Abstract
When we contract an infection, we typically feel sick and behave accordingly. Symptoms of sickness behavior (SB) include anorexia, hypersomnia, depression, and reduced social interactions. SB affects species spanning from arthropods to vertebrates, is triggered nonspecifically by viruses, bacteria, and parasites, and is orchestrated by a complex network of cytokines and neuroendocrine pathways; clearly, it has been naturally selected. Nonetheless, SB seems evolutionarily costly: it promotes starvation and predation and reduces reproductive opportunities. How could SB persist? Former explanations focused on individual fitness, invoking improved resistance to pathogens. Could prevention of disease transmission, propagating in populations through kin selection, also contribute to SB?
Highlights
We propose that reduced transmission of infectious disease among related individuals contributed to the evolution of sickness behavior (SB)
More intense SB is expected among species that live in dense colonies and engage in close physical contact
SB would intensify with population viscosity and the length of care for offspring
Summary
Different pathogens invoke SB of varying intensities. Through an evolutionary process, more virulent pathogens would come to provoke stronger behavioral responses. When a pathogen is deadly, the individual loses little (as it would die anyway) and gains much (as it saves its relatives from death) from a debilitating behavioral response. When a pathogen is avirulent, the optimal behavioral response would be a subclinical one, invoking no SB even if an immune response is activated
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