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Register a new userDisease Detectives: Using Mathematics to Forecast the Spread of Infectious Diseases
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The COVID-19 pandemic has led to significant changes in how people are currently living their lives. To determine how to best reduce the effects of the pandemic and start reopening societies, governments have drawn insights from mathematical models of the spread of infectious diseases. In this article, we give an introduction to a family of mathematical models (called compartmental models) and discuss how the results of analyzing these models influence government policies and human behavior, such as encouraging mask wearing and physical distancing to help slow the spread of the disease.
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Major advances in public health have resulted from disease prevention. However, prevention of a new infectious disease by vaccination or pharmaceuticals is made difficult by the slow process of vaccine and drug development. We propose an additional intervention that allows rapid control of emerging infectious diseases, and can also be used to eradicate diseases that rely almost exclusively on human-to-human transmission. The intervention is based on (1) testing every individual for the disease, (2) repeatedly, and (3) isolation of infected individuals. We show here that at a sufficient rate of testing, the reproduction number is reduced below 1.0 and the epidemic will rapidly collapse. The approach does not rely on strong or unrealistic assumptions about test accuracy, isolation compliance, population structure or epidemiological parameters, and its success can be monitored in real time by following the test positivity rate. In addition to the compliance rate and false negatives, the required rate of testing depends on the design of the testing regime, with concurrent testing outperforming random sampling. Provided that results are obtained rapidly, the test frequency required to suppress an epidemic is monotonic and near-linear with respect to R0, the infectious period, and the fraction of susceptible individuals. The testing regime is effective against both early phase and established epidemics, and additive to other interventions (e.g. contact tracing and social distancing). It is also robust to failure: any rate of testing reduces the number of infections, improving both public health and economic conditions. These conclusions are based on rigorous analysis and simulations of appropriate epidemiological models. A mass-produced, disposable test that could be used at home would be ideal, due to the optimal performance of concurrent tests that return immediate results.
We develop a mathematical framework to study the economic impact of infectious diseases by integrating epidemiological dynamics with a kinetic model of wealth exchange. The multi-agent description leads to study the evolution over time of a system of kinetic equations for the wealth densities of susceptible, infectious and recovered individuals, whose proportions are driven by a classical compartmental model in epidemiology. Explicit calculations show that the spread of the disease seriously affects the distribution of wealth, which, unlike the situation in the absence of epidemics, can converge towards a stationary state with a bimodal form. Furthermore, simulations confirm the ability of the model to describe different phenomena characteristics of economic trends in situations compromised by the rapid spread of an epidemic, such as the unequal impact on the various wealth classes and the risk of a shrinking middle class.
Background: The global spread of the severe acute respiratory syndrome (SARS) epidemic has clearly shown the importance of considering the long-range transportation networks in the understanding of emerging diseases outbreaks. The introduction of extensive transportation data sets is therefore an important step in order to develop epidemic models endowed with realism. Methods: We develop a general stochastic meta-population model that incorporates actual travel and census data among 3 100 urban areas in 220 countries. The model allows probabilistic predictions on the likelihood of country outbreaks and their magnitude. The level of predictability offered by the model can be quantitatively analyzed and related to the appearance of robust epidemic pathways that represent the most probable routes for the spread of the disease. Results: In order to assess the predictive power of the model, the case study of the global spread of SARS is considered. The disease parameter values and initial conditions used in the model are evaluated from empirical data for Hong Kong. The outbreak likelihood for specific countries is evaluated along with the emerging epidemic pathways. Simulation results are in agreement with the empirical data of the SARS worldwide epidemic. Conclusions: The presented computational approach shows that the integration of long-range mobility and demographic data provides epidemic models with a predictive power that can be consistently tested and theoretically motivated. This computational strategy can be therefore considered as a general tool in the analysis and forecast of the global spreading of emerging diseases and in the definition of containment policies aimed at reducing the effects of potentially catastrophic outbreaks.
In this chapter, an application of Mathematical Epidemiology to crop vector-borne diseases is presented to investigate the interactions between crops, vectors, and virus. The main illustrative example is the cassava mosaic disease (CMD). The CMD virus has two routes of infection: through vectors and also through infected crops. In the field, the main tool to control CMD spreading is roguing. The presented biological model is sufficiently generic and the same methodology can be adapted to other crops or crop vector-borne diseases. After an introduction where a brief history of crop diseases and useful information on Cassava and CMD is given, we develop and study a compartmental temporal model, taking into account the crop growth and the vector dynamics. A brief qualitative analysis of the model is provided,i.e., existence and uniqueness of a solution,existence of a disease-free equilibrium and existence of an endemic equilibrium. We also provide conditions for local (global) asymptotic stability and show that a Hopf Bifurcation may occur, for instance, when diseased plants are removed. Numerical simulations are provided to illustrate all possible behaviors. Finally, we discuss the theoretical and numerical outputs in terms of crop protection.
In the study of infectious diseases on networks, researchers calculate epidemic thresholds to help forecast whether a disease will eventually infect a large fraction of a population. Because network structure typically changes in time, which fundamentally influences the dynamics of spreading processes on them and in turn affects epidemic thresholds for disease propagation, it is important to examine epidemic thresholds in temporal networks. Most existing studies of epidemic thresholds in temporal networks have focused on models in discrete time, but most real-world networked systems evolve continuously in time. In our work, we encode the continuous time-dependence of networks into the evaluation of the epidemic threshold of a susceptible--infected--susceptible (SIS) process by studying an SIS model on tie-decay networks. We derive the epidemic-threshold condition of this model, and we perform numerical experiments to verify it. We also examine how different factors---the decay coefficients of the tie strengths in a network, the frequency of interactions between nodes, and the sparsity of the underlying social network in which interactions occur---lead to decreases or increases of the critical values of the threshold and hence contribute to facilitating or impeding the spread of a disease. We thereby demonstrate how the features of tie-decay networks alter the outcome of disease spread.
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