Viruses I/II Flashcards

1
Q

Why is viral DNA larger and more complex than viral RNA?

A

The DNA pol can proofread, but RNA is not proofread; the RNA will contain many errors and therefore be nonfunctional if it is too large

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2
Q

What is a segmented genome?

A

RNA virus genome may be broken into pieces, which function like chromosomes

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3
Q

Function of a capsid?

A

Protect the vulnerable genetic material

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4
Q

3 basic morphological structures of viruses.

A

Complex, helical, Icosahedral

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5
Q

What makes the Icosahedral structure so stable?

A

Triangular pieces form the best ratio of volume to surface area without additional support

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6
Q

What’s remarkable about the proteins in a helical virus?

A

During synthesis, the proteins self assemble onto the helical protein surrounding the nucleic acid (so it is rarely exposed)

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7
Q

Why does RNA require more “protection” than DNA?

A

More readily degraded

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8
Q

How will additional nucleic acid length affect self assembling capsomeres?

A

They will continue to add no matter the length

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9
Q

What is a capsomere?

A

Individual component of capsid structure

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10
Q

How does the construction of the icosahedron capsid structure progress?

A

Via self assembly of capsomeres, which join into pentomer units

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11
Q

What is a procapsid?

A

Shell without nucleic acid

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12
Q

What is sequential assembly?

A

Capsid synthesized separately from nucleic acid.

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13
Q

What happens if too much DNA is put into a capsid?

A

Increased turgor pressure; places too much pressure onto interior of capsid, resulting in “blowing up”

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14
Q

Headful packaging

A

The right amount of DNA in a capsid

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15
Q

Concerted assembly is for _____ viruses (type of viral structure)

A

Helical

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16
Q

Sequential assembly is for _____ viruses (type of viral structure)

A

Headful packaging

Icosahedral?

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17
Q

Nucleocapsid

A

Genome + capsid

Virion for naked viruses

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18
Q

Enveloped viruses

A

Nucleocapsid + membrane

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19
Q

What is the function of virally encoded glycoproteins?

A
  1. Attach and penetrate cells

2. target immune response

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20
Q

Where is viral membrane derived from?

A

Host

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21
Q

Why do viruses use repeating subunits to build capsids?

A

More efficient than building various specialized proteins (like animal cells) due to limited genome

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22
Q

What are the consequences of having an envelope (versus a virus not having an envelope)?

A

Less stable than naked virus, need aqueous environment

  • -more susceptible to drying
  • -sensitive to detergents and etoh
  • -can’t survive in GI tract (acid)

**limited spread

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23
Q

T/F: Enveloped viruses may spread fecally and orally.

A

F: can’t survive acid of GI tract

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24
Q

Why is it important to determine receptors utilized by viruses?

A

By blocking these receptors, viruses ability to enter cell is blocked.

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25
Describe the methods of viral endocytosis
Takes advantage of the cells normal processes: virus attaches, enters cell within vesicle, pinches into endosome allowing nucleocapsid to be released into cell
26
T/F: Endocytosis is limited to enveloped viruses
F: enveloped and nonenveloped
27
Fusion proteins.
Proteins that disrupt vesicle or cause merging of envelope/vesicle, releasing nucleocapsid.
28
The role of pH in membrane fusion.
Fusion proteins are activated in low pH, and undergo a conformational change.
29
This type of virus fuses directly with the plasma membrane.
Enveloped
30
pH independent penetration
plasma membrane fusion
31
pH dependent penetration
endocytosis
32
Proteins contained within the envelope of viruses that undergo plasma membrane fusion
Fusion and attachment proteins
33
Fusion and attachment proteins
Proteins contained within the envelope of viruses that undergo plasma membrane fusion
34
Two ways that antivirals affect viral penetrance.
1) can't release itself from the endosome | 2) changes ridgity of the cell membrane in order to block envelope fusion
35
What happens to the capsid during uncoating?
Complete disassembly
36
What occurs after early transcription?
genome replication
37
Early transcription yields...
Proteins/enzymes necessary for replication
38
When is RNA dependent RNA pol transcribed?
Early transcription
39
What is the downside to replicating so many genomes so quickly?
Introduction of many errors (even more if it is RNA)
40
What is created during late transcription?
Structural proteins
41
RNA viruses replicate/assemble within the _____ of cells
cytoplasm
42
DNA viruses replicate/assemble in the _____ of cells
nucleus
43
Lysis
release of naked virus from host
44
Budding
release of enveloped virus (does not kill cell)
45
Release of enveloped virus
Budding
46
Release of naked virus from host
Lysis
47
The original glycoproteins on the enveloped virus
are reacquired when the virus buds from the host.
48
Naked genome is likely what shape?
Icosahedral, because the nucleic acid isn't being shielded as it is synthesized.
49
(+/-) RNA viruses look like messenger RNA
+
50
Internal Ribosomal Entry Site
Viral substitue for our 5' cap structure; provides a site for ribosome binding
51
Location where ribosomes bind on (+) RNA
internal ribosomal entry site
52
What is the function of protease in RNA synthesis?
Cuts long polyprotein synthesized into the appropriate pieces
53
What is necessary to synthesized the 3' to 5' strand during (+) RNA virus replication?
RNA dependent RNA polymerase
54
RNA dependent RNA polymerase
encoded by virus to create RNA from an RNA template
55
Complement strand synthesized by (+) RNA makes
Templates (more + strand RNA for progeny) or translates into capsid proteins (this will be in 3' to 5')
56
When should RNA dependent RNA polymerase be made in (+) RNA?
First, so additional RNA can be created
57
First event for (+) RNA
Translation of RNA dependent RNA polymerase
58
First event for (-) RNA
Transcription of (+) strand RNA (5' to 3')
59
What is the biggest difference between (+) and (-) RNA?
(-) must package and bring RNA dependent RNA polymerase with it into the cell
60
Translates individual proteins
(-) RNA
61
What components of (-) RNA continue on to infect the next cell?
RNA polymerase,
62
Retrovirus are (+/-) RNA
+
63
How does a retrovirus affect cells?
It integrates into host DNA
64
What enzyme does a DNA virus use to transcribe viral genes?
RNA pol III
65
How do small DNA viruses signal transcription enzymes?
Encode viral gene promoters to redirect host RNA pol II
66
What enzyme does a large DNA virus use to replicate viral genes?
its own DNA pol (target for antiviral drugs)
67
What enzyme does a small DNA virus use to replicate viral genes?
host DNA pol
68
"Hole" in a confluent monolayer of cells left after cell lysis
Plaque
69
Plaque
"Hole" in a confluent monolayer of cells left after cell lysis
70
Lysate
Suspension of virions in culture medium that results from unrestricted growth of the virus on a monolayer of cells
71
Suspension of virions in culture medium that results from unrestricted growth of the virus on a monolayer of cells
Lysate
72
Biological assay of infectivity, measured in pfu/mL lysate
Plaque Assay
73
What is determined by a plaque assay?
Number of infectious viruses in a suspension
74
Particle to pfu ratio
Number of particles compared to the number of INFECTIOUS virions (assumes that not all viruses are capable of infection)
75
Multiplicity of Infection
ratio of infectious particles to number of target cells to be infected
76
What does a low particle to pfu ratio demonstrate?
Most of the cells are capable of infection
77
What does an MOI of 5-10 signify?
All cells are infected
78
2 reasons that viruses have high mutation frequencies:
1) Large number of genome copies | 2) High error rate among RNA polymerases
79
Complementation
Protein sharing among viruses (such as sharing a functional protein with a virus lacking that functional protein)
80
One way to repair a defective DNA virus.
Recombination
81
Reassortment
In segmented RNA viruses, segments of RNA can exchange (AABB + aabb --> AaBb + aAbB)
82
Common example of reassortment
Especially virulent strands of the flu virus
83
How does reassortment affect viral immunity?
The virus may have different epitopes, unfamiliar to immune system
84
When you infect cells at an MOI of 0.1, no lysate is obtained; when you infect at an MOI of 10, a lysate is obtained. Why?
Coinfection (such as complementation) is necessary to produce progeny (virus cannot leave cell if 1 defective virus infects the cell)
85
Most common route for viral infection
respiratory
86
Two ways for localized spread
1) Release of progeny and infection of surrounding cell | 2) Syncytia
87
Synctia
Fusion of infected cell and uninfected cells, forming a large multinucleated cell; does not require release and reentry
88
Viremia
Viruses within bloodstream
89
Viruses spread in the body via:
bloodstream and lymphatics
90
Methods for viruses gaining access to CNS:
1) circumventing the BBB 2) CSF 3) direct uptake in peripheral nerves (polio)
91
Acute phase
symptomatic phase
92
Viral genome remains in cell indefinitely, but virus particles are not produced unless activated
Latent viral infection
93
Virus is produced at low levels throughout persistent infection
Chronic viral infection
94
Viral genome integrates into cellular DNA and changes cells, i.e. cancer
Transforming (oncogenic) viral infection
95
First immune defense against viruses
NK cells and IFN
96
Induced by viral PAMPS binding to Toll-like receptors and PRRs
IFN
97
Three pathways induced by IFN
PKR, 2-5A system, Mx pathway
98
Inactivates/phosphorylates translation initiation factor eIF-2, which inhibits viral AND cellular protein translation
Protein kinase pathway
99
Activates RNase L, which cleaves RNA and destroys the genome or inhibits viral transcription
2-5A System
100
PKR
Inactivates/phosphorylates translation initiation factor eIF-2, which inhibits viral protein translation
101
2-5A System
Activates RNase L, which cleaves RNA and destroys the genome or inhibits viral transcription
102
Mx Pathway
GTPase proteins inhibit RNA polymerase activity
103
GTPase proteins inhibit RNA polymerase activity
Mx Pathway
104
Antigen specific imune responses:
CD8+ cytotoxic cells and Neutralizing antibodies
105
What activates PKR pathway?
dsRNA
106
Immune Mechanisms of viruses:
Infection of neural cells (no MHC I), cytokine homologs, inhibition of antigen presention, antigen variation
107
When may a vaccine be impractical?
1) If many disease-causing strains exist | 2) Variation exhibited in dominant antigen structure (epitope)
108
Antibody responses from live vaccine.
IgG and IgA
109
Vaccine form that does not require injection
Live
110
Vaccine form with a single dosing that results in long term immunity
Live
111
Non-heat labile vaccine form
Inactivated
112
Benefit of IgA antibodies against a virus.
The virus is inactivated in the gut, so it is not shed/spread to others
113
Form of vaccine that may revert to virulence
Live
114
Derived from only ONE viral protein expressed in yeast so it cannot cause disease (but requires multiple injections)
Subunit vaccine (HBV and HPV)