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MIMM 324 > 36. Emerging Viruses > Flashcards

36. Emerging Viruses Flashcards

1
Q

what is an emerging virus?

A

causes new or previously unrecognized infection

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2
Q

5 examples of emerging virus

A
  1. 1918 influenza
  2. 2002 SARS
  3. 2009 swine flu (H1N1)
  4. 2014 chikungunya
  5. 2015 zika
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3
Q

how do emerging viruses expand their host range?

A
  1. secondary hosts or vector
  2. spillover
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4
Q

what is zoonosis?

A

transmission of virus from wild or domesticated animal to humans

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5
Q

what % of human emerging infectious viruses are zoonotic?

A

60-80%

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6
Q

example of virus that expanded host range by secondary host

A

rhabdovirus

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7
Q

example of virus that expanded host range by spillover

explain

A

Nipah virus –> natural host is bats but switch to other animals then humans

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8
Q

2 roles of evolution for emerging viruses

A
  1. mutations allow for biodiversity of pathogens in nature
  2. selection allows for pathogens to adapt to new hosts and environments
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9
Q

4 types of host-virus interactions

A
  1. stable
  2. evolving
  3. dead-end
  4. resistant
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10
Q

what is a STABLE host-virus interaction?

A

virus is maintained in the ecosystem –> both the host and virus populations survive and multiply

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11
Q

describe host and virus populations vs individual host and virus in STABLE host-virus interactions

does the population or individual matter in STABLE host-virus interaction?

A

virus population: more or less virulent
host population: develop mechanism to attenuate viral effects (more tolerant to infection, dampen immune response)

individual virus: can infect but may be cleared or establish infection
individual host: get infection and become sick

host and virus POPULATION that survives and multiplies is most importrant

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12
Q

when can stable host-virus interactions be permanent?

A

if there is only 1 host

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13
Q

4 examples where humans are the only host

A
  1. measles
  2. HSV
  3. HCMV
  4. smallpox
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14
Q

3 examples of viruses where stable host-virus interactions include infection of >1 species

A
  1. influenza A
  2. flavivirus
  3. togavirus
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15
Q

why are there are rarely influenza pandemics?

A

influenza maintains stable infections in their hosts so only get outbreaks rather than pandemics

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16
Q

what are EVOLVING host-virus infections?

A

virus transmits to naive populations

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17
Q

2 hallmarks of EVOLVING host-virus interactions?

A
  1. instability
  2. unpredictability
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18
Q

characteristic of pathogen in EVOLVING host-virus interaction

A

mutations select for increased spread or virulence in best environment

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19
Q

characteristic of host in EVOLVING host-virus interaction

A

reduced resistance to virus

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20
Q

outcome of EVOLVING host-virus interaction

A

range from benign to death

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21
Q

3 examples of EVOLVING host-virus interaction

A
  1. introduction of smallpox and measles to Indigenous peoples by colonizers
  2. introduction of west nile virus to western hemisphere
  3. introduction of pox virus to rid Australia of rabbits
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22
Q

what is a DEAD-END host-virus interaction?

A

transmission is 1-way to 1 individual of a species, does not spread within species

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23
Q

when do DEAD-END host-virus interactions occur?

A

frequent outcome of cross-species infection

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24
Q

how do DEAD-END host-virus interactions contribute to the spread of natural infection?

A

very little contribution to the spread of natural infection

25
Q

what is a RESISTANT host-virus infection?

A

host blocks infection completely –> host cells are not susceptible and body’s defenses are strong

26
Q

how common are DEAD-END host-virus interactions?

A

most human encounters with viruses are dead-end

27
Q

what is the relationship between the different host-virus interactions?

A

very dynamic –> can switch from one type of interaction to other

28
Q

based on host-virus interactions which viruses have the best chance at being emerging?

A

stable –> evolving

stable –> dead-end

29
Q

3 things that affect emerging infections

A
  1. introduction of virus into cell (role of the virus)
  2. establishment and dissemination (role of the host)
  3. cross-species transmission and emergence of endemic + pandemic (role of environment/behaviour)
30
Q

describe 3 ways that the introduction of the virus into cells affects emerging viruses

A
  1. genetic instability
  2. cell tropism
  3. immune evasion
31
Q

how does genetic instability affect emerging infections?

A

allows mutations for rapid evolution to adapt to the ever-changing environment (common for RNA viruses)

32
Q

how does cell tropism affect emerging infections? (3)

A
  1. cell receptors for virus entry
  2. ability to circumvent innate immune responses
  3. antigenic immunodominance
33
Q

4 factors in the establishment and dissemination of the virus in emerging infections

A
  1. access to susceptible and permissible cells
  2. population density and health
  3. genetic variation in hosts
  4. virus populations only endure in nature because of serial infections (chain of transmission)
34
Q

describe infection of SARS-CoV-2 vs Ebola virus

A

covid can transmit BEFORE symptoms onset whereas ebola can only transmit AFTER symptoms onset

35
Q

what are 6 factors in cross-species transmission and emergence of endemic+pandemic?

A
  1. air travel
  2. air conditioning
  3. blood transfusion
  4. long distance transport of livestock, birds
  5. deforestation
  6. hunting

etc.

36
Q

what is the key determinant of disease emergence?

A

environment / human activities

37
Q

how do coronaviruses make the species jump?

A

subtle changes (in spike protein for ex.) can alter the cell/tissue tropism, host range, and disease manifestation

38
Q

3 determinants for host-switching

A
  1. evolutionary closeness of donor and recipient
  2. viral quasispecies
  3. pathogen opportunities
39
Q

how do we determine the evolutionary closeness of the donor and recipient host?

A

look at fitness valleys

40
Q

what are fitness valleys?

A

reflect the adaptational barriers that need to be crossed

41
Q

steep vs shallow fitness valley

A

steep = many mutations must be made

shallow = fewer mutations must be made

42
Q

how do viruses overcome adaptational barriers? (3)

A
  1. point mutations
  2. recombinations
  3. reassortment
43
Q

what are viral quasispecies?

A

virus evolves as a diverse array of species with diff levels of fitness

44
Q

benefit of viral quasispecies

A

enhances adaptation flexibility

45
Q

how do pathogen opportunities help host-switching?

A

a virus poorly fit to a host can adapt to a new host if given enough chances

46
Q

how common is host-switching?

A

usually dead-end, very rare to produce sustained transmission

47
Q

can we predict host-switching?

A

no but we can possibly assess the viruses that are out there and be prepared

48
Q

5 ways for managing and surveilling emerging infections

A
  1. research and development in academia and industry
  2. early detection and identification technology
  3. database of viral genomes in ecosystem
  4. first responder actions + rapid communication
  5. public health action + widespread compliance
  6. surveillance and cooperation by governmental and international agencies
49
Q

what animal is a common source of zoonotic infection?

A

BATS

50
Q

describe the diversity of bats

A

bat species occupy 25% of mammal species

51
Q

what allows for the transmission of viruses from bats?

A

bats have wide geographical distribution

52
Q

how does flight affect bats as a virus host?

A

bats adapting to flight leads to dampening of inflammation

53
Q

how does hibernation affect bats as a virus host?

A

reduced body temperature and metabolic rate suppresses immune response and delays viral clearance

54
Q

5 things that happen to cause immune tolerance in bats

A
  1. STING-dependent type I IFN response was dampened via point mutation
  2. NLRP3 is dampened
  3. PYHIN gene family is lost
  4. reduced activation of inflammatory cytokines
  5. reduced inflammatory cell deaths
55
Q

what is STING?

A

PRR induced by cytosolic DNA

56
Q

what is NLRP3?

A

inflammasome sensor that recognizes cellular stresses and pathogen invasion

57
Q

2 examples of genes in the PYHIN gene family and their role

A

AIM2 and IFI16 which are inflammasome sensors for intracellular DNA

58
Q

inflammasome activation in human/mouse vs bats

A

human/mouse –> RNA viruses activate inflammasome to induce cell death and cytokine secretion

bat –> dampened PRR priming, therefore dampened inflammasome activation and reduced cytokine secretion

MIMM 324 (37 decks)

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