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Sem 1: Parasite and pathogen ecology > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is the strict definition of co-evolution?

A

The joint evolution of two (or more) ecologically interacting species, each of which evolves in response to selection imposed by the other

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2
Q

What is the loose definition of co-evolution?

A

The evolution of one species caused by its interaction with another

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3
Q

What is the general definiton of co-evolution?

A

Each party exerts selective pressure on the other, thereby affecting each others evolution

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4
Q

What is the relationship between hosts and pathogens?

A

Pathogens want to consume host tissue/energy to covert it into more pathogens
Hosts limit damage by slowing or killing the pathogen
This places a strong selection pressure on both hosts and pathogens

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5
Q

What are the 3 co-evolutionary concepts for parasites and hosts?

A

1 - Specific host and pathogen co-evolve
2- Several species involved and their efffects are not independant (host many evolve to more than one pathogen)
3- Host species evolves a major new defence against pathogens, escape 1 pathogen and another evolves later

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6
Q

How can host species escape a pathogen?

A

Evolves a new defence against pathogens
Escapes pathogens and can proliferate and diversify
Later new pathogens adapt to host clade and therefore also diversify

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7
Q

What is used to analyse co-evolution?

A

Phylogenetic analysis

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8
Q

What are some issues with assessing co-evolution?

A

Most congruent phylogeny - some mismatches
Host switching
Extinction of Lineages

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9
Q

What is relationship between pigeons, wing and body lice?

A

Body lice competitively superior to wing lice
More host switching in wing lice
Both transmit vertically - parent to child
Wing lice also has phoretic horizontal transmission

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10
Q

What are examples of specific parasite co-evolutions adaptation?

A

Parasitic trematode larvae (Leucochloridium) - migrats to the eye stalk of its intermidiate host (land snail)

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11
Q

What are examples of specific host co-evolutions defences?

A

Wild parsnips (Pastinaca Sativa) produce chemical defence furanocoumarins against insects (webworms)
Vertebrates - Major Histocompatability Complex

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12
Q

What is the costs of furanocoumarin production in wild parsnips?

A

High energetic cost to produce furanocoumarins
Can be up to 10% energy costs
Parsnips with high furanocoumarins produce less seeds

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13
Q

What are the 3 outcomes of a pathogen and host relationship?

A

Unending arms race
Extinction of one of the species
Stable genetic equilibrium

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14
Q

What are the 2 complex models of co-evolution?

A

Attack and defence
Cost and benefits

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15
Q

What are the mechanisms of pathoegn-mediated selection?

A

Frequency dependance
Heterozygote advantage
Fluctuating selection

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16
Q

What is virulence?

A

The relarive ability of a pathogen to cause a disease
The host’s loss of fitness due to the pathogen
Virulence depends on host-pathogen co-evolution

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17
Q

What is coincidental evolution?

A

Accidental virulence with selection of other traits

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18
Q

What is an example of conincidental evolution?

A

Tetnus (Claustridium tetane)
Chemical secretions - selected for life in soil
Neurotoxin in humans

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19
Q

What is short-sighted evolution?

A

Generations of evolution within a host before transmission
Trsits for within host firtness evolve
Even if detrimental to transmission to new host

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20
Q

What is an example of short-sighted evolution?

A

Poliovirus in humans - normally in gut lining
May evolve to exploit nervous system
But will never be transmitted

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21
Q

What is the trade off hypothesis?

A

Selection favours pathogens that strike the optimal balance between the cost and benefits of harming their hosts - to optimise transmission rates

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22
Q

What factors affect trade off and therefore virulence?

A

Multiple infections - competition between different strains of pathogens within host
Speed/effectiveness of the host’s immune system
Pathogen transmission
- Form of transmission - horizontal vs vertical
- Means of transmission - vector vs direct contact

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23
Q

As shown in bacteriophages in E.Coli, what is the method for horizontal transmission?

A

Virus induces cell to produce and secrete new phages- but this slows E.Coli cell growth

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24
Q

As shown in bacteriophages in E.Coli, what is the method for vertical transmission?

A

E.Coli divides - virus copies in both daughter cells

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25
How can you block different forms of transmission of bacteriophages?
1 - Anti virals to block horizontal 2 - To block vertical transmission move phages to new uninfected E.Coli cultures every generation
26
What was the experiments done by Messenger in 1999?
Created 2 sets of selection lines of virus (13 in each) 1 set can only vertical transmission virus lines and the other horizontal transmission
27
What were the predictions for the Messenger experiments based off of trade off hypothesis?
1 - Correlation between phage reproduction rate and virulence - virus lines that reproduce the most - slow host growth most 2 - Mainly vertical transmission lines - evolves lower phage reproduction rates and lower virulence (allow their host to reproduce more) 3 - Mainly horizontal transmission lines - favour viral strains that reproduce quicker - more virulent
28
What was the result of the Messenger experiments?
The predictions where found to be correct horizontal transmission has high virulence and vertical transmission had low virulence with a positive correlation between virulence and phage reproduction rate
29
How does transmission form impact virulence?
Vector born pathogens - carried away from severly debilitated host Pathogens transmitted by direct contact - cannot afford to be too virulent
30
What happened to the Myxoma virus in the European rabbit (Oryctologus cuniculus) populations in Australia?
Introduced to Australia (1950) Spread by fleas, mosquitos and man Causes localised skin tumours Kills 99.8% rabbits but soon dropped off
31
Why did the rabbit death percentage drop off?
Myxoma epidemics exerted strong selective pressure for resistance Rabbits populations that had been exposed to more epidemics had lower mortality Genetic variation conferring resistance to myxoma before indroduction of virus
32
What happened to the virulence of the myxoma virus?
Virus strains that didn't kill hosts were more readily disperse to new hosts - stabilises at an intermediate level
33
What is the endosymbiotic theory?
A rickettsia species of bacteria has so co-evolved that it only lives in cells
34
What is the Major Histocompatibility complex?
Set of genes coding for cell surface glycoprotein molecules in all vertebrates
35
What is the major histocompatibility complex called in human?
Human leukocyte anitgen (HLA) complex
36
How was the HLA first identified?
Organ transplants
37
What is the function of major histocompatibility complex?
Distinguishing self from non-self
38
What does the major histocompatibility complex code for?
Molecules that bind and present antigens on the cell surface
39
What are antigens?
Non-self peptides
40
How does the major histocompatibility complex help in immune response?
Major role in determining acquires immune response
41
How many classes of major histocompatibility complex are there?
3
42
What is the function of class 1 major histocompatibility complex?
Present antigenic peptides to Cytotoxic cells Endogenously derived peptides Used against intracellular pathogens
43
What are class 2 major histocompatibility complexes?
Present antigenic peptides to T helper cells Process exogenous antigens Extracellular pathogens e.g Gut parasites
44
What are class 3 major histocompatibility complexes?
Secrete proteins that have an immune function Involved in inflammation
45
What are major histocompatibility complex genes?
Complicated set of replictaed genes (multiple gene duplications
46
Are major histocompatibility complex genes linked?
Yes, they are linked together in a haplotype (set of alleles across loci)
47
How are major histocompatibility complex inherited?
Inherited as a haplotype - little recombination
48
How are the 2 sets of major histocompatibility complex genes expressed?
Believed to be co-dominant
49
What are possibilities for different individuals?
Heterozygous or homozygous
50
What does MHC genes means for host variation?
Results in lots of MHC molecules with slightly different structure on each cell
51
What is Peptide Binding Region (PBR)?
PBR are key area of MHC loci
52
How does PBR change per molecule?
Different amino acids at the PBR - result in different binding properties
53
Are PBR limit to only complementary binding?
Potentially promiscuous binding
54
What are examples of MHC allele pathogen associations in Humans?
Malaria HIV progression
55
What are examples of MHC allele pathogen associations in other animals?
Sheep and nemotodes Chickens and merek disease Chickens and avian flu Passerines and avian malaria
56
How many alleles are there of the HLA-B gene?
499 alleles
57
How does natural selection promote variation in the MHC?
Maintains genetic polymorphism across individuals within a population
58
How can you detect evidence for historical balancing selection?
Ratio of non-synonymous (amino acid altering) to synonymous (silent) substitutions in the DNA dN:dS
59
What happens if the dN:dS ratio is greater than 1?
Postive selection
60
What happens if the dN:dS ratio is less than 1?
Negative selection
61
What happens if the dN:dS ratio is equal to 1?
Neutral
62
What is trans-species persistance of MHC alleles?
Related of MHC genes across species
63
What is an example of trans-species persistance?
At MHC loci, chimp alleles can be more closely related to human alleles than to other chimp alleles
64
What do the dN:dS ratios and trans-species persistance mean?
That the balancing selection has been operated for some time
65
What are the 3 main models for how balancing selection maintains variation?
Heterozygote advantage Rare allele advantage Fluctuating selection
66
What is the heterozygote advantage?
Heterozygote gentotypes have an advantage over homozygote ones
67
How does being heterozygous provide an advantage?
2 different alleles at a locus allow for: Detect more pathogen strains Better detection of any single pathogen strain
68
Why is heterozygous dominant?
More likely to contain the 'best' allele
69
Why are heterzygous overdominant?
Combination of alleles in Hz is better than both alleles alone
70
What evidence is there for heterozygous domiance?
Hz more resistant Over-representation of Hz gentotypes in a population ( deviation from Hardy-Weinberg expectations in adult popualtion and deviation from medelian proportions in offspring)
71
What is the rare allele advantage?
Relative fitness of an allele declines when the frequency of that allele is high
72
What is the advantage of having a new/rare MHC alleles?
Better able to detect pathogen variants that have evolves to evade common MHC alleles
73
How many generations does it take for allele frequency to decrease from 1% to 0.1%?
1000 generations
74
What is the theoritcal support for rare allele advantage?
Mechanistic models
75
Is there empirical eveidence for rare allele advantage?
Very hard to show as changes occur evolutionary time
76
How is rare allele advantage inferred?
Spatial variation in relationship between resistance to a specific pathogen and MHC alleles Changes in allele frequencies over time in a population Correlation between frequency of MHC allele and resistance
77
What is fluctuating selection?
Spatio-fluctuations in pathogens infecting host and thus selection This selects for different MHC alleles at different places at different times Host gene flow and temporal fluctuations - maintains MHC variation in metapopulation
78
What is the evidence fluctating selection for MHC?
Greater among subpopulations variations at MHC than at neutral markers Shows different selection acting in different places at different times
79
Which of the theories are most likely?
All three causing a positive reinforce
80
What are side benefits of MHC variation?
May help determine quantitive traits like size or secondary sexual characteristics Linked to individual fitness behaviour in natural populations
81
What is the romantic model?
Females prefer males with compatible MHC genes to their own which is determined by direct clues like smell
82
What is the Hotshot model?
Individual survival is partially determined by the MHC genes they carry, this is boosted by diversity and specific alleles
83
How is MHC-dependant mate choice seen in humans?
T-shirt tests Hutterite couples Dissimilar European american couples
84
How is MHC variation impacting Seychelles warbler?
Positive association between MHC diversity and juvenile survival Mean life span: less than 4 alleles = 1 year More than 4 alleles = 2.5 years
85
What pre-copulatory factors drive MHC-dependant fertilisation patterns?
MHC based mate choice MHC dependant male-male competition
86
What post-copulatory factors drive MHC-dependant fertilisation patterns?
MHC related selective fertilisation MHC dependant selective abortion MHC dependant mortality of eggs/embryos
87
Why is conservation important for MHC?
Individuals with greater MHC variations mean can combat wder range of pathogens Populations with greater MHC variations can identify an process larger number of antigens therefore combat larger number of pathogens

Sem 1: Parasite and pathogen ecology (11 decks)

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