lecture_29_Mar 24_Co-evolution of parasites and hosts

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Transcript lecture_29_Mar 24_Co-evolution of parasites and hosts

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
– Host-parasite
– Plant- herbivore
– Predator-Prey
– Mutualisms
Parasites may evolve rapidly due to:
Short generation times
High fecundity
Founder effects and drift
High mutation rates
Consider plants and insects: it is sometimes difficult to determine whether
plants' secondary compounds arose for the purpose of preventing herbivores
from eating 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, symbiosis, mutualism, etc. is not
synonymous with coevolution. In one sense there has definitely been "evolution
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 insect 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 adaptations 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 commensalism- 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 inbreeding depression 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 infection; 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 fitness (population biologist’s definition)
Evolution of virulence
•
Why are some symbionts commensal and others
virulent?
•
Why do mortality rates following infection vary?
•
What causes qualitative and quantitative variation
in disease symptoms?
The conventional wisdom
•
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.
The conventional wisdom
•
The logic behind this view is pleasing to human
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?
The conventional wisdom
•
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
humans
•
In other older diseases, like rabies, humans play a
negligible role in the transmission of the parasite
The conventional wisdom
•
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 malaria 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?
The conventional wisdom
•
The conventional wisdom runs up against a big
problem when it comes to articulating the
mechanism responsible for the alleged
evolutionary pressure toward benign associations
•
For a parasite to evolve to become gentle and
prudent in its treatment of its host requires some
form of group selection since natural selection
operating at the level of the individual parasite
often favors virulence
The conventional wisdom
•
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 Australia
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
3
1
4
Grade
107
5
Low
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
Myxoma virus
•
Trade-off between virulence and transmission: highly
virulent forms killed too quickly, reducing chance of
being picked up by vector
•
Viruses that were too attenuated (mild) had fewer
lesions and lower viral load, again translating into
less chance of being picked up by vector
•
Happy medium selected for, rather than ever-more
benign forms
R0: The basic reproductive rate
The fundamental epidemiological quantity
R0 represents the average number of secondary
infections 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
R0
= βH
α+µ+b
β =transmission rate, H= number of hosts
α = parasite induced host mortality (a measure of virulence)
µ= parasite mortality rate within the host, b=natural host death
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.
R0: The basic reproductive rate
•
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 transmission.
The parasitemia of trypanosomes (sleeping sickness), or
Plasmodium (malaria) may affect virulence which may affect
host behaviour and the probability that an infected individual will
be bitten by a vector.
Costs of parasitism 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 producedeasily 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 Cell- 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 Red Queen Hypothesis
“ Here, you see, it takes all the running you can do just to stay in one place”
– Red Queen (Alice Through the Looking Glass)