Transcript Evolution of sex

Evolution of virulence
Conventional wisdom
“Given enough time a state of peaceful coexistence
eventually becomes established between any host
and parasite.”
–Rene Dubos (1965)
“Disease usually represents the inconclusive
negotiation for symbiosis…a biological
misinterpretation of borders.” –Lewis Thomas (1972)
“The ideal of parasitism is actually commensalism”
-Paul D. Hoeprich (1989)
Pathogens have an evolutionary edge
• Rapid replication rate relative to host
• Many mechanisms of increasing genetic variability
• Sporulation and biofilms
– Long-term durability in the environment
Mechanisms of variation
Segmented genome with
recombining fragments
Variable repeats, e.g.
ATATATATATAT
Cassette switching
(Neisseria, trypanosomes)
Plasmids and viruses
“Competence” = picking up foreign DNA from environment
Parasite fitness is dependent upon
transmission to susceptible hosts
Why virulence evolves
• Correlation between replication rate of pathogen
and harm to host (presumed, poorly supported)
• Faster replication = better competition within
hosts
• Slower replication = better competition between
hosts??
– Is this an evolutionarily stable strategy (ESS?)
Survey of parasite strategies
• Direct transmission (host-to-host contact)
• Vectorborne (versus direct transmission)
– Malaria, dengue, sleeping sickness, etc etc
• Vertical transmission (versus horizontal)
– Lots of plant pathogens transmitted through seed
• “Sit and wait” (durable pathogens)
– Anthrax, baculoviruses
Survey of parasite strategies II
• Intracellular immune avoidance
– Mycobacterium tuberculosis and M. leprae
– Legionella
– Rickettssia pathogens (e.g typhus, Rocky Mtn spotted fever)
• Waterborne transmission
– Diarrheal pathogens
• Attendant-borne transmission
– Group B Strep, Staph (esp. MRSA), Serratia, Klebsiella
– Canine parvovirus
– Agricultural pathogens (Cadang-cadang, Ilarviruses)
Parasite fitness is dependent upon
transmission to susceptible hosts
Each of these strategies offer
distinct evolutionary predictions
Is the current host-pathogen relationship optimal
from the parasite’s perspective?
• Alternative hypotheses (sensu Ewald 1994):
 Restricted adaptation (insufficient time)
 Adaptive severity
• Mode of transmission
– Is host mobility critical for transmission or not?
Why virulence may increase when
hosts are dense
• (i) The extinction rate of virulent lineages may decline
because ‘herd immunity’ is less likely to reduce the pool
of susceptibles below a critical transmission threshold for
parasite maintenance (Fine 1993).
• (ii) High host density may reduce the dependence on
host mobility for transmission and permit greater host
exploitation (Ewald 1994; Lenski & May 1994).
• (iii) Virulent variants may gain a numerical advantage
during epidemic spread because of more frequent
transmission (Anderson 1991).
• (iv) Transmission during the early stage of an infection
may be enhanced.
Timing of transmission and the evolution of virulence of an
insect virus
• System: Lymantria dispar (gypsy moth) NPV
• Experimenters: 3 consecutive years of
Amherst College undergraduate honors students
• Treatments: Early versus Late Transmission
• Transmission simulated early versus late, 9 cycles of
transmission
Viruses transmitted early became more lethal
Percent larval morality
80
70
*
60
50
40
30
20
10
0
Early
Late
Gypchek
Viruses transmitted late were more productive
100
14.0 days
25.9 days
721.3mg
1946.6mg
Early
Late
10
12.2mg
14.5mg
1
0.1
5 days post-inoculation
Larval death or pupation
Time of Viral Harvest
Group selection and interparasite conflict
• Superinfection = two strains of the same pathogen
co-infecting and competing within the same host
• Between host competition = parasite populations
within different hosts will compete over the longer
term
– Parasites within hosts, while related, will still act selfishly
given sufficient genetic variance
• These two dynamics may play against each other in
an ecological “metapopulation” setting