Theoretical Population Biology最新文献

This paper considers Lotka-Volterra competitive systems characterizing laboratory experiment by Hu et al. (Science, 378:85-89, 2022). Using dynamical systems theory and projection method, we give theoretical analysis and numerical simulation on the model with four species by demonstrating equilibrium stability, periodic oscillation and chaotic fluctuation in the systems. It is shown that varying one competition strength could lead to emergent phases and phase transitions between stable full coexistence, stable partial coexistence, stable persistence of a unique species, persistent periodic oscillation, and persistent chaotic fluctuation in a smooth fashion. Here, the stronger the competition is, the less the number of stable coexisting species, or the higher the amplitude of periodic oscillation, or the more irregular the fluctuation. Our results are consistent with experimental observation and provide new insight. This work is important in understanding effect of competition on emergent phases and phase transitions in competitive systems.

Ordinary differential equation models such as the classical SIR model are widely used in epidemiology to study and predict infectious disease dynamics. However, these models typically assume that populations are homogeneously mixed, ignoring possible variations in disease prevalence due to spatial heterogeneity. To address this issue, reaction-diffusion models have been proposed as an alternative approach to modeling spatially continuous populations in which individuals move in a diffusive manner. In this study, we explore the conditions under which such spatial structure must be explicitly considered to accurately predict disease spread, and when the assumption of homogeneous mixing remains adequate. In particular, we derive a critical threshold for the diffusion coefficient below which disease transmission dynamics exhibit spatial heterogeneity. We validate our analytical results with individual-based simulations of disease transmission across a two-dimensional continuous landscape. Using this framework, we further explore how key epidemiological parameters such as the probability of disease establishment, its maximum incidence, and its final epidemic size are affected by incorporating spatial structure into SI, SIS, and SIR models. We discuss the implications of our findings for epidemiological modeling and identify design considerations and limitations for spatial simulation models of disease dynamics.

Phages use bacterial host resources to replicate, intrinsically linking phage and host survival. To understand phage dynamics, it is essential to understand phage-host ecology. A key step in this ecology is infection of bacterial hosts. Previous work has explored single and multiple, sequential infections. Here we focus on the theory of simultaneous infections, where multiple phages simultaneously attach to and infect one bacterial host cell. Simultaneous infections are a relevant infection dynamic to consider, especially at high phage densities when many phages attach to a single host cell in a short time window. For high bacterial growth rates, simultaneous infection can result in bi-stability: depending on initial conditions phages go extinct or co-exist with hosts, either at stable densities or through periodic oscillations of a stable limit cycle. This bears important consequences for phage applications such as phage therapy: phages can persist even though they cannot invade. Consequently, through spikes in phage densities it is possible to infect a bacterial population even when the phage basic reproductive number is less than one. In the regime of stable limit cycles, if timed right, only small densities of phage may be necessary.

Mutation accumulation (MA) experiments play an important role in understanding evolution. For microbial populations, such experiments often involve periods of population growth, such that a single individual can make a visible colony, followed by severe bottlenecks. Previous work has quantified the effect of positive and negative selection on MA experiments, demonstrating for example that with 20 generations of growth between bottlenecks, big-benefit mutations can be over-represented by a factor of five or more (Wahl and Agashe, 2022). This previous work assumed a deterministic model for population growth. We now develop a fully stochastic model, including realistic offspring distributions that incorporate genetic drift and allow for the loss of rare lineages. We demonstrate that when stochastic offspring distributions are considered, selection bias is even stronger than previously predicted. We describe several analytical and numerical methods that offer an accurate correction for the effects of selection on the observed distribution of fitness effects, describe the practical considerations in implementing each method, and demonstrate the use of this correction on simulated MA data.

We model natural selection for or against an anti-parasite (or anti-predator) defense allele in a host (or prey) population that is structured into many demes. The defense behavior has a fitness cost for the actor compared to non defenders ("cheaters") in the same deme and locally reduces parasite growth rates. Hutzenthaler et al. (2022) have analytically derived a criterion for fixation or extinction of defenders in the limit of large populations, many demes, weak selection and slow migration. Here, we use both individual-based and diffusion-based simulation approaches to analyze related models. We find that the criterion still leads to accurate predictions for settings with finitely many demes and with various migration patterns. A key mechanism of providing a benefit of the defense trait is genetic drift due to randomness of reproduction and death events leading to between-deme differences in defense allele frequencies and host population sizes. We discuss an inclusive-fitness interpretation of this mechanism and present in-silico evidence that under these conditions a defense trait can be altruistic and still spread in a structured population.

Infinitely many distinct trait values may arise in populations bearing quantitative traits, and modeling their population dynamics is thus a formidable task. While classical models assume fixed or infinite population size, models in which the total population size fluctuates due to demographic noise in births and deaths can behave qualitatively differently from constant or infinite population models due to density-dependent dynamics. In this paper, I present a stochastic field theory for the eco-evolutionary dynamics of finite populations bearing one-dimensional quantitative traits. I derive stochastic field equations that describe the evolution of population densities, trait frequencies, and the mean value of any trait in the population. These equations recover well-known results such as the replicator-mutator equation, Price equation, and gradient dynamics in the infinite population limit. For finite populations, the equations describe the intricate interplay between natural selection, noise-induced selection, eco-evolutionary feedback, and neutral genetic drift in determining evolutionary trajectories. My work uses ideas from statistical physics, calculus of variations, and SPDEs, providing alternative methods that complement the measure-theoretic martingale approach that is more common in the literature.