End of Chapter 6 Flashcards

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1
Q

Multiplication of Retroviridae

A

Reverse Transcriptase
RNA-dependent
DNA-polymerase
1. Retrovirus enters by fusion between attachment spikes and the host cell receptors
2. Uncoating releases the two viral RNA genomes and the viral enzymes reverse transcriptase, integrase, and protease
3. Reverse transcriptase copies viral RNA to produce double-stranded DNA
4. The new viral DNA is transported into the host cell’s nucleus, where it is integrated into a host cell chromosome as a provirus by viral integrase. The provirus may be replicated when the host cell replicates
5. Transcription of the provirus may also occur, producing RNA for new retrovirus genomes and RNA that encodes the retrovirus capsid, enzymes and envelope proteins
6. Viral proteins are processed by viral protease; some of the viral proteins are moved to the host plasma membrane
7. Mature retrovirus leaves host cell, acquiring an envelope and attachment spikes as it buds out

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2
Q

Damage to Host Cells

A

Cytopathic effects- CPE’s

  1. Changes in size and shape
  2. Cytoplasmic inclusion bodies
  3. Inclusion bodies
  4. Cells fuse to form multinucleated cells
  5. Cell lysis
  6. Alter DNA
  7. Transform cells into cancerous cells
    ex: Herpes simplex: cells fuse to form multinucleated syncytia
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3
Q

Prions

A

Proteinaceous infectious particles
-noncellular infectious agents (no nucleic acid)
-Abnormal version of a normal protein
>a prion can induce spontaneous abnormal folding in normal proteins (can happen if you had a mutation)
-extremely resistant to control methods
-Cause transmissible spongiform encephalopathies TSE’s:
>chronic degenerative fatal brain disease
>long latent period (several years) before symptoms appear
>loss of nerve and glial cells leads to sponge-like appearance of brain tissue
>patient loses motor coordination then sensory and cognitive abilities

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4
Q

Prions Cause Transmissible Spongiform Encephalopathies (TSE’s)

A
  • chronic degenerative fatal brain disease
  • long latent period (several years) before symptoms appear
  • loss of nerve and glial cells lead to sponge-like appearance of brain tissue
  • patient loses motor coordination then sensory and cognitive abilities
    ex: Mad Cow disease. chronic waste disease (CWD)
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5
Q

Prion Cycle

A
  1. Prion protein infects a nerve cell
  2. Upon contact with normal proteins, the prions are able to shift the configuration of the normal proteins, converting them to prions
  3. When this process creates large numbers of prions, they bind tightly together and form elongate chains
  4. As the chains build up, they form fibers within the cell, which interfere with the cell’s function and destroy it
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6
Q

Prion Diseases

A
  • Creutzfeldt-Jakob Disease (CJD)
  • Kuru
  • Fatal Familial Insomnia
  • Bovine Spongiform Encephalopathy (Mad Cow)
  • Scrapie (sheep)
  • Chronic Waste Disease (CWD), elk, deer, mink (not killed by cooking temperatures)
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7
Q

Other Noncellular Infectious Agents: Satellite Viruses

A

Dependent on other viruses for replication

  • Adeno-associated virus: replicates only in cells infected with adenovirus
  • Delta agent: naked strand of RNA expressed only in the presence of hepatitis B virus
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8
Q

Noncellular Infectious Agents: Satellite Viruses: Adeno-Associated Virus

A

replicates only in cells infected with adenovirus

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9
Q

Noncellular Infectious Agents: Satellite Viruses: Delta Agent

A

naked strand of RNA expressed only in the presence of hepatitis B virus

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10
Q

Other Noncellular Infectious Agents: Viroids

A

short pieces of RNA, no protein coat; only been identified in plants

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