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Home , Coevolution, Evolutionary pressure, Group selection

Coevolution: a pattern of reciprocal , caused by two evolving in close association. is a change in the genetic composition of one species (or group) in response to a genetic change in another. More generally, the idea of some reciprocal evolutionary change in interacting species is a requisite for coevolution

– -parasite – - – Predator-Prey – Mutualisms

Parasites may evolve rapidly due to: Short generation times High fecundity Founder effects and drift High rates Consider and : it is sometimes difficult to determine whether plants' secondary compounds arose for the purpose of preventing from plant tissue. Certain plants may have produced certain compounds as waste products and herbivores attacked those plants that they could digest.

Parasites and hosts: when a parasite invades a host, it will successfully invade those hosts whose defence traits it can circumvent because of the abilities it carries at that time. Thus presence of a parasite on a host does not constitute evidence for coevolution. These criticisms are quite distinct from the opportunity for coevolution once a parasite has established itself on a host.

The main point is that any old interaction, , , etc. is not synonymous with coevolution. In one sense there has definitely been " together" but whether this fits our strict definition of coevolution needs to be determined by careful 1) observation, 2) experimentation and 3) phylogenetic analysis The classic analogy is the coevolutionary arms race: a plant has chemical defenses, an evolves the biochemistry to detoxify these compounds, the plant in turn evolves new defenses that the insect in turn "needs" to further detoxify.

At present the evidence for these types of reciprocal is limited, but the suggestive evidence of plant animal interactions is widespread. An important point is the relative timing of the evolution of the various traits that appear to be part of the coevolution. If the presumed reciprocally induced, sequential traits actually evolved in the plant host before the insect became associated with it, we should not call it coevolution.

That is, the central problem in coevolutionary studies is to understand the ecological and genetic conditions that permit interacting species to undergo repeated bouts of reciprocal genetic change specifically because of the interaction Coevolution, Coexistence, Conflict ?

Conventional thought: the good, or better adapted, parasite does not unduly harm its host. Any exceptions can be viewed as new or more recent associations compared with benign interactions

Therefore are all the parasites we have seen new associations?

When hosts encounter “harmful” parasites, that drain resources and take actions to counter the effect of the parasites- is this peaceful coexistence or a stalemate?

Should the relationship develop towards - or can a certain level of pathogenicity be tolerated? Coevolution between hosts and parasites is continuous reciprocal evolution. As parasites are suggested to track the common host genotypes coevolution can lead to adaptation by parasites to their local hosts.

Isolation of populations may enhance the local adaptation process by diverging selection and reducing migration. Selection for parasites depends on the host resistance alleles present in the population and the host’s alleles for resistance are themselves under selection by parasites.

In small isolated populations the probability of mating among relatives is increased. Host inbreeding might affect the observation of local adaptation by parasites in two ways. First, due to inbreeding the within population variation in host resistance might be fixed within homozygous lineages thereby enforcing local coevolutionary processes. On the other hand, inbreeding might confound the observation of local adaptation by parasites as the resulting may increase the hosts’ susceptibility. The concept that parasite-host relationships evolve / coevolve to negligible pathogenicity has become so strong that it now acts as a paradigm.

Should parasites be virulent or avirulent? • Virulence is the harm done by a pathogen to the host following an ; parasite-mediated morbidity and mortality in infected hosts

• Virulence is of course the result of complex interactions between both the parasite and its host.

• “Harm” here can mean specific symptoms and pathologies (clinician’s definition) or a reduction in host (population biologist’s definition) EvolutionEvolution ofof virulencevirulence

• Why are some symbionts commensal and others virulent?

• Why do mortality rates following infection vary?

• What causes qualitative and quantitative variation in disease symptoms? TheThe conventionalconventional wisdomwisdom

• Biologists traditionally believed that all pathogen populations would evolve toward ever-lower virulence

• Why?

Damage to the host must ultimately be detrimental to the interests of the pathogens that live within it. TheThe conventionalconventional wisdomwisdom

• The logic behind this view is pleasing to sensibilities: a fully-evolved parasite would not harm the host it needs for its survival, proliferation, and transmission

• The corollary is that pathogenesis is evidence of recent associations between parasites and their hosts. Virulence is an indication that not enough time has elapsed for a benign association to evolve…Is this view correct? TheThe conventionalconventional wisdomwisdom

• Many observations are consistent with the conventional wisdom: Legionnaire’s disease, Lyme disease, ebola, and SARS are consequences of human infection with symbionts of other species that have recently jumped into

• In other older diseases, like rabies, humans play a negligible role in the transmission of the parasite TheThe conventionalconventional wisdomwisdom

• Other observations don’t fit so well, however.

• For some virulent pathogens like Shigella and Neisseria gonorrhoeae humans are the unique or dominant host

• For other, like and tuberculosis, there is evidence of a long association with humans

• Is “long” not long enough, or could it be that some pathogens evolve to become increasingly virulent? TheThe conventionalconventional wisdomwisdom

• The conventional wisdom runs up against a big problem when it comes to articulating the mechanism responsible for the alleged toward benign associations

• For a parasite to evolve to become gentle and prudent in its treatment of its host requires some form of since operating at the level of the individual parasite often favors virulence TheThe conventionalconventional wisdomwisdom

• In the 1980, evolutionary biologists realized that if transmission and virulence were positively coupled, natural selection acting on individuals could favor the evolution and maintenance of some level of virulence

• It comes down to elucidating the relationship between the rate of parasite-mediated mortality and the rate of transmission. If the relationship is positive, some level of virulence may be favored

• In other words, if killing your host is correlated with higher transmission, natural selection may well favor virulence Coevolution: a pattern of reciprocal adaptation, caused by two species evolving in close association. coevolution is a change in the genetic composition of one species (or group) in response to a genetic change in another. More generally, the idea of some reciprocal evolutionary change in interacting species is a requisite for coevolution Questions: How do parasites and hosts evolve? Do parasites evolve to lose virulence? Should they? Do parasites cause less disease because hosts mount counter measures? Are we in an arm’s race or in a negotiated settlement?

Can the parasite increase virulence and the host increase defences indefinitely? Can this continue forever?

What about the costs to the parasite and host of increasing virulence and defences? Will overall fitness of both be affected?

In theory when costs are present on either side some “compromise” is likely History of myxomatosis virus.

Isolated in S. America 1890s sent to Introduced into Australia in 1950s. Intention: kill introduced rabbits. Initially killed 100% of infected hosts. Kill rate declined over time. Rabbits evolved resistance. Myxomatosis evolved lower virulence- why? 1 High 1 3 4 Grade 107

Low 5 5 time time

Now host responses maintain low viremia: virus increasing viremia just to reach threshold to maintain transmission Coevolution of parasites and their hosts virus virus

Myxoma Myxoma highly virulent forms killed too quickly, reducing chance of being picked up by vector lesions and lower viral load, again translating into less chance of being picked up by vector benign forms • between virulence and transmission: Trade-off • Viruses that were too attenuated (mild) had fewer • Happy medium selected for, rather than ever-more y (a measure of virulence) in the host, b=natural host death : The basic reproductive rate : The basic reproductive rate

0 H

0 + µ + b β

R R α = represents the average number of secondary

0 0 = parasite induced host mortalit =transmission rate, H= number of hosts β generated by one primary case in a susceptible population Can be used to estimate the level of immunization or behavioural change required to control an epidemic The fundamental epidemiological quantity R0 α R R µ= parasite mortality rate with Parasite-imposed and host-imposed selection can operate together in determining features of parasite-host interactions.

Parasite virulence can incur costs for parasite and host- if parasites incur too much suffering on their hosts. Anderson and May:

R0 = βH α + µ + b

Parasite net reproductive rate (R0) and virulence (α) are inversely related If parasite virulence brings no benefit to parasite, there is nothing to stop virulence from evolving to zero (commensalism) or even a positive relationship (mutualism). If the parameters were independent of each other the predictions derived in this equation would suggest that parasites to become benign. . transmission an infected individual will : The basic reproductive rate : The basic reproductive rate 0 0 R R If all parameters were independent, benign parasites would evolve Natural selection would favor highly transmissible, incurable commensals or symbionts On the other hand, if transmission and virulence were positively coupled, some level of virulence will be favored Link between virulence and increased fitness is The parasitemia of trypanosomes (sleeping sickness), or virulence which may affect Plasmodium (malaria) may affect host behaviour and the probability that be bitten by a vector. • • • Costs of for parasite and host and their interdependencies between costs and benefits may lead to trade offs and compromises. In natural populations the fitness costs of parasitism and immune defences are complex and sometimes difficult to separate. Costs of fitness often are measured in terms of number of offspring produced- easily measured. If we activate the immune response we may find immune defences are energetically costly: and should have a negative correlation with other fitness-related traits. But normally we activate only a component of the immune response and cannot measure costs directly. Immune responses to a challenge may be short-lived; less than a day. Unless these are very energetically costly these are unlikely to reveal fitness costs. In wild animals the immune stimulus may be broad and long: response may be stimulated by a series of pathogens. Many subtle responses may reduce reserves until other traits are affected. How do we interpret the synergistic interactions between infections? Plasmodium infections in humans:

Severe infections, hosts may die: What responses have humans developed?

Human malaria: adaptations to the parasite Sickle - single point mutation- abnormal shape of a percentage of RBC Only benefit is to heterozygous individuals: double dominant are susceptible double recessive often die from anemia

G-6-Phosphate dehydrogenase deficiency: results in reduced parasitemias

Duffy Blood group: double recessive- completely resistant to P. vivax. parasite cannot find receptors to enter RBC Found in 80% of W. African black population Lizard malaria reduces clutch size. Infected males interact less with females and other males, results in maintenance of inferior territories, decreased ability to compete for females, inability to attract females.

Infection may be associated with significant reduction in fitness, although no direct effect on survival. Genetically controlled resistance mechanisms also have a cost:

1) Immune responses may be harmful themselves 2) Structures for passive immunity or infrastructure for a response (thymus and spleen) are expensive to produce and maintain 3) Mounting an immune response may be energetically expensive

What are the costs for developing an immune response? Does this depend on the probability of encountering a parasite or the costs of having a parasite? Take home message

• Coevolution is a pattern of reciprocal adaptation, caused by 2 species evolving in close association.

• Examples include host-parasite, predator-prey, mutualisms etc.: interspecific relationships.

• Antagonistic interactions can result in arms race: species evolve countermeasures just to “stay in one place” The

“ Here, you see, it takes all the running you can do just to stay in one place”

– Red Queen (Alice Through the Looking Glass)