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VIROLOGY > 5 – Virus Host Interactions > Flashcards

5 – Virus Host Interactions Flashcards

1
Q

Cytopathic

A
  • Infection kills the cell
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2
Q

Productive

A
  • Progeny virions produced and released
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3
Q

Abortive, non-productive

A
  • Progeny virions not produced and released
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4
Q

Permissive

A
  • Refers to a cell that supports virus replication and progeny virion release
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5
Q

Non-permissive

A
  • Refers to cell that does NOT support virus replication or progeny virion release
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6
Q

Persistent

A
  • Refers to an infection that lasts a long time
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7
Q

Latent

A
  • Infection remains but NO progeny virions produced
    o May re-enter a productive cycle of infection (reactivation)
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8
Q

Transformation

A
  • Changes in growth or phenotype of cell
    o often cancerous phenotype induced by oncogenic viruses
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9
Q

Cytopathic effect (CPE)

A
  • Morphological changes to the cell due to infection
    o Infected cell monolayers gradually visibly develop evidence of cell damage as infection progresses
  • *useful for IDing infecting virus (under light microscopy)
    o can cause multipe CPE
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10
Q

Enterovirus CPE

A
  • Rounding of cells
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11
Q

Herpesvirus CPE

A
  • Enlarged rounded cells
  • Plaque formation
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12
Q

Paramyxovirus CPE

A
  • Areas of sued cells (syncytia)
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13
Q

Pseudorabies virus CPE

A
  • Enlarged rounded cells
  • Areas of used cells
  • Plaque formation: where cells have been killed by infection
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14
Q

Plague assay

A
  • A way to determine concentration of infectious virus
  • 10-fold dilution series
  • *Each one represents one infectiou virus
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15
Q

Can use immunofluorescent imaging

A
  • Ex. FMD
  • Cell organelles and cytoskeleton can be rearranged during infection
  • *morphological changes are more PRONOUCED as infection progresses
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16
Q

Electron microscopy imaging

A
  • Ex. FMD
  • Early-stage infection: organelles accumulate in perinuclear region
    o Virus-like particles evident
  • Late stage infection: cytoplasm largely filled by replication site, which contains many membranous vesicles
    o Accumulations of virus-like particles in replication site
17
Q

Syncytia form when cellular membranes fuse: ex. respiratory syncytial virus (RSV)

A
  • Viral proteins on cell surface cause neighbouring cell membranes to MERGE and create large multinucleated ‘cells’
18
Q

Hemadsorption: orthomyxoviruses, paramyxoviruses, togaviruses

A
  • Some viruses infected cells can bind to RBCs on their surfaces
  • Due to viral proteins expressed at infected cell plasma membrane that bind to RBCs
19
Q

Hemagglutination assay

A
  • Erythrocytes are agglutinated by virues
  • Free virus particles cause the erythrocytes to aggregate
  • Can be used to quantify viruses
  • *if no virus=RBCs to a button
  • *if virus=homongenous layer
  • *last dilation without a button=titre
20
Q

Inclusion bodies

A
  • Aggregates (proteins, virus particles) that form during replication
  • May represent areas of viral synthesis/assembly (ex. viral factories)
  • May be nuclear, cytoplasmic or both
21
Q

Inclusion bodies: intranuclear examples

A
  • Herpesviruses
  • Adenoviruses
  • Parvoviruses
  • *replication compartment are the sites of viral DNA replication
22
Q

Inclusion bodies: intracytoplasmic examples

A
  • Paramyxoviruses
  • Reoviruses
  • Rabies virus
  • Pox viruses
  • *large cytoplasmic viral inclusions appear around the vacuoles or eosinophilic bodies (Bollinger bodies)
  • *TEM image can show numerous viral particles (ex. Avian pox)
23
Q

What are negri bodies?

A
  • Matrix of granular or filamentous material made up of viral nucleoprotein
  • Ex. rabies virus
24
Q

Cytomegalovirus inclusion bodies

A
  • Intranuclear and intracytoplasmic
  • *resemble ‘owl’s eyes’
25
Q

Canine distemper virus inclusion bodies

A
  • Intranuclear and intracytoplasmic
26
Q

What are 2 ways viruses can kill cells?

A
  1. Apoptosis: immunologically silent
  2. Necrosis: proinflammatory death=body responds
27
Q

Apoptosis

A
  • Can be induced by virus infection
    o Can be rapid (mins)
  • Mechanism to protect from infection: cell dies BEFORE many viral progeny are made
  • Viruses often have mechanisms to interfere with and prevent apoptosis
  • *variety of signals can activate
28
Q

What are the pathways to induce apoptosis?

A
  • Extrinsic death receptor pathway
  • Intrinsic death receptor pathway
    o Mitochondria and ER
29
Q

Cells can fight back against infection

A
  • Intrinsic antiviral response
30
Q

Intrinsic antiviral response

A
  • FIRST LINE of intracellular defense
  • Mediated by constitutively expressed cellular proteins that DIRECTLY INHIBIT viral infection at MULTIPLE STEPS
  • Viral proteins antagonize cellular antiviral restriction factors
31
Q

What do intrinsic antiviral factors and viral antagonism of their antiviral activities contribute to?

A
  • Zoonotic transmission
    Ex. Nef antagonizes so virions can be released
  • Nef needs to gain function to inhibit anti-viral activity of tetherin
32
Q

Interferon response

A
  • Cellular proteins recognize viral components
    o Cellular pattern recognition receptors recognize PAMPs and induce signalling cascades that activate expression of antiviral signals
     Inflammatory cytokines
     Chemokines
     Type 1 interferons
  • *signals from infected cell can bind neighbouring cells to stimulate expression of IFN-responsive genes
    o Adjacent cells are ready to combat virus BEFORE they are infected
33
Q

PAMPs

A
  • Pathogen associated molecular patterns
34
Q

Superinfection resistance

A
  • *viral interference
  • Previous exposure of a cell to a virus that inhibits infection by another virus
  • Initial infeiton may stimulate an antiviral state (Interferon)
35
Q

When might superinfection resistance (viral interference) occur?

A
  • Vaccines composed of live-attenuated viruses
    o Vaccines may disrupt infection by unreleated viruses
    o Wild viruses may render live-attenuated vaccines LESS effective
  • *persistently infected cells may resist further infection

VIROLOGY (12 decks)

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