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• W2979886058 abstract "Host defense mechanisms fundamentally shape disease dynamics and virulence evolution. Feeding behaviors may play a critical, but overlooked, role in host defense and evolutionary epidemiology. Specifically, hosts typically reduce their feed intake in response to both realized and potential infections, despite the fact that defense mechanisms are energetically costly. The decline in feeding (‘illness-mediated anorexia’) shifts within-host energetics, metabolism, physiology, and immune functions in ways that alter the selective pressures facing parasites. Consequentially, illness-mediated anorexia may drive the evolution of higher or lower virulence, depending on its interactive effects on immunological and parasitological processes. Examining illness-mediated anorexia through the lens of evolutionary epidemiology carries important implications for disease management, especially for livestock and fish. The loss of appetite that typically accompanies infection or mere exposure to parasites is traditionally considered a negative byproduct of infection, benefitting neither the host nor the parasite. Numerous medical and veterinary practices directly or indirectly subvert this ‘illness-mediated anorexia’. However, the ecological factors that influence it, its effects on disease outcomes, and why it evolved remain poorly resolved. We explore how hosts use anorexia to defend against infection and how parasites manipulate anorexia to enhance transmission. Then, we use a coevolutionary model to illustrate how shifts in the magnitude of anorexia (e.g., via drugs) affect disease dynamics and virulence evolution. Anorexia could be exploited to improve disease management; we propose an interdisciplinary approach to minimize unintended consequences. The loss of appetite that typically accompanies infection or mere exposure to parasites is traditionally considered a negative byproduct of infection, benefitting neither the host nor the parasite. Numerous medical and veterinary practices directly or indirectly subvert this ‘illness-mediated anorexia’. However, the ecological factors that influence it, its effects on disease outcomes, and why it evolved remain poorly resolved. We explore how hosts use anorexia to defend against infection and how parasites manipulate anorexia to enhance transmission. Then, we use a coevolutionary model to illustrate how shifts in the magnitude of anorexia (e.g., via drugs) affect disease dynamics and virulence evolution. Anorexia could be exploited to improve disease management; we propose an interdisciplinary approach to minimize unintended consequences. the set of quantitative trait values expressed by both the host and the parasite that cannot be invaded by nearby trait values for either the host or parasite. The strategies we examine here are anorexia, exploitation, and virulence. the value of a quantitative trait (of the host or parasite) such that a population expressing this trait cannot be invaded by populations expressing a nearby trait value. the rate at which parasites steal resources from the host for their own growth and development, which, in turn, can affect virulence with concomitant changes in the shedding of infectious propagules into the environment. refers to the reproductive success of an individual (host or parasite), which involves both reproduction and survival and is measured in terms of genetic representation in the next generation. a usually temporary but substantial reduction in voluntary food intake that accompanies exposure to or infection by infectious agents (parasites and pathogens) and other antigenic challenges [e.g., lipopolysaccharide (LPS) or poly(I:C), which mimic generalized bacterial and viral infections, respectively]; can occur in uninfected and infected individuals alike; also known as parasite-induced anorexia, foraging-rate depression, often studied using calorie restriction. Illness-mediated anorexia is the most frequently used term for this condition, so we use it here for consistency’s sake, although there are likely to be many other, more appropriate terms. Note, it should not be confused with anorexia cachexia (a life-threatening condition associated with several pathologies and characterized by massive loss of body mass, anorexia, general inflammation, and pronounced muscle wasting) or anorexia nervosa (an emotional dysregulation characterized by an obsessive desire to lose weight by refusing to eat). harm, hypersensitivity, or disease arising from activity of the immune system. used here to refer to the trait value that maximizes a fitness expression, given a set of constraints or life-history trade-offs. the ability to control parasite levels; can occur by preventing the establishment of parasite infection or reducing the infective dose (known as ‘anti-infection resistance’ or avoidance) or reducing the parasite growth or burden within infected hosts (known as ‘antigrowth resistance’ or clearance). use of a third species or compounds by hosts to reduce the likelihood of specific compounds infection (can occur in uninfected and infected individuals alike) or to fight or inhibit parasite growth once infected (occurs in infected individuals). stereotypical behavioral changes that accompany different phases of exposure to or infection by parasites and pathogens – anorexia, fever, lethargy, somnolence, and decreased libido. a reduction in infection-induced pathology (e.g., fecundity loss, mortality) that does not reduce parasite infection or growth. parasite-induced reduction in host fitness; often equated with the disease-induced mortality rate and therefore involves both direct harm from the parasite and associated immunopathology." @default.
• W2979886058 created "2019-10-18" @default.
• W2979886058 creator A5011739264 @default.
• W2979886058 creator A5062076247 @default.
• W2979886058 creator A5069951693 @default.
• W2979886058 date "2020-01-01" @default.
• W2979886058 modified "2023-10-12" @default.
• W2979886058 title "Starving the Enemy? Feeding Behavior Shapes Host-Parasite Interactions" @default.
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• W2979886058 doi "https://doi.org/10.1016/j.tree.2019.08.004" @default.
• W2979886058 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31604593" @default.
• W2979886058 hasPublicationYear "2020" @default.
• W2979886058 type Work @default.

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