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20.1 Fever 20.1.a. Explain how “behavioral fever” in certain ectothermic vertebrates suggests that fever is advantageous in dealing with infection. 20.1.b. Describe the proximate mechanisms responsible for fever in mammals. 20.1.c. Give evidence that supports the hypothesis that fever is an adaptation, including fitness costs and benefits. 20.1.d. Apply the principle of asymmetric harm to both smoke detectors and fevers. 20.2 Vulnerability to Disease 20.2.a. Describe how Tinbergen’s four levels of explanation can be applied to illness, disease, and medicine. 20.2.b. List Nesse and Williams’ six classes of evolutionary explanation for vulnerability to disease. 20.3 Coevolutionary Arms Races between Pathogens and Hosts 20.3.a. Identify the advantages that pathogens have in the coevolutionary arms race with their hosts. 20.3.b. Describe three ways that host immune systems can limit the ability of a pathogen population to outrun the host despite the pathogen’s rapid evolution. 20.3.c. Explain the role of clonal selection in the vertebrate adaptive immune system, including how V(D)J recombination generates a diverse repertoire of antibodies. 20.3.d. Give examples of ways that pathogens can subvert the host immune system. 20.3.e. Explain how host immune systems affect the phylogenetic pattern of pathogen evolution, including the role of viral escape variants in reinfection. 20.4 The Evolution of Virulence 20.4.a. Define “virulence” and name one metric for quantifying the virulence of a pathogen. 20.4.b. Discuss how virulence of the myxoma virus changed following its initial introduction into Australian rabbit populations in the 1950s and explain how this scenario exemplifies early views on the evolution of virulence. 20.4.c. List three possible reasons for why host mortality can change after the introduction of a novel pathogen into a wild population. 20.4.d. Distinguish between the trade-off and short-sighted evolution models of virulence evolution.
20.4.e .Describe the changes in SARS-CoV-2 fatality rates between spring 2020 and summer 2022 and discuss possible explanations for the observed changes. 20.5 Phylogenetic Constraint and Vulnerability to Choking 20.5.a. Identify the proximate cause of choking. 20.5.b. Define “phylogenetic constraint” and explain how this concept relates to the human vulnerability to choking. 20.6 Senescence 20.6.a. Define “senescence” and describe the pattern of senescence seen across organisms. 20.6.b. Summarize the rate-of-living hypothesis and explain why it cannot fully explain senescence. 20.6.c. Contrast the strength of natural selection on early-acting mutations with late- acting mutations and explain its relevance to senescence with regard to the mutation accumulation hypothesis. 20.6.d. Discuss how the antagonistic pleiotropy hypothesis can account for senescence. 20.6.e. Describe the relationship between the rate of senescence and the extrinsic mortality rate. 20.6.f. Summarize the disposable soma hypothesis and explain how this hypothesis can account for the large number of alleles that show antagonistic pleiotropy. 20.6.g. Explain how aging in bacteria relates to the various hypotheses about the evolution of senescence.