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Resources, mortality, and disease ecology: importance of positive feedbacks between host growth rate and pathogen dynamics

Smith, Val H., Holt, Robert D., Smith, Marilyn S., Niu, Yafen, Barfield, Michael
Israel journal of ecology & evolution 2015 v.61 no.1 pp. 37-49
cell culture, death, epidemiology, fungi, host-pathogen relationships, hosts, infectious diseases, metabolism, models, mortality, pathogens, physiological state
Resource theory and metabolic scaling theory suggest that the dynamics of a pathogen within a host should strongly depend upon the rate of host cell metabolism. Once an infection occurs, key ecological interactions occur on or within the host organism that determine whether the pathogen dies out, persists as a chronic infection, or grows to densities that lead to host death. We hypothesize that, in general, conditions favoring rapid host growth rates should amplify the replication and proliferation of both fungal and viral pathogens. If a host population experiences an increase in mortality, to persist it must have a higher growth rate, per host, often reflecting greater resource availability per capita. We hypothesize that this could indirectly foster the pathogen, which also benefits from increased within-host resource turnover. We first bring together in a short review a number of key prior studies which illustrate resource effects on viral and fungal pathogen dynamics. We then report new results from a semi-continuous cell culture experiment with SHIV, demonstrating that higher mortality rates indeed can promote viral proliferation. We develop a simple model that illustrates dynamical consequences of these resource effects, including interesting effects such as alternative stable states and oscillatory dynamics. Our paper contributes to a growing body of literature at the interface of ecology and infectious disease epidemiology, emphasizing that host abundances alone do not drive community dynamics: the physiological state and resource content of infected hosts also strongly influence host–pathogen interactions.