9. Lecture Flashcards

1
Q

what is a virus environment

A
  • another virus
  • host cell
  • host organism
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2
Q

when does interaction btw viruses occur

A

Only during multiplication (vegetative virus)

Simultaneous infection of the same cell

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3
Q

virus interaction can occur btw. which types of viruses

A

― usually related viruses, but not always

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4
Q

types of virus interaction

A
  • Advantageous
  • Disadvantageous (interference)
  • Neutral (virusexaltation)
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5
Q

Advantageous interaction

A

on nucleic acid level (recombination)

on protein level (complementation, phenotype mixing)

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6
Q

• Disadvantageous interaction

A

interference

One virus inhibits the multiplication of the other

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7
Q

recombination

A

•Exchange of genetic information
→ new virus generation – inherited new properties
At least 20-40 nucleotide homology between the viruses is needed

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8
Q

Intramolecular recombination occurance:

A
  • derailing of the polymerase during replication
  • Aujeszky’s disease virus: even 70% transfer
  • sometimes between non-related viruses (Polyoma – Adenovirus)
  • also with RNA viruses (i.e. FMDV)
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9
Q

•Genetic reassortment definition

A

• Viruses with segmented genome (ie. Orthomyxoviridae)
• Exchange of segments during viral assembly
• Sudden, major antigenic changes
→ antigenic shift

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10
Q

Reactivation types

A

Cross-reactivation
Multiple reactivation

latent cell -> lytic stage (replication)

→ Do not use different live vaccines within a short time interval!

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11
Q

•Cross-reactivation

  • btw who, example
  • how
A
  • Attenuated vaccine strain + related virus
  • Repair of the defected virulence-genes
  • i.e. herpesviruses
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12
Q

•Multiple reactivation

  • btw who, example
  • how
A
  • Between two attenuated virus-strains
  • Different defected genomic regions
  • Mutual completion
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13
Q

Complementation

A

• Between defective and competent (helper) viruses
• Exchange of enzymes (mainly polymerase)
→ multiplication of the defected virus
• heat-sensitive mutant + wild type virus
• avirulent virus + inactivated virulent virus (pox)
• dependovirus + adenovirus

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14
Q

Phenotype mixing

A
  • Exchange of structural proteins
  • Leukosis + sarcoma virus: acquiring envelope proteins
  • Transcapsidation (Polio- + Coxsackievirus)

NON-HERITABLE!

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15
Q

Adsorption interference

A

Competition for the same cell-surface receptor
• related viruses, or
• after phenotype mixing, or
• different viruses, but the same receptor (ie. CAR)

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16
Q

Autointerference

A

• complete and incomplete forms of the same virus
• also at adsorption
• incomplete virion: shorter nucleic acid
→ higher mobility, polymerase affinity
• competition for enzymes, ribosomes
→ defective interfering particles (DI)
• large amounts of incomplete progeny viruses
→ self-limiting infections (Paramyxo-, Rhabdoviridae)

17
Q

•Heterologous interference

A
  • non-related viruses
  • viral suppressor protein production
  • ie.: herpes, adenovirus – inhibits pox
18
Q

Virusexaltation - neutral virus interaction

A

The viruses are able to multiplicate independently

The simultaneous infection does not effect the multiplication
BUT
changes the viral influence on the host cell or organism:
• Increased pathogenicity
• Cytopathic effect appears

19
Q

lytogenic cycle of viruses

A

after the multiplication of viruses, cell death occur

20
Q

lysogenic cycle of viruses

A

cells incorporate the viruses NA into its own for exchange of survival