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Register a new userAgentization of Two Population-Driven Models of Mathematical Biology
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John C. Stevenson
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Single species population models and discrete stochastic gene frequency models are two standards of mathematical biology important for the evolution of populations. An agent based model is presented which reproduces these models and then explores where these models agree and disagree under relaxed specifications. For the population models, the requirement of homogeneous mixing prevents prediction of extinctions due to local resource depletion. These models also suggest equilibrium based on attainment of constant population levels though underlying population characteristics may be nowhere close to equilibrium. The discrete stochastic gene frequency models assume well mixed populations at constant levels. The models predictions for non-constant populations in strongly oscillating and chaotic regimes are surprisingly good, only diverging from the ABM at the most chaotic levels.
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Malaria is a mosquito-borne, lethal disease that affects millions and kills hundreds of thousands of people each year. In this paper, we develop a model for allocating malaria interventions across geographic regions and time, subject to budget constraints, with the aim of minimizing the number of person-days of malaria infection. The model considers a range of several conditions: climatic characteristics, treatment efficacy, distribution costs, and treatment coverage. We couple an expanded susceptible-infected-recovered (SIR) compartment model for the disease dynamics with an integer linear programming (ILP) model for selecting the disease interventions. Our model produces an intervention plan for all regions, identifying which combination of interventions, with which level of coverage, to use in each region and year in a five-year planning horizon. Simulations using the model yield high-level, qualitative insights on optimal intervention policies: The optimal policy is different when considering a five-year time horizon than when considering only a single year, due to the effects that interventions have on the disease transmission dynamics. The vaccine intervention is rarely selected, except if its assumed cost is significantly lower than that predicted in the literature. Increasing the available budget causes the number of person-days of malaria infection to decrease linearly up to a point, after which the benefit of increased budget starts to taper. The optimal policy is highly dependent on assumptions about mosquito density, selecting different interventions for wet climates with high density than for dry climates with low density, and the interventions are found to be less effective at controlling malaria in the wet climates when attainable intervention coverage is 60% or lower. However, when intervention coverage of 80% is attainable, then malaria prevalence drops quickly.
We study the effectiveness of tracking and testing in mitigating or suppressing epidemic outbreaks, in combination with or as an alternative to quarantines and global lockdowns. We study these intervention methods on a network-based SEIR model, augmented with an additional probability to model symptomatic, asymptomatic and pre-symptomatic cases. Our focus is on the basic trade-offs between economic costs and human lives lost, and how these trade-offs change under different lockdown, quarantine, tracking and testing policies. Our main findings are as follows: (i) Tests combined with patient quarantines reduce both economic costs and mortality, but require a large-scale testing capacity to achieve a significant improvement; (ii) Tracking significantly reduces both economic costs and mortality; (iii) Tracking combined with a limited number of tests can achieve containment without lockdowns; (iv) If there is a small flow of new incoming infections, dynamic On-Off lockdowns are more efficient than fixed lockdowns. Our simulation results underline the extreme effectiveness of tracking and testing policies in reducing both economic costs and mortality and their potential to contain epidemic outbreaks without imposing social distancing restrictions. This highlights the difficult social question of trading-off these gains with the privacy loss that tracking necessarily entails.
The human adaptive immune response is known to weaken in advanced age, resulting in increased severity of pathogen-born illness, poor vaccine efficacy, and a higher prevalence of cancer in the elderly. Age-related erosion of the T-cell compartment has been implicated as a likely cause, but the underlying mechanisms driving this immunosenescence have not been quantitatively modeled and systematically analyzed. T-cell receptor diversity, or the extent of pathogen-derived antigen responsiveness of the T-cell pool, is known to diminish with age, but inherent experimental difficulties preclude accurate analysis on the full organismal level. In this paper, we formulate a mechanistic mathematical model of T-cell population dynamics on the immunoclonal subpopulation level, which provides quantitative estimates of diversity. We define different estimates for diversity that depend on the individual number of cells in a specific immunoclone. We show that diversity decreases with age primarily due to diminished thymic output of new T-cells and the resulting overall loss of small immunoclones.
We present a new mathematical model to explicitly capture the effects that the three restriction measures: the lockdown date and duration, social distancing and masks, and, schools and border closing, have in controlling the spread of COVID-19 infections $i(r, t)$. Before restrictions were introduced, the random spread of infections as described by the SEIR model grew exponentially. The addition of control measures introduces a mixing of order and disorder in the systems evolution which fall under a different mathematical class of models that can eventually lead to critical phenomena. A generic analytical solution is hard to obtain. We use machine learning to solve the new equations for $i(r,t)$, the infections $i$ in any region $r$ at time $t$ and derive predictions for the spread of infections over time as a function of the strength of the specific measure taken and their duration. The machine is trained in all of the COVID-19 published data for each region, county, state, and country in the world. It utilizes optimization to learn the best-fit values of the models parameters from past data in each region in the world, and it updates the predicted infections curves for any future restrictions that may be added or relaxed anywhere. We hope this interdisciplinary effort, a new mathematical model that predicts the impact of each measure in slowing down infection spread combined with the solving power of machine learning, is a useful tool in the fight against the current pandemic and potentially future ones.
It is well-established that including spatial structure and stochastic noise in models for predator-prey interactions invalidates the classical deterministic Lotka-Volterra picture of neutral population cycles. In contrast, stochastic models yield long-lived, but ultimately decaying erratic population oscillations, which can be understood through a resonant amplification mechanism for density fluctuations. In Monte Carlo simulations of spatial stochastic predator-prey systems, one observes striking complex spatio-temporal structures. These spreading activity fronts induce persistent correlations between predators and prey. In the presence of local particle density restrictions (finite prey carrying capacity), there exists an extinction threshold for the predator population. The accompanying continuous non-equilibrium phase transition is governed by the directed-percolation universality class. We employ field-theoretic methods based on the Doi-Peliti representation of the master equation for stochastic particle interaction models to (i) map the ensuing action in the vicinity of the absorbing state phase transition to Reggeon field theory, and (ii) to quantitatively address fluctuation-induced renormalizations of the population oscillation frequency, damping, and diffusion coefficients in the species coexistence phase.
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