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Lora Billings

Publications and source records attributed to Lora Billings.

11 recordsLinked to original sources

Model Reduction in Stochastic Environments

We present a general theory of stochastic model reduction which is based on a normal form coordinate transform method of A.J. Roberts. This nonlinear, stochastic projection allows for the deterministic and stochastic dynamics to interact correctly on the lower-dimensional manifold so that the dynamics predicted by the reduced, stochastic system agrees well with the dynamics predicted by the original, high-dimensional stochastic system. The method may be applied to any system with well-separated time scales. In this article, we consider a physical problem that involves a singularly perturbed Duffing oscillator as well as a biological problem that involves the prediction of infectious disease outbreaks.

math.DS

Analysis and control of pre-extinction dynamics in stochastic populations

We consider a stochastic population model where the intrinsic or demographic noise causes cycling between states before the population eventually goes extinct. A master equation approach coupled with a WKB (Wentzel-Kramers-Brillouin) approximation is used to construct the optimal path to extinction. In addition, a probabilistic argument is used to understand the pre-extinction dynamics and approximate the mean time to extinction. Analytical results agree well with numerical Monte Carlo simulations. A control method is implemented to decrease the mean time to extinction. Analytical results quantify the effectiveness of the control and agree well with numerical simulations.

q-bio.PE

Noise Induced Switching and Extinction in Systems with Delay

We consider the rates of noise-induced switching between the stable states of dissipative dynamical systems with delay and also the rates of noise-induced extinction, where such systems model population dynamics. We study a class of systems where the evolution depends on the dynamical variables at a preceding time with a fixed time delay, which we call hard delay. For weak noise, the rates of inter-attractor switching and extinction are exponentially small. Finding these rates to logarithmic accuracy is reduced to variational problems. The solutions of the variational problems give the most probable paths followed in switching or extinction. We show that the equations for the most probable paths are acausal and formulate the appropriate boundary conditions. Explicit general results are obtained for small delay compared to the relaxation rate. We also develop a direct variational method to find the rates. We find that the analytical results agree well with the numerical simulations for both switching and extinction rates.

cond-mat.stat-mech

Intervention-Based Stochastic Disease Eradication

Disease control is of paramount importance in public health with infectious disease extinction as the ultimate goal. Although diseases may go extinct due to random loss of effective contacts where the infection is transmitted to new susceptible individuals, the time to extinction in the absence of control may be prohibitively long. Thus intervention controls, such as vaccination of susceptible individuals and/or treatment of infectives, are typically based on a deterministic schedule, such as periodically vaccinating susceptible children based on school calendars. In reality, however, such policies are administered as a random process, while still possessing a mean period. Here, we consider the effect of randomly distributed intervention as disease control on large finite populations. We show explicitly how intervention control, based on mean period and treatment fraction, modulates the average extinction times as a function of population size and rate of infection spread. In particular, our results show an exponential improvement in extinction times even though the controls are implemented using a random Poisson distribution. Finally, we discover those parameter regimes where random treatment yields an exponential improvement in extinction times over the application of strictly periodic intervention. The implication of our results is discussed in light of the availability of limited resources for control.

nlin.AO

Disease Persistence in Epidemiological Models: The Interplay between Vaccination and Migration

We consider the interplay of vaccination and migration rates on disease persistence in epidemiological systems. We show that short-term and long-term migration can inhibit disease persistence. As a result, we show how migration changes how vaccination rates should be chosen to maintain herd immunity. In a system of coupled SIR models, we analyze how disease eradication depends explicitly on vaccine distribution and migration connectivity. The analysis suggests potentially novel vaccination policies that underscore the importance of optimal placement of finite resources.

physics.bio-ph

Set-based corral control in stochastic dynamical systems: Making almost invariant sets more invariant

We consider the problem of stochastic prediction and control in a time-dependent stochastic environment, such as the ocean, where escape from an almost invariant region occurs due to random fluctuations. We determine high-probability control-actuation sets by computing regions of uncertainty, almost invariant sets, and Lagrangian Coherent Structures. The combination of geometric and probabilistic methods allows us to design regions of control that provide an increase in loitering time while minimizing the amount of control actuation. We show how the loitering time in almost invariant sets scales exponentially with respect to the control actuation, causing an exponential increase in loitering times with only small changes in actuation force. The result is that the control actuation makes almost invariant sets more invariant.

nlin.AO

Switching barrier scaling near bifurcation points for non-Gaussian noise

We study noise-induced switching of a system close to bifurcation parameter values where the number of stable states changes. For non-Gaussian noise, the switching exponent, which gives the logarithm of the switching rate, displays a non-power-law dependence on the distance to the bifurcation point. This dependence is found for Poisson noise. Even weak additional Gaussian noise dominates switching sufficiently close to the bifurcation point, leading to a crossover in the behavior of the switching exponent.

cond-mat.stat-mech

Accurate Noise Projection for Reduced Stochastic Epidemic Models

We consider a stochastic Susceptible-Exposed-Infected-Recovered (SEIR) epidemiological model. Through the use of a normal form coordinate transform, we are able to analytically derive the stochastic center manifold along with the associated, reduced set of stochastic evolution equations. The transformation correctly projects both the dynamics and the noise onto the center manifold. Therefore, the solution of this reduced stochastic dynamical system yields excellent agreement, both in amplitude and phase, with the solution of the original stochastic system for a temporal scale that is orders of magnitude longer than the typical relaxation time. This new method allows for improved time series prediction of the number of infectious cases when modeling the spread of disease in a population. Numerical solutions of the fluctuations of the SEIR model are considered in the infinite population limit using a Langevin equation approach, as well as in a finite population simulated as a Markov process.

nlin.AO

Thermally activated switching in the presence of non-Gaussian noise

We study the effect of a non-Gaussian noise on interstate switching activated primarily by Gaussian noise. Even weak non-Gaussian noise can strongly change the switching rate. The effect is determined by all moments of the noise distribution. The explicit analytical results are compared with the results of simulations for an overdamped system driven by white Gaussian noise and a Poisson noise. Switching induced by a purely Poisson noise is also discussed.

cond-mat.stat-mech

Using dimension reduction to improve outbreak predictability of multistrain diseases

Multistrain diseases have multiple distinct coexisting serotypes (strains). For some diseases, such as dengue fever, the serotypes interact by antibody-dependent enhancement (ADE), in which infection with a single serotype is asymptomatic, but contact with a second serotype leads to higher viral load and greater infectivity. We present and analyze a dynamic compartmental model for multiple serotypes exhibiting ADE. Using center manifold techniques, we show how the dynamics rapidly collapses to a lower dimensional system. Using the constructed reduced model, we can explain previously observed synchrony between certain classes of primary and secondary infectives (Schwartz et al., Phys. Rev. E 72: 066201, 2005). Additionally, we show numerically that the center manifold equations apply even to noisy systems. Both deterministic and stochastic versions of the model enable prediction of asymptomatic individuals that are difficult to track during an epidemic. We also show how this technique may be applicable to other multistrain disease models, such as those with cross-immunity.

nlin.CD

Chaotic desynchronization of multi-strain diseases

Multi-strain diseases are diseases that consist of several strains, or serotypes. The serotypes may interact by antibody-dependent enhancement (ADE), in which infection with a single serotype is asymptomatic, but infection with a second serotype leads to serious illness accompanied by greater infectivity. It has been observed from serotype data of dengue hemorrhagic fever that outbreaks of the four serotypes occur asynchronously. Both autonomous and seasonally driven outbreaks were studied in a model containing ADE. For sufficiently small ADE, the number of infectives of each serotype synchronizes, with outbreaks occurring in phase. When the ADE increases past a threshold, the system becomes chaotic, and infectives of each serotype desynchronize. However, certain groupings of the primary and second ary infectives remain synchronized even in the chaotic regime.

physics.bio-ph