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VET 413: Infectious Disease/Immunology > Virology III - Infection & Disease > Flashcards

Virology III - Infection & Disease Flashcards

1
Q

virulence

A

ability of a virus to cause disease (pathogenicity)

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2
Q

why do viruses cause disease

A

to optimize survival
- want the clinically sick animal to shed the virus

can also be an accidental by product of infection

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3
Q

what are the factors that determine virulence

A

host
virus
environment

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4
Q

what virus factors determine virulence

A
  • genome sequence
  • epigenetic factors
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5
Q

what host factors determine virulence

A
  • genome sequence
  • epigenetic factors
  • adaptive & innate response
  • receptor distribution
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6
Q

what does receptor distribution determine

A

viral tropism for specific hosts/sites/tissues

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7
Q

what is the iceberg of disease severity

A

assessment of most common virulence outcomes

  1. exposure w/o infection
  2. subclinical infection
  3. mild disease
  4. moderate disease
  5. severe disease
  6. death
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8
Q

what are the steps of host infection

A
  1. entry and replication into initial host cell types
  2. local or generalized spread in host
  3. shedding from host
  4. clearance from host
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9
Q

what are the routes of entry into a host

A
  • respiratory
  • alimentary
  • conjunctiva
  • skin
  • systemic (capillary)
  • scratch/bite
  • urogenital tract
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10
Q

what is required by the virus in order to spread locally or systemically

A

must evade host immune system and inflammatory responses/barriers

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11
Q

what is important for adequate shedding of the virus

A

virus must reach the correct site for shedding at a concentration high enough to ensure infection of the next host

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12
Q

what mediates clearance of a virus

A

adaptive immune response

may not be complete - can get intermittent shedding of chronic infections

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13
Q

local infections

A

route of virus entry = route of shedding

ex. respiratory pathogen that gets shed via the respiratory tract

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14
Q

systemic infections

A

route of virus entry = one route of shedding, but shedding also occurs at an additional site

ex. respiratory pathogen that gets shed via the respiratory and urogenital tract

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15
Q

what are the steps of viral spread

A
  1. virus crosses epithelium
  2. primary replication occurs inside macrophages OR free in blood
  3. travels to LN
  4. secondary replication occurs in LN
  5. virus travels in blood either cell-free or cell-associated
  6. causes viremia
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16
Q

why might a virus target dead end sites (ex. brain)

A

dead end sites = locations in the body where the virus is not able to shed

goal is to alter behavior to make shedding more likely

ex. rabies - shed in saliva but travels to the brain in order to increase biting behavior –> increases transmission in saliva

17
Q

what are the 5 mechanisms of invading the CNS

A
  1. neuromuscular junctions
  2. sensory neurons
  3. neurons in nasal epithelium
  4. leukocytes that enter BBB
  5. endothelium
18
Q

steps and example of NMJ invasion

A
  1. bite wound injects virus into muscle
  2. replicates in muscle cells
  3. crosses NMJ
  4. travels up motor neuron
  5. replicates in CNS cells
  6. infects salivary glands

ex. rabies - site of bite wound determines time required to show clinical signs

19
Q

steps and example of endothelial invasion

A
  1. virus in blood (viremia) infects endothelium
  2. crosses BBB
  3. replicates in CNS cells in brain and spinal cord

ex. WNV; may also use “Trojan horse” mechanism of hijacking WBCs

20
Q

what are the 4 ways that viruses can cause injury/disease

A
  1. cell injury (cytocidal)
  2. persistent, productive
  3. persistent, non-productive
  4. transformation
21
Q

cell injury/cytocidal

A
  • has cytopathic effects
  • causes inhibition of host protein, RNA, and DNA synthesis –> apoptosis
  • HAS production of infectious virus

cytopathic effects: lysis, apoptosis, necrosis, syncytia, cytoskeletal disruption, etc

22
Q

persistent, productive

A
  • NO cytopathic effects
  • tries to “hide” from the host cell
  • some loss of cell division/metabolic disturbance
  • HAS production of infectious virus
23
Q

persistent, non-productive

A
  • no loss of host cell functions
  • does NOT result in production of infectious virus

resumption of productive infection may be triggered by trauma

24
Q

transformation

A
  • alters cell morphology to produce tumors

oncogenic DNA virus: do NOT produce infectious virus

oncogenic retroviruses: DO produce infectious virus

25
Q

mechanism of GI injury

A
  1. infection of GI enterocytes
  2. lysis of enterocytes –> reduced absorptive surface –> diarrhea
  3. diarrhea causes loss of fluid and electrolytes
  4. causes clinical signs
26
Q

clinical signs of viral GI injury

A

dehydration, hemoconcentration, acidosis, hypoglycemia, electrolyte imbalances

27
Q

mechanisms of CNS injury

A
  1. systemic or nerve cell infection
  2. virus crosses BBB or BCSFB via neuroinvasion mechanisms
  3. infects neurons and glial cells
  4. causes inflammatory cell influx
  5. inflammation –> meningitis, encephalitis, myelitis
  6. causes clinical signs (neurologic dysfunction)
28
Q

what are persistent viral infections

A

viral shedding can begin before, during, or after clinical signs appear

infectiousness increases and decreases with intermittent viral shedding

VET 413: Infectious Disease/Immunology (38 decks)

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