Dataset Information

Bridging scales in the evolution of infectious disease life histories: application.

ABSTRACT: Within- and between-host disease processes occur on the same timescales, therefore changes in the within-host dynamics of parasites, resources, and immunity can interact with changes in the epidemiological dynamics to affect evolutionary outcomes. Consequently, studies of the evolution of disease life histories, that is, infection-age-specific patterns of transmission and virulence, have been constrained by the need for a mechanistic understanding of within-host disease dynamics. In a companion paper (Day et al. 2011), we develop a novel approach that quantifies the relevant within-host aspects of disease through genetic covariance functions. Here, we demonstrate how to apply this theory to data. Using two previously published datasets from rodent malaria infections, we show how to translate experimental measures into disease life-history traits, and how to quantify the covariance in these traits. Our results show how patterns of covariance can interact with epidemiological dynamics to affect evolutionary predictions for disease life history. We also find that the selective constraints on disease life-history evolution can vary qualitatively, and that "simple" virulence-transmission trade-offs that are often the subject of experimental investigation can be obscured by trade-offs within one trait alone. Finally, we highlight the type and quality of data required for future applications.

SUBMITTER: Mideo N

PROVIDER: S-EPMC3937741 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature

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Bridging scales in the evolution of infectious disease life histories: application.

Mideo Nicole N Nelson William A WA Reece Sarah E SE Bell Andrew S AS Read Andrew F AF Day Troy T

Evolution; international journal of organic evolution 20110721 11

Within- and between-host disease processes occur on the same timescales, therefore changes in the within-host dynamics of parasites, resources, and immunity can interact with changes in the epidemiological dynamics to affect evolutionary outcomes. Consequently, studies of the evolution of disease life histories, that is, infection-age-specific patterns of transmission and virulence, have been constrained by the need for a mechanistic understanding of within-host disease dynamics. In a companion ...[more]

PMID: 22023593

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Project description:Life history is a robust correlate of relative brain size: larger-brained mammals and birds have slower life histories and longer lifespans than smaller-brained species. The cognitive buffer hypothesis (CBH) proposes an adaptive explanation for this relationship: large brains may permit greater behavioural flexibility and thereby buffer the animal from unpredictable environmental challenges, allowing for reduced mortality and increased lifespan. By contrast, the developmental costs hypothesis (DCH) suggests that life-history correlates of brain size reflect the extension of maturational processes needed to accommodate the evolution of large brains, predicting correlations with pre-adult life-history phases. Here, we test novel predictions of the hypotheses in primates applied to the neocortex and cerebellum, two major brain structures with distinct developmental trajectories. While neocortical growth is allocated primarily to pre-natal development, the cerebellum exhibits relatively substantial post-natal growth. Consistent with the DCH, neocortical expansion is related primarily to extended gestation while cerebellar expansion to extended post-natal development, particularly the juvenile period. Contrary to the CBH, adult lifespan explains relatively little variance in the whole brain or neocortex volume once pre-adult life-history phases are accounted for. Only the cerebellum shows a relationship with lifespan after accounting for developmental periods. Our results substantiate and elaborate on the role of maternal investment and offspring development in brain evolution, suggest that brain components can evolve partly independently through modifications of distinct developmental phases, and imply that environmental input during post-natal maturation may be particularly crucial for the development of cerebellar function. They also suggest that relatively extended post-natal maturation times provide a developmental mechanism for the marked expansion of the cerebellum in the apes.

Dataset Information

Bridging scales in the evolution of infectious disease life histories: application.

Publications

Bridging scales in the evolution of infectious disease life histories: application.

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