Lecture 3: General Virology 3 Flashcards

(32 cards)

1
Q

Define vial transmisson

A

Virus Transmission: passing of viral infection between hosts (ether naive or susceptible)

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2
Q

Describe the transmission between species of influenza virus

A
  • Bird reservoir with minimal clinic signs
  • Infect domestic poultry and swine from wild birds
  • Infect people from domestic poultry and swine
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3
Q

What is the most important influenza virus type

A
  • Type A is the most important because it infects the most number of species
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4
Q

what are 2 types of transmission

A

vertical
horizontal

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5
Q

What are the mechanisms of vertical transmission? Add examples of diseases and consequences of infection

A
  • Vertical: parent to offspring
    o in utereo: BVDV/Blue tongue/feline parvo
    o birth: canine herpes
    o After birth/milk: CAE/Meadi-visna
    o Causing abortion (PRRS)/congential dz (BVDV/border dz)/congenital defects (akabana virus/blue tongue/feline parvo)
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6
Q

What are horizontal transmission mechanisms

A
  • Horizontal: Between individuals in a population
    o Direct:
    o Indirect:
    o Aerosols:
    o Arthropods:
    o Iatrogenic:
    o Nosocomial:
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7
Q

What are mechanisms of direct viral transmission + examples

A

o Direct: lick/rub/bite (rabies)/ sexual contact (herpes)/abrasions (papilloma)
o Indirect: iatrogenic/fomite

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8
Q

What are mechanisms of aerosol viral transmission + examples

A

o Aerosols: smaller particles travel farther (Marek’s dz)

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9
Q

What are mechanisms of arthropod viral transmission + examples

A

o Arthropods: mosquito (equine encephalitis)/ticks (African swine fever)/culicoides (blue tongue dz)

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10
Q

What are mechanisms of iatrogenic viral transmission + examples

A

o Iatrogenic: non-sterile/poor hygiene (equine infectious anemia/bovine leukemia)

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11
Q

What are mechanisms of nosocomial viral transmission + examples

A

o Nosocomial: canine parvo/calci virus

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12
Q

How is equine encephalitis virus transmitted

A

o Ex. equine encephalitis: equine/humans are dead end hosts – virus cycles between birds and mosquitoes

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13
Q

How is bovine leukemia virus controlled

A

o Ex. bovine leukemia controlled by good hygiene – milk pasteurization/reduce flies/disinfect equipment

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14
Q

Compare features of low and high stability viruses in the environment (with examples)

A
  • Low environmental stability: respiratory transmission, enveloped
    o Except Marek’s dz (wrapped in keratin)
  • High environmental stability: fecal-oral, non-enveloped (adeno/circo viruses)
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15
Q

Compare the stability of viruses in a clinical vs subclinical infection

A
  • Clinical infection = more productive
  • Subclinical infection = better used for dissemination
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16
Q

What are the strategies are used to impact viral survival/stability

A
  • Factors: maintenance of serial infections
    o Acute/self limiting: Transmission affected by population size
    o Persistent infection
    o Vector maintenance
17
Q

What are the features of transmission of a virus that causes acute/self limiting dz (+examples)

A

o Acute/self limiting: Transmission affected by population size
 Virus disappear with recovery + high load during dz
 Require consistent supply of hosts
 Ex. influenza/rota viral diarrhea/infectious bursal dz

18
Q

What are the 3 features of transmission of a virus that causes persistent dz (+examples)

A

 Persistent: clinical dz after years of subclinical shedding (BVDV)
 Chronic: similar to acute initially (high viral shedding) + low level shedding for years after (foot and mouth/feline calcivirus)
 Latent: intermittent shedding without clinical consequence (herpes)
* +/- clinical signs during re-activation
* Cannot detect infection in latent period (no viral protein prod.)

19
Q

What type of strategy does bovine herpes virus use to maintain infection/transmission

A
  • Ex. BVH-1 (bovine herpes) replicated in nasal mucosa – latent in trigeminal ganglia/t cells in tonsils -> stress/low immunity re-activates to create productive infection in primary replication sites
20
Q

What are 3 factors that affect how emerging viral dz develop

A
  • Host: must overcome host defences
  • Environmental change: ecological or human (translocation of virus/vector)
  • Viral determinants: evolution with short generation time/high mutation rate
21
Q

What are some mechanisms viruses evolve slowly/gradually

A

o Variants depend on selective pressure – vary in virulence/tropism
o Antigenic drift: DNA virus (except Pox) use cell proofreading – RNA virus don’t = mutate more
o Higher mutation size = lower genome size
o Quasi species: small variations in virus due to mutation

22
Q

What are some mechanisms viruses uses to evolve quickly

A

o Recombination;
o Reassortment:

23
Q

How do viruses change via recombination + an example

A

o Recombination; 2 viral genomes combine – require co-infection
 Ex. sinbis-like virus + eastern equine encephalitis = western equine encephalitis
 Single stranded RNA or DNA viruses

24
Q

How do viruses change via reassortment + examples

A

o Reassortment: exchange segments of genome
 2 segments: arena/birna
 3 segments: bunyaviridae
 6-8 segments: orthomyzoviridae
 12 segments: Reoviridae

25
What is the mechanism influenza uses to evolve
 Influenza A: can do triple reassortment (swine + human + avian = NA swine flu, + euro-asian swine flue = H1N1 ) * HA binds sialic acid receptors on host * Avian = highest affinity for 2-3 sialic receptors in gut/lung * Human = affinity for 2-6 sialic receptors in airway * Quail and pig type viruses have both types of receptors * Receptor types/affinities can change due to reassortment and antigenic shift (quail/pig) * Quails and pigs act at ‘mixing pot’ for reassortment – because both types of viruses can enter one cell * Infected cell will produce both initially infecting viruses + new reassorted virus
26
Briefly explain the genetic interaction you can expect if a quail is infected with human adapted H1N1 and avian adapted H6N2 influenza A viruses. (3 marks)
mark 1:Quail have a2-3 and a2-6 (human and avian) receptors for influenza. mark 2: If they infect the same cell, reassortment can occur. mark 3: If reassortment occurs there will be a novel progeny that is different from the initially infecting parent viruses.
27
Which animal species can act as a mixing vessel for influenza virus reassortment A Cattle B Chicken C Swine D Felines E Bovines
C
28
During latency of herpes virus infection, you may observe A Virus replication B Viral protein synthesis C Mild clinical signs D Severe clinical signs E No virus shedding
E
29
Can a virus replicate in a target cell with nonfunctional ribosomes? Briefly explain your answer. (2 marks)
No. Viruses rely on host cell machinery to produce viral proteins. Without ribosomes no protein production can occur.
30
What are the consequences (at least 2 points) of mutation in viral genome? (2 marks)
mark 1: A mutation may lead to a new biological variant that mark 2: The tropism may change. Resulting in the colonization of different host or organs. mark 3: A change in virulence may occur. It can increase or decrease mark 4: The virus may be non-viable.
31
What is meant by 'vertical transmission'? How is this different from 'horizontal transmission? (2 marks)
Vertical transmission occurs between mother and offspring. It can occur trans-placentally, during birth, or via milk. Horizontal transmission occurs between individuals in the population at risk. It can be direct or indirectly transmitted for example via airborne aerosols, consumption of milk/meat, nosocomial.
32
What are the 3 types of 'emerging' viral dz
Types: * Newly recognized * Newly evolved * Increased incidence