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Register a new userMetapopulation dynamics of a respiratory disease with infection during travel
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We formulate a compartmental model for the propagation of a respiratory disease in a patchy environment. The patches are connected through the mobility of individuals, and we assume that disease transmission and recovery are possible during travel. Moreover, the migration terms are assumed to depend on the distance between patches and the perceived severity of the disease. The positivity and boundedness of the model solutions are discussed. We analytically show the existence and global asymptotic stability of the disease-free equilibrium. Without human movement, the global stability of the endemic equilibrium point is also established using Lyapunov functions. We study three different network topologies numerically and find that underlying network structure is crucial for disease transmission. Further numerical simulations reveal that infection during travel has the potential to change the stability of disease-free equilibrium from stable to unstable. The coupling strength and transmission coefficients are also very crucial in disease propagation. Different exit screening scenarios indicate that the patch with the highest prevalence may have adverse effects but other patches will be benefited from exit screening. Furthermore, while studying the multi-strain dynamics, it is observed that two co-circulating strains will not persist simultaneously in the community but only one of the strains may persist in the long run. Transmission coefficients corresponding to the second strain are very crucial and show threshold like behavior with respect to the equilibrium density of the second strain.
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Chloroplast microsatellites are becoming increasingly popular markers for population genetic studies in plants, but there has been little focus on their potential for demographic inference. In this work the utility of chloroplast microsatellites for the study of population expansions was explored. First, we investigated the power of mismatch distribution analysis and the F(S) test with coalescent simulations of different demographic scenarios. We then applied these methods to empirical data obtained for the Canary Island pine (Pinus canariensis). The results of the simulations showed that chloroplast microsatellites are sensitive to sudden population growth. The power of the F(S) test and accuracy of demographic parameter estimates, such as the time of expansion, were reduced proportionally to the level of homoplasy within the data. The analysis of Canary Island pine chloroplast microsatellite data indicated population expansions for almost all sample localities. Demographic expansions at the island level can be explained by the colonization of the archipelago by the pine, while population expansions of different ages in different localities within an island could be the result of local extinctions and recolonization dynamics. Comparable mitochondrial DNA sequence data from a parasite of P. canariensis, the weevil Brachyderes rugatus, supports this scenario, suggesting a key role for volcanism in the evolution of pine forest communities in the Canary Islands.
We study the extinction risk of a fragmented population residing on a network of patches coupled by migration, where the local patch dynamics include the Allee effect. We show that mixing between patches dramatically influences the populations viability. Slow migration is shown to always increase the populations global extinction risk compared to the isolated case. At fast migration, we demonstrate that synchrony between patches minimizes the populations extinction risk. Moreover, we discover a critical migration rate that maximizes the extinction risk of the population, and identify an early-warning signal when approaching this state. Our theoretical results are confirmed via the highly-efficient weighted ensemble method. Notably, our analysis can also be applied to studying switching in gene regulatory networks with multiple transcriptional states.
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We present a robust data-driven machine learning analysis of the COVID-19 pandemic from its early infection dynamics, specifically infection counts over time. The goal is to extract actionable public health insights. These insights include the infectious force, the rate of a mild infection becoming serious, estimates for asymtomatic infections and predictions of new infections over time. We focus on USA data starting from the first confirmed infection on January 20 2020. Our methods reveal significant asymptomatic (hidden) infection, a lag of about 10 days, and we quantitatively confirm that the infectious force is strong with about a 0.14% transition from mild to serious infection. Our methods are efficient, robust and general, being agnostic to the specific virus and applicable to different populations or cohorts.
We review research papers which use game theory to model the decision making of individuals during an epidemic, attempting to classify the literature and identify the emerging trends in this field. We show that the literature can be classified based on (i) type of population modelling (compartmental or network-based), (ii) frequency of the game (non-iterative or iterative), and (iii) type of strategy adoption (self-evaluation or imitation). We highlight that the choice of model depends on many factors such as the type of immunity the disease confers, the type of immunity the vaccine confers, and size of population and level of mixing therein. We show that while early studies used compartmental modelling with self-evaluation based strategy adoption, the recent trend is to use network-based modelling with imitation-based strategy adoption. Our review indicates that game theory continues to be an effective tool to model intervention (vaccination or social distancing) decision-making by individuals.
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