Browsing by Author "Koelle, K"

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    Navigating the devious course of evolution: the importance of mechanistic models for identifying eco-evolutionary dynamics in nature.
    (Am Nat, 2013-05) Luo, S; Koelle, K
    In proposing his genetic feedback mechanism, David Pimentel was one of the first biologists to argue that the reciprocal interplay of ecological and evolutionary dynamics is an important process regulating population dynamics and ultimately affecting community composition. Although the past decade has seen an increase in research activity on these so-called eco-evolutionary dynamics, there remains a conspicuous lack of compelling natural examples of such feedback. Here we argue that this lack may be due to an inherent difficulty in detecting eco-evolutionary dynamics in nature. By examining models of virulence evolution, host resistance evolution, and antigenic evolution, we show that the influence of evolution on ecological dynamics can often be obscured by other ecological processes that yield similar dynamics. We then show, however, that mechanistic models can be used to navigate this, in Pimentel's words, "devious" course of evolution when effectively combined with empirical data. We argue that these models, improving upon Pimentel's original mathematical models, will therefore play an increasingly important role in identifying more subtle, but possibly ubiquitous, eco-evolutionary dynamics in nature. To highlight the importance of identifying these potentially subtle dynamics in nature, we end by considering our ability to anticipate the effect of population control strategies in the presence of these eco-evolutionary feedbacks.
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    Phylodynamic inference and model assessment with approximate bayesian computation: influenza as a case study.
    (PLoS Comput Biol, 2012) Ratmann, O; Donker, G; Meijer, A; Fraser, C; Koelle, K
    A key priority in infectious disease research is to understand the ecological and evolutionary drivers of viral diseases from data on disease incidence as well as viral genetic and antigenic variation. We propose using a simulation-based, Bayesian method known as Approximate Bayesian Computation (ABC) to fit and assess phylodynamic models that simulate pathogen evolution and ecology against summaries of these data. We illustrate the versatility of the method by analyzing two spatial models describing the phylodynamics of interpandemic human influenza virus subtype A(H3N2). The first model captures antigenic drift phenomenologically with continuously waning immunity, and the second epochal evolution model describes the replacement of major, relatively long-lived antigenic clusters. Combining features of long-term surveillance data from The Netherlands with features of influenza A (H3N2) hemagglutinin gene sequences sampled in northern Europe, key phylodynamic parameters can be estimated with ABC. Goodness-of-fit analyses reveal that the irregularity in interannual incidence and H3N2's ladder-like hemagglutinin phylogeny are quantitatively only reproduced under the epochal evolution model within a spatial context. However, the concomitant incidence dynamics result in a very large reproductive number and are not consistent with empirical estimates of H3N2's population level attack rate. These results demonstrate that the interactions between the evolutionary and ecological processes impose multiple quantitative constraints on the phylodynamic trajectories of influenza A(H3N2), so that sequence and surveillance data can be used synergistically. ABC, one of several data synthesis approaches, can easily interface a broad class of phylodynamic models with various types of data but requires careful calibration of the summaries and tolerance parameters.
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    Viral phylodynamics.
    (PLoS Comput Biol, 2013) Volz, EM; Koelle, K; Bedford, T
    Viral phylodynamics is defined as the study of how epidemiological, immunological, and evolutionary processes act and potentially interact to shape viralphylogenies. Since the coining of the term in 2004, research on viral phylodynamics has focused on transmission dynamics in an effort to shed light on how these dynamics impact viral genetic variation. Transmission dynamics can be considered at the level of cells within an infected host, individual hosts within a population, or entire populations of hosts. Many viruses, especially RNA viruses, rapidly accumulate genetic variation because of short generation times and high mutation rates. Patterns of viral genetic variation are therefore heavily influenced by how quickly transmission occurs and by which entities transmit to one another. Patterns of viral genetic variation will also be affected by selection acting on viral phenotypes. Although viruses can differ with respect to many phenotypes, phylodynamic studies have to date tended to focus on a limited number of viral phenotypes. These include virulence phenotypes, phenotypes associated with viral transmissibility, cell or tissue tropism phenotypes, and antigenic phenotypes that can facilitate escape from host immunity. Due to the impact that transmission dynamics and selection can have on viral genetic variation, viral phylogenies can therefore be used to investigate important epidemiological, immunological, and evolutionary processes, such as epidemic spread[2], spatio-temporal dynamics including metapopulation dynamics[3], zoonotic transmission, tissue tropism[4], and antigenic drift[5]. The quantitative investigation of these processes through the consideration of viral phylogenies is the central aim of viral phylodynamics.