidemiological model with voluntary quarantine strategies governed by evolutionary game dynamics

During pandemic events, strategies such as social distancing can be fundamental to curb viral spreading. Such actions can reduce the number of simultaneous infections and mitigate the disease spreading, which is relevant to the risk of a healthcare system collapse. Although these strategies can be suggested, their actual implementation may depend on the population perception of the disease risk. The current COVID-19 crisis, for instance, is showing that some individuals are much more prone than others to remain isolated, avoiding unnecessary contacts. With this motivation, we propose an epidemiological SIR model that uses evolutionary game theory to take into account dynamic individual quarantine strategies, intending to combine in a single process social strategies, individual risk perception, and viral spreading. The disease spreads in a population whose agents can choose between self-isolation and a lifestyle careless of any epidemic risk. The strategy adoption is individual and depends on the perceived disease risk compared to the quarantine cost. The game payoff governs the strategy adoption, while the epidemic process governs the agent's health state. At the same time, the infection rate depends on the agent's strategy while the perceived disease risk depends on the fraction of infected agents. Results show recurrent infection waves, which were seen in previous epidemic scenarios with quarantine. Notably, the risk perception is found to be fundamental for controlling the magnitude of the infection peak, while the final infection size is mainly dictated by the infection rates. Low awareness leads to a single and strong infection peak, while a greater disease risk leads to shorter, although more frequent, peaks. The proposed model spontaneously captures relevant aspects of a pandemic event, highlighting the fundamental role of social strategies