Lecture 19 Evolution and human health
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1 Lecture 19 Evolution and human health
2 The evolution of flu viruses
3 The evolution of flu viruses Google Flu Trends data US data Check out:
4 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution.
5 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution. host-pathogen coevolution is also referred to as an evolutionary arms race.
6 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution. host-pathogen coevolution is also referred to as an evolutionary arms race. Adaptation Host Pathogen Counter Adaptation
7 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution. host-pathogen coevolution is also referred to as an evolutionary arms race. Example: the influenza A virus
8 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution. host-pathogen coevolution is also referred to as an evolutionary arms race. Example: the influenza A virus influenza A is a retrovirus with 11 genes (on 8 RNA strands).
9 The evolution of flu viruses the evolution of viruses and their hosts is a form of antagonistic coevolution. host-pathogen coevolution is also referred to as an evolutionary arms race. Example: the influenza A virus influenza A is a retrovirus with 11 genes (on 8 RNA strands). responsible for annual flu epidemics (killing about 30,000 to 35,000 Americans per year).
10 Influenza A virus also causes serious global pandemics:
11 Influenza A virus also causes serious global pandemics: Year Deaths in US Spanish flu ,000
12 Influenza A virus also causes serious global pandemics: Year Deaths in US Spanish flu ,000 Asian flu ,000
13 Influenza A virus also causes serious global pandemics: Year Deaths in US Spanish flu ,000 Asian flu ,000 Hong Kong flu ,000
14 The influenza A virus N H
15 The influenza A virus N H
16 The evolution of antigenic sites
17 The evolution of antigenic sites influenza A s major coat protein is hemagglutinin.
18 The evolution of antigenic sites influenza A s major coat protein is hemagglutinin. hemagglutinin is the main target of our immune system.
19 The evolution of antigenic sites influenza A s major coat protein is hemagglutinin. hemagglutinin is the main target of our immune system. amino acid sites in hemagglutinin that our immune system recognizes (and remembers) are called antigenic sites.
20 Locations of antigenic sites in hemagglutinin molecule
21 Phylogenetic analysis of influenza A
22 Phylogenetic analysis of influenza A Fitch et al. (1991) examined the phylogenetic relationships among flu strains over a 20-year period using hemagglutinin sequences.
23 Phylogenetic analysis of influenza A Fitch et al. (1991) examined the phylogenetic relationships among flu strains over a 20-year period using hemagglutinin sequences. this is equivalent to 20 million years of human evolution!
24 Hemagglutinin evolved at a constant rate!
25 Hemagglutinin evolved at a constant rate! Is this neutral evolution?
26 Hemagglutinin evolved at a constant rate! Is this neutral evolution? NOT LIKELY!
27 Annual flu epidemics arise from a single lineage!
28 Why did only a single flu strain persist?
29 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites?
30 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites? Surviving Extinct lineage lineages
31 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites? Surviving Extinct lineage lineages antigenic sites 33 31
32 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites? Surviving Extinct lineage lineages antigenic sites non-antigenic sites 10 35
33 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites? Surviving Extinct lineage lineages antigenic sites non-antigenic sites
34 Why did only a single flu strain persist? due to differences in mutations at antigenic vs. nonantigenic sites? Surviving Extinct lineage lineages antigenic sites non-antigenic sites Conclusion: The surviving lineage had significantly more mutations at antigenic sites
35 Positive selection in the hemagglutinin gene
36 Positive selection in the hemagglutinin gene positive selection occurs when the rate of replacement substitution exceeds the rate of silent substitution.
37 Positive selection in the hemagglutinin gene positive selection occurs when the rate of replacement substitution exceeds the rate of silent substitution. in influenza A, there are 18 codons exhibiting higher rates of replacement substitution!
38 Positive selection in the hemagglutinin gene positive selection occurs when the rate of replacement substitution exceeds the rate of silent substitution. in influenza A, there are 18 codons exhibiting higher rates of replacement substitution! why is this important?
39 Positive selection in the hemagglutinin gene positive selection occurs when the rate of replacement substitution exceeds the rate of silent substitution. in influenza A, there are 18 codons exhibiting higher rates of replacement substitution! why is this important? because this allows us to predict surviving strains and thus make flu vaccines!
40 Strains that persist have the most changes in hemagglutinin antigenic sites
41 * * * A phylogeny of influenza A based on the nucleoprotein gene * * * * * * * *
42 Influenza A can move between humans, birds, and pigs
43 Where did H3 come from?
44 H3 jumped into humans from birds
45 Influenza A can move between humans, birds and pigs
46 The origin of pandemic flu strains Human strain Bird strain Recombination in swine host Reinfect human host
47 H1N1 is a triple-reassortment virus
48 H1N1 is a triple-reassortment virus Segment Origin PB2 Avian North America PB1 Human circa 1993 PA Swine Eurasia HA Swine North America NP Swine Eurasia NA Swine Eurasia MP Swine Eurasia NS Swine Eurasia
49 The evolution of virulence
50 The evolution of virulence virulence is a term that describes the effect a pathogen has on its host.
51 The evolution of virulence virulence is a term that describes the effect a pathogen has on its host. high virulence major effect on host s fitness
52 The evolution of virulence virulence is a term that describes the effect a pathogen has on its host. high virulence major effect on host s fitness low virulence minor effect on its host s fitness
53 The evolution of virulence virulence is a term that describes the effect a pathogen has on its host. high virulence major effect on host s fitness low virulence minor effect on its host s fitness Example: rabbits and the myxoma virus in Australia
54 The evolution of virulence Example: rabbits and the myxoma virus in Australia
55 The evolution of virulence Example: rabbits and the myxoma virus in Australia in 1859, 12 rabbits were bought by Mr. Thomas Austin.
56 The evolution of virulence Example: rabbits and the myxoma virus in Australia in 1859, 12 rabbits were bought by Mr. Thomas Austin. 6 years later, there were 30,000!
57 The evolution of virulence Example: rabbits and the myxoma virus in Australia in 1859, 12 rabbits were bought by Mr. Thomas Austin. 6 years later, there were 30,000! they escaped from his farm and exploded in abundance all over the country.
58 The evolution of virulence Example: rabbits and the myxoma virus in Australia in 1859, 12 rabbits were bought by Mr. Thomas Austin. 6 years later, there were 30,000! they escaped from his farm and exploded in abundance all over the country. the myxoma virus was introduced in the 1950 s to control the rabbit population.
59 The evolution of virulence Example: rabbits and the myxoma virus in Australia Virulence grade high low I II IIIa IIIb IV V
60 The evolution of virulence Example: rabbits and the myxoma virus in Australia Virulence grade high low I II IIIa IIIb IV V
61 The evolution of virulence Example: rabbits and the myxoma virus in Australia Virulence grade high low I II IIIa IIIb IV V
62 The evolution of virulence virulence is a term that describes the effect a pathogen has on its host. high virulence major effect on host s fitness low virulence minor effect on its host s fitness three models have been proposed to account for the evolution of virulence.
63 1. The coincidental evolution hypothesis
64 1. The coincidental evolution hypothesis the virulence of many human pathogens is a result of selection acting on that pathogen in a different environment.
65 1. The coincidental evolution hypothesis the virulence of many human pathogens is a result of selection acting on that pathogen in a different environment. Example: tetanus
66 1. The coincidental evolution hypothesis the virulence of many human pathogens is a result of selection acting on that pathogen in a different environment. Example: tetanus caused by a soil bacteria Clostridium tetani.
67 1. The coincidental evolution hypothesis the virulence of many human pathogens is a result of selection acting on that pathogen in a different environment. Example: tetanus caused by a soil bacteria Clostridium tetani. produces a deadly toxin not directed at humans but at something in the soil.
68 2. The short-sighted evolution hypothesis
69 2. The short-sighted evolution hypothesis since pathogens reproduce within hosts, traits that increase their short-term fitness may actually be detrimental.
70 2. The short-sighted evolution hypothesis since pathogens reproduce within hosts, traits that increase their short-term fitness may actually be detrimental. the virus is short-sighted and virulence higher than expected.
71 2. The short-sighted evolution hypothesis since pathogens reproduce within hosts, traits that increase their short-term fitness may actually be detrimental. the virus is short-sighted and virulence higher than expected. Example: poliovirus.
72 2. The short-sighted evolution hypothesis since pathogens reproduce within hosts, traits that increase their short-term fitness may actually be detrimental. the virus is short-sighted and virulence higher than expected. Example: poliovirus. normally infects cells that line the digestive tract and cause few symptoms.
73 2. The short-sighted evolution hypothesis since pathogens reproduce within hosts, traits that increase their short-term fitness may actually be detrimental. the virus is short-sighted and virulence higher than expected. Example: poliovirus. normally infects cells that line the digestive tract and cause few symptoms. occasionally, the virus infects cells of the nervous system with tragic consequences.
74 3. The trade-off hypothesis
75 3. The trade-off hypothesis pathogens should evolve to the point where fitness costs to the host are balanced by its capacity to propagate itself to other hosts.
76 3. The trade-off hypothesis pathogens should evolve to the point where fitness costs to the host are balanced by its capacity to propagate itself to other hosts. pathogens may thus evolve to where they harm their hosts considerably.
77 3. The trade-off hypothesis pathogens should evolve to the point where fitness costs to the host are balanced by its capacity to propagate itself to other hosts. pathogens may thus evolve to where they harm their hosts considerably. An experiment: E. coli and the phage f1 by Messenger et al. (1999).
78 3. The trade-off hypothesis pathogens should evolve to the point where fitness costs to the host are balanced by its capacity to propagate itself to other hosts. pathogens may thus evolve to where they harm their hosts considerably. An experiment: E. coli and the phage f1 by Messenger et al. (1999). phage f1 can propagate both vertically (parent to daughter cell) and horizontally (to a new host).
79 Treatment 1: 8 day vertical () + brief horizontal ()
80 Treatment 1: 8 day vertical () + brief horizontal () Treatment 2: 1 day vertical () + brief horizontal ()
81 Treatment 1: 8 day vertical () + brief horizontal () Treatment 2: 1 day vertical () + brief horizontal () After 24 days measured:
82 Treatment 1: 8 day vertical () + brief horizontal () Treatment 2: 1 day vertical () + brief horizontal () After 24 days measured: 1. Phage virulence (growth rate of infected hosts).
83 Treatment 1: 8 day vertical () + brief horizontal () Treatment 2: 1 day vertical () + brief horizontal () After 24 days measured: 1. Phage virulence (growth rate of infected hosts). 2. Phage growth rate (rate of virion secretion from infected hosts).
84 Trade-off between virulence and reproductive rate in phage f1
85 What factors can select for increased virulence?
86 What factors can select for increased virulence? 1. Live host not needed for transmission
87 What factors can select for increased virulence? 1. Live host not needed for transmission Examples: ebola virus, parasitic fungi
88 What factors can select for increased virulence? 1. Live host not needed for transmission Example: ebola virus, parasitic fungi 2. Multiple infections in same host
89 What factors can select for increased virulence? 1. Live host not needed for transmission Example: ebola virus, parasitic fungi 2. Multiple infections in same host leads to competition among pathogens within hosts
90 What factors can select for increased virulence? 1. Live host not needed for transmission Example: ebola virus, parasitic fungi 2. Multiple infections in same host leads to competition among pathogens within hosts 3. Transmission is horizontal (i.e., from individual to individual), not vertical (i.e., parent to offspring)
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