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Micro 3010 > Unit 8 - Prions > Flashcards

Unit 8 - Prions Flashcards

1
Q

What are prions?

A

Protineacous infectious particle that lacks nucleic acid

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2
Q

How are prions different from classical pathogens?

A

They have nucleic acid genomes, where prions lack nucleic acid

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3
Q

Give an example of a disease caused by prions in cattle

A

mad cow disease (bovine spongiform encephalopathy)

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4
Q

Give an example of a disease caused by prions in sheep

A

Scrapie

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5
Q

Give an example of a disease caused by prions in elk

A

Chronic wasting disease

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6
Q

Give an example of a disease caused by prions in humans

A

Kuru, Creutzfeldt-Jakob disease

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7
Q

Describe the pathology of prions

A

Large vacuoles in CNS, motor disturbances

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8
Q

Prions cause ____ disease

A

slow

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9
Q

_____ years between infection and symptoms

A

1-35

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10
Q

______ kDA host-encoded glycoprotein

A

30-35

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11
Q

PrP stands for?

A

Prion Protein

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12
Q

Normal cells express PrPc at the ____ _______ as linear proteins

A

cell membrane

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13
Q

PrPSc exists as a _____ ______ _________

A

free globular glycoprotein

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14
Q

PrPSc can interact with ____

A

PrPc

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15
Q

PrPc is released from the ___ _______

A

cell membrane

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16
Q

PrPc is released from the cell membrane and is converted into ____

A

PrPSc

17
Q

Cells then produce more ____ and the cycle is repeated

A

PrPc

18
Q

PrPSc accumulates as ____ and is internalized by cells

A

plaques

19
Q

What is the misfolded protein in TSE?

A

PrPSc

20
Q

What is the misfolded protein in AA amyloidosis?

A

SAA

21
Q

What is the misfolded protein in Alzheimers; cerebral B-amyloidosis?

A

AB

22
Q

What is the misfolded protein in Parkinsons’?

A

alpha-synuclein (Lewy bodies)

23
Q

What is the misfolded protein in Alzheimer’s; tauopathies?

A

Tau

24
Q

What is the misfolded protein in ALS?

A

SOD 1

25
Q

What is the misfolded protein in Huntington’s?

A

Huntington, polyQ expansions

26
Q

In what 2 ways is there development and transmission of prion disease?

A

1) Mutations in codon 129 of PrPc in chromosome 20

2) Exposure to infective agent (more common)

27
Q

Describe “Mutations in codon 129 of PrPc in chromosome 20”

A

-CJD and two other human diseases: Gertsmann-Straussler-Scheinker syndrome and fatal familial insomnia

28
Q

Describe “Exposure to infective agent (more common)”

A
  • Contaminated food (eating infected cow meat uncooked)
  • Contaminated medical products (blood, transplants)
  • Contaminated surgical instruments (strong binding to metal surfaces)
  • Mother-fetus transmission? (Animals can for sure have mother-fetus transmission, there has only been one recorded case in humans of mother-fetus transmission)
29
Q

How are prions shed?

A
  • skin
  • feces
  • urine
  • milk
  • nasal secretions
  • saliva
  • placenta (still an investigated theory)
30
Q

How can scrapie in sheep/goats be spread to humans?

A

Not spread directly!

  • spreads to cattle first
  • then a few cases have resulted in CJD in humans
31
Q

How is kuru in humans spread?

A

cannibalism

32
Q

What causes conversion of protein into the pathogenic form?

A

Mutations at amino acid residue 129 of the prion protein.

33
Q

Describe diagnosis and treatment of prion infections

A
  • Difficult
  • No culturing, serology
  • No inflammation
  • Tonsillar tissue, good source of PrPSc
  • No treatment to date right now, experimental studies in rodents, polyanionic and tricyclic compounds

*Not a virus, not a bacterium, not a fungi - cannot culture and study these

34
Q

Give a brief summary of prions

A
  • Unusual infectious agents
  • Host-derived glycoproteins, lack nucleic acid genome
  • Resistant to disinfection procedures
  • Transmission: Ingestion or Latrogenic
35
Q

List & Define the two types of transmission of prions

A

1) Ingestion: eating infected foods

2) Latrogenic: infection from medical procedures

Micro 3010 (20 decks)

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