Papillomaviruses and Polyomaviruses Flashcards

1
Q

Shope papillomavirus

A
  • First mammalian model of cancer caused by a virus
  • Dr. Richard E. Shope
  • Ex. possible source of myths about a jackalope (rapid with horns of an antelope)
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2
Q

Papillomaviruses and polyomaviruses properties

A
  • Naked, icosahedral virions, spherical in outline
  • dsDNA
  • replication in nucleus
  • most have not been cultured, but can TRANSFORM cultured cells
  • polyoma: transcribed from both strands
  • papilloma: transcribed from one strand
  • *may be oncogenic
  • Transmitted by contact
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3
Q

What is papillomaviruses distinguished based on?

A
  • Host range and DNA sequence relatedness
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4
Q

Properties of genomes

A
  • Similar to human PV
  • *generally have multiple genera and multiple serotypes that are species specific
    o Usually difficult to grow in vitro
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5
Q

How do papillomaviruses replicate?

A
  • Pathogens of epithelial cells
    o Tightly related to growth of epithelium
    o Outside of chromosome in basal layer
    o As cell matures the virus matures as well
  • Infects dermal layer and EARLY gene expression can be detected
  • Late gene expression of structural proteins and vegetative DNA synthesis is restricted to TERMINALLY DIFFERENTIATED CELLS OF EPIDERMIS
  • **link between cellular differentiation and viral gene expression
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6
Q

Papillomavirus replication highlights

A
  • Binds proteoglycan and enters through receptor-mediated endocytosis
  • Expression of genome is complicated (3 reasons)
  • *only 1 strand of genome is transcribed
  • 2 classes of proteins produced
  • Virions assembled in nucleus, release on death of cell often as a consequence of cellular replacement
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7
Q

What are the reasons why the expression of papillomavirus genome is complex?

A
  • Multiple promoters
  • Alternative splicing patterns
  • Link between differentiation and gene expression
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8
Q

What are the 2 classes of proteins produced in papillomavirus replication?

A
  • Early: non-structural regulatory proteins (trans-acting transcriptional regulators)
  • Late: structural
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9
Q

Canine papillomatosis

A
  • Caused by at least 16 canine PV in 3 different genera
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10
Q

What is the most common papillomavirus-induced disease (primarily by CPV-1) in dogs?

A
  • Oral papilloma’s
    o Typically start on lips
    o Spread to buccal mucosa, tongue, palate, pharynx
    o Develop 4-8 week AFTER INFECTION
    o *most regress within 8 weeks
    o Extensive ones require intervention
  • *clinical diagnosis
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11
Q

What does CPV-2 and CPV-6 cause?

A
  • Cutaneous papilloma’s=’warts’
    o Most common on FEET of young dogs
    o Can developed in nailbed epithelium
     Cause distortion of claw
     Destruction of bone
  • *Skin trauma and immunosuppression predispose to wart development
  • *clinical diagnosis
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12
Q

Why do the warts go away?

A
  • If squeeze a wart=expose virus to immune system=promote a better immune response
    *people will NOT get warts from their dog: species specific!
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13
Q

If a dog has an unusual skin lesion, what should you think?

A
  • Papillomavirus: more than just regular warts
  • *specific staining shows extent of DNA: see it throughout
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14
Q

Equine papillomatosis consists of

A
  • Warts: EpPV-1 (regress after 1-9 months)
  • Aural plagues: EqPV-2 (association with squamous cell carncinoma?)
  • Genital papilloma’s: EqPV-2
  • **clinical diagnosis
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15
Q

How is equine papilloma virus transmitted?

A
  • Contaminated fomites (halters, etc), rubbing posts
  • Direct contact
    o Sexual transmission NOT required for genital papillomas
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16
Q

Bovine papillomatosis

A
  • *most commonly affected domestic species
  • 2 subtypes of papilloma’s (often multiple types in same lesions and normal skin)
  • Associated with neoplasia
    o Bladder cancer (BPV-2)
    o Upper alimentary tract (BPV-4)
  • More common in HOUSED vs. pasture
  • Hyperplasia and degeneration begin about 4-6 weeks
  • Resolved in 4-6 months: self-limiting
17
Q

What are the 2 subtypes of papillomas with bovine papillomatosis?

A
  • Squamous: BPV-4
    o Caudal oral cavity, esophagus, rumen
    o Flat with broad base
  • Fibropapillomas: BPV-1, 2, 5
    o Head, neck, teats, udder, shoulders
    o Small nodules to cauliflower-like growths
18
Q

How is bovine PV transmitted?

A
  • Contaminated fomites (halters, etc.), rubbing posts, direct contact, abrasions
19
Q

Vaccines for bovine papillomatosis?

A
  • vaccines have been tried: doesn’t make sense to use in MANY animals
    o not a single serotype, if not all in vaccine=not great protection
  • *they work, but no cross protection!
20
Q

What does bovine PV cause in horses?

A
  • Equine (and feline) sarcoids: BPV-1 and BPV-2
    o Classified based on appearance
    o Clinical diagnosis
    o Variable success of therapy
21
Q

HPV and cervical cancer

A
  • Showed virus in lesions
  • *big deal!
22
Q

Transformation of papillomaviruses to cause cancer

A
  • Complex
  • Depends on EARLY GENE PRODUCTS
    o At least 2 early proteins cooperate to give a transforming phenotype
  • *some ‘transforming genes’ maintained in tumour, but other times the virus DNA is lost after transformation (‘hit and run’ mechanism)
23
Q

HPV serotype-specific vaccines

A
  • Multiple ones with various serotypes (ex. 9 serotypes)
  • *serotype makes all the difference in the world
    o If don’t include relevant serotype=wont get a response against them (enough of a difference between them!)
  • *first example of needing a specific serotype
24
Q

What are the properties of polyomaviruses?

A
  • Infect wide variety of vertebrates
  • Solid tumors at many sites
  • *lytic and non-lytic pathway
25
Q

Lytic pathway of polyomaviruses

A
  • In permissive cells leading to production of virus particles, INTRANUCELAR INCLUSIONS and cell death
26
Q

Non-lytic pathway of polyomaviruses

A
  • In non-permissive cells which leads to TRANSFORMATION
27
Q

What is Budgerigar Fledgling disease?

A
  • Polyoma viral disease affecting ALL PSITTACINES
  • Leading cause of young birds
  • Birds that survive will have abnormal feathers (DDx for PBFD)
  • Incubation: 7-14days
  • *in non-budgerigar psittacine birds=peractue death with non signs
  • *’french moult’ (loss of tail feathers)
28
Q

How is the virus passed in Budgerigar Fledgling disease?

A
  • Feces
  • Urates
  • Feather dander
  • Regurgitated fluids
  • **Can remain and infect birds for 2-12 months=HIGHLY CONTAGIOUS
29
Q

Budgerigar Fledgling disease: clinical signs

A
  • *Multisystemic disease
  • Depression
  • Delayed crop emptying
  • Regurgitation in baby birds
  • Diarrhea and/or polyuria
  • Bright yellow urine with strings of mucus and urates
  • Bleeding under skin
  • Abnormal feathering in fledgling birds
  • Sudden death
30
Q

Budgerigar Fledgling disease: diagnosis

A
  1. Blood tests to detect viral DNA particles in blood (indicates exposure)
  2. Fecal/urate swab to detect viral DNA in excrement (indicts virus present)
  3. In situ hybridization on tissue
31
Q

Budgerigar Fledgling disease: prevention

A
  • Vaccination
  • Do not sell, ship or accept unweaned, non-vaccinated baby birds
  • Use biosecurity shipping containers
  • Maintain a closed airway
  • Use separate feeding utensil for each clutch of baby birds
  • Limit exposure of your birds to non-vaccinated birds