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ISCI 350 > Arms Race > Flashcards

Arms Race Flashcards

1
Q

organism x environement

A

-> evolutionary change

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2
Q

components of an organism’s environment

A
  • abiotic

- biotic

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3
Q

abiotic components of an organism’s environment

A
  • temperature, humidity, water salinity, substrate colour, etc
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4
Q

biotic components of an organism’s environment (5)

A
  • predators
  • food/prey
  • competitors (same or other species)
  • partners (same or other species)
  • pathogens and parasites
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5
Q

what can biotic interactions lead to?

A
  • antagonistic coevolution/”arms races”
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6
Q

possible facets of a prey and predator relationship

A

better/faster:

  • hiding
  • mimicry, camo
  • running
  • size, strength
  • group hunting/defense
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7
Q

running adaptations (3)

A
  • running on toe tips
  • longer foot bones
  • tibia and fibula fusion
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8
Q

snail defence adaptation as prey

A
  • proportion of snail subfamilies with thickened shells and narrowed apertures has increase through time
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9
Q

what are the characteristics of pathogens and parasites? (4)

A
  • short life spans
  • huge population sizes
  • high mutation rates
  • these traits allow pathogens to evolve as much in a day as we can in 1000 years
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10
Q

how can humans combat the evolutionary mismatch with pathogens?

A
  • adaptive immunity
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11
Q

adaptive immune response (3)

A
  • immune cells recognize epitopes on the surface of pathogens to mount a highly specific response against that pathogen
  • jawed vertebrates only
  • presence of lymphocytes (WBC): B cells (antibodies) and T cells ( helper and killer cells)
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12
Q

how does adaptive immunity combat rapid evolution of pathogens? (3)

A
  • involves evolution by natural selection within the individual
  • clonal selection yields cell lines that recognize and attack specific pathogens
  • a memory is retained to guard against future infections by the same pathogen strains
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13
Q

how is variability generated in adaptive immune response?

A
  • gene rearrangement and somatic hypermutation produces a large primary repertoire of antibody-producing B cells
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14
Q

innate immunity (4)

A
  • all animals
  • skin/exoskeleton
  • phagocytosis by blood cells
  • antimicrobial peptides
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15
Q

T cells

A
  • cell-mediated response against intracellular pathogens
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16
Q

B cells (2)

A
  • antibody-mediated (humoral) response against extracellular pathogens and paracites
  • antigen + helper T cell simulation produces memory B cells and plasma cells (anitbodies)
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17
Q

adaptive immunity (3)

A
  • somatic (within individual) evolution by natural selection
  • individual protection against future infections by same strain of pathogen
  • specific response not inherited by offspring
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18
Q

antigenic variation (2)

A
  • continual switching of surface antigens through variable surface glycoproteins
  • how the african sleeping virus escapes immune system and kills the host
19
Q

how does influenza escape host defences (2)

A
  • antigenic drift: mutation + selection (several strains can infect same species)
  • antigenic shift: recombination (ability for virus to jump species)
20
Q

how does the SARS-CoV2 escape host defences? (3)

A
  • successful mutations increase transmissibility, evade immunity, or both
  • rapid expansion of delta variant in India
  • reduced sensitivity to neutralizing antibodies from sera following infection or vaccination
21
Q

history of pandemics (6)

A
  • spanish flu, bubonic plague, HIV, malaria, COVID-19
22
Q

problem of antibiotic resistance (4)

A
  • rapid bacterial evolution
  • horizontal transfer of resistance factors
  • cost of resistance can be compensated
  • expression controlled by regulatory genes (adaptive resistance)
23
Q

horizontal transfer of resistance factors (3)

A
  • conjugation: bacteria to bacteria
  • transduction: virus vector
  • transformation: from environment
24
Q

compensatory mutation

A
  • create “fitness valleys” that prevent pathogen from reverting to sensitive type in absence of the antibiotic
25
Q

fitness valleys and antibiotic resistance (4)

A

Relative fitness in the absence of the antibiotic

  1. wild type (sensitive) and uncompensated
  2. resistant and compensated
  3. resistant and uncompensated
  4. sensitive and compensated
26
Q

disease emergence and examples (4)

A
  • transfer of novel pathogens from animals to humans
  • influenza from birds and pigs
  • COVID-19 from bats
  • HIV fro other primates
27
Q

stages of pathogen emergence (5)

A
  1. agent in animal only (no human transmission)
  2. primary infection (only transmitted from animals)
  3. limited outbreak (from animals or few humans)
  4. long outbreak (from animals or many humans)
  5. exclusive human agent (only from humans)
28
Q

R0

A
  • mean # of secondary infections arising from one infected individual in a totally susceptible population (no interventions and all transmission routes considered)
29
Q

R0 < 1

A
  • emergence does not occur, likely a newly introduced strain
30
Q

R0 > 1

A
  • emergence occurs, most likely an evolved strain
31
Q

what is characteristic of diseases with higher R0 (2)

A
  • harder to control

- needs higher percentage of vaccination for herd immunity

32
Q

virulence (3)

A
  • reduction in lifetime reproductive success of host due to harm done by pathogen
  • % mortality due to pathogen
  • it is the outcome of host/pathogen coevolution
33
Q

what determines equilibrium levels of virulence in pathogens? (2)

A
  • mode of transmission

- opportunity for transmission

34
Q

vertical vs horizontal mode of transmission (2)

A
  • higher virulence in horizontal transmission because survival of host is less important
  • lower virulence in vertical transmission because host must survive to spread pathogen
35
Q

R0 formula

A

R0 = (betas)/(gammamuv)

36
Q

what is beta in the R0 formula

A
  • transmission rate: rate of contact between susceptible and infectious individuals x probability of transmission
37
Q

what is S in the R0 formula

A
  • density of susceptibles
38
Q

what is gamma in the R0 formula

A
  • rate at which an infected host clears the disease
39
Q

what is mu in the R0 formula

A
  • background mortality rate of host
40
Q

what is v in the R0 formula

A
  • mortality rate due to infection (virulence)
41
Q

how does parasite increase fitness and transmission?

A
  • increase transmission (increases beta)

- prolong the infection (decreases gamma or v)

42
Q

mode of transmission (2)

A
  • vertical vs horizontal

- direct vs vector driven

43
Q

opportunity for transmission (2)

A
  • host/vector: behaviour

- population structure and density

ISCI 350 (14 decks)

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