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Register a new userEstimating the impact of preventive quarantine with reverse epidemiology
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The impact of mitigation or control measures on an epidemics can be estimated by fitting the parameters of a compartmental model to empirical data, and running the model forward with modified parameters that account for a specific measure. This approach has several drawbacks, stemming from biases or lack of availability of data and instability of parameter estimates. Here we take the opposite approach -- that we call reverse epidemiology. Given the data, we reconstruct backward in time an ensemble of networks of contacts, and we assess the impact of measures on that specific realization of the contagion process. This approach is robust because it only depends on parameters that describe the evolution of the disease within one individual (e.g. latency time) and not on parameters that describe the spread of the epidemics in a population. Using this method, we assess the impact of preventive quarantine on the ongoing outbreak of Covid-19 in Italy. This gives an estimate of how many infected could have been avoided had preventive quarantine been enforced at a given time.
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When an epidemic spreads into a population, it is often unpractical or impossible to have a continuous monitoring of all subjects involved. As an alternative, algorithmic solutions can be used to infer the state of the whole population from a limited amount of measures. We analyze the capability of deep neural networks to solve this challenging task. Our proposed architecture is based on Graph Convolutional Neural Networks. As such it can reason on the effect of the underlying social network structure, which is recognized as the main component in the spreading of an epidemic. We test the proposed architecture with two scenarios modeled on the CoVid-19 pandemic: a generic homogeneous population, and a toy model of Boston metropolitan area.
A great variety of complex physical, natural and artificial systems are governed by statistical distributions, which often follow a standard exponential function in the bulk, while their tail obeys the Pareto power law. The recently introduced $kappa$-statistics framework predicts distribution functions with this feature. A growing number of applications in different fields of investigation are beginning to prove the relevance and effectiveness of $kappa$-statistics in fitting empirical data. In this paper, we use $kappa$-statistics to formulate a statistical approach for epidemiological analysis. We validate the theoretical results by fitting the derived $kappa$-Weibull distributions with data from the plague pandemic of 1417 in Florence as well as data from the COVID-19 pandemic in China over the entire cycle that concludes in April 16, 2020. As further validation of the proposed approach we present a more systematic analysis of COVID-19 data from countries such as Germany, Italy, Spain and United Kingdom, obtaining very good agreement between theoretical predictions and empirical observations. For these countries we also study the entire first cycle of the pandemic which extends until the end of July 2020. The fact that both the data of the Florence plague and those of the Covid-19 pandemic are successfully described by the same theoretical model, even though the two events are caused by different diseases and they are separated by more than 600 years, is evidence that the $kappa$-Weibull model has universal features.
We study the coevolutionary dynamics of the diversity of phenotype expression and the evolution of cooperation in the Prisoners Dilemma game. Rather than pre-assigning zero-or-one interaction rate, we diversify the rate of interaction by associating it with the phenotypes shared in common. Individuals each carry a set of potentially expressible phenotypes and expresses a certain number of phenotypes at a cost proportional to the number. The number of expressed phenotypes and thus the rate of interaction is an evolvable trait. Our results show that nonnegligible cost of expressing phenotypes restrains phenotype expression, and the evolutionary race mainly proceeds on between cooperative strains and defective strains who express a very few phenotypes. It pays for cooperative strains to express a very few phenotypes. Though such a low level of expression weakens reciprocity between cooperative strains, it decelerates rate of interaction between cooperative strains and defective strains to a larger degree, leading to the predominance of cooperative strains over defective strains. We also find that evolved diversity of phenotype expression can occasionally destabilize due to the invasion of defective mutants, implying that cooperation and diversity of phenotype expression can mutually reinforce each other. Therefore, our results provide new insights into better understanding the coevolution of cooperation and the diversity of phenotype expression.
The stabilizing effects of local enrichment are revisited. Diffusively coupled host-parasitoid and predator-prey metapopulations are shown to admit a stable fixed point, limit cycle or stable torus with a rich bifurcation structure. A linear toy model that yields many of the basic qualitative features of this system is presented. The further nonlinear complications are analyzed in the framework of the marginally stable Lotka-Volterra model, and the continuous time analog of the unstable, host-parasitoid Nicholson-Bailey model. The dependence of the results on the migration rate and level of spatial variations is examined, and the possibility of nonlocal effect of enrichment, where local enrichment induces stable oscillations at a distance, is studied. A simple method for basic estimation of the relative importance of this effect in experimental systems is presented and exemplified.
Interactions among multiple infectious agents are increasingly recognized as a fundamental issue in the understanding of key questions in public health, regarding pathogen emergence, maintenance, and evolution. The full description of host-multipathogen systems is however challenged by the multiplicity of factors affecting the interaction dynamics and the resulting competition that may occur at different scales, from the within-host scale to the spatial structure and mobility of the host population. Here we study the dynamics of two competing pathogens in a structured host population and assess the impact of the mobility pattern of hosts on the pathogen competition. We model the spatial structure of the host population in terms of a metapopulation network and focus on two strains imported locally in the system and having the same transmission potential but different infectious periods. We find different scenarios leading to competitive success of either one of the strain or to the codominance of both strains in the system. The dominance of the strain characterized by the shorter or longer infectious period depends exclusively on the structure of the population and on the the mobility of hosts across patches. The proposed modeling framework allows the integration of other relevant epidemiological, environmental and demographic factors opening the path to further mathematical and computational studies of the dynamics of multipathogen systems.
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