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CMD Block 2 > Viruses I/II > Flashcards

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
Q

Describe the methods of viral endocytosis

A

Takes advantage of the cells normal processes: virus attaches, enters cell within vesicle, pinches into endosome allowing nucleocapsid to be released into cell

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26
Q

T/F: Endocytosis is limited to enveloped viruses

A

F: enveloped and nonenveloped

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27
Q

Fusion proteins.

A

Proteins that disrupt vesicle or cause merging of envelope/vesicle, releasing nucleocapsid.

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28
Q

The role of pH in membrane fusion.

A

Fusion proteins are activated in low pH, and undergo a conformational change.

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29
Q

This type of virus fuses directly with the plasma membrane.

A

Enveloped

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30
Q

pH independent penetration

A

plasma membrane fusion

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31
Q

pH dependent penetration

A

endocytosis

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32
Q

Proteins contained within the envelope of viruses that undergo plasma membrane fusion

A

Fusion and attachment proteins

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33
Q

Fusion and attachment proteins

A

Proteins contained within the envelope of viruses that undergo plasma membrane fusion

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34
Q

Two ways that antivirals affect viral penetrance.

A

1) can’t release itself from the endosome

2) changes ridgity of the cell membrane in order to block envelope fusion

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35
Q

What happens to the capsid during uncoating?

A

Complete disassembly

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36
Q

What occurs after early transcription?

A

genome replication

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37
Q

Early transcription yields…

A

Proteins/enzymes necessary for replication

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38
Q

When is RNA dependent RNA pol transcribed?

A

Early transcription

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39
Q

What is the downside to replicating so many genomes so quickly?

A

Introduction of many errors (even more if it is RNA)

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40
Q

What is created during late transcription?

A

Structural proteins

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41
Q

RNA viruses replicate/assemble within the _____ of cells

A

cytoplasm

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42
Q

DNA viruses replicate/assemble in the _____ of cells

A

nucleus

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43
Q

Lysis

A

release of naked virus from host

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44
Q

Budding

A

release of enveloped virus (does not kill cell)

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45
Q

Release of enveloped virus

A

Budding

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46
Q

Release of naked virus from host

A

Lysis

47
Q

The original glycoproteins on the enveloped virus

A

are reacquired when the virus buds from the host.

48
Q

Naked genome is likely what shape?

A

Icosahedral, because the nucleic acid isn’t being shielded as it is synthesized.

49
Q

(+/-) RNA viruses look like messenger RNA

A

+

50
Q

Internal Ribosomal Entry Site

A

Viral substitue for our 5’ cap structure; provides a site for ribosome binding

51
Q

Location where ribosomes bind on (+) RNA

A

internal ribosomal entry site

52
Q

What is the function of protease in RNA synthesis?

A

Cuts long polyprotein synthesized into the appropriate pieces

53
Q

What is necessary to synthesized the 3’ to 5’ strand during (+) RNA virus replication?

A

RNA dependent RNA polymerase

54
Q

RNA dependent RNA polymerase

A

encoded by virus to create RNA from an RNA template

55
Q

Complement strand synthesized by (+) RNA makes

A

Templates (more + strand RNA for progeny) or translates into capsid proteins (this will be in 3’ to 5’)

56
Q

When should RNA dependent RNA polymerase be made in (+) RNA?

A

First, so additional RNA can be created

57
Q

First event for (+) RNA

A

Translation of RNA dependent RNA polymerase

58
Q

First event for (-) RNA

A

Transcription of (+) strand RNA (5’ to 3’)

59
Q

What is the biggest difference between (+) and (-) RNA?

A

(-) must package and bring RNA dependent RNA polymerase with it into the cell

60
Q

Translates individual proteins

A

(-) RNA

61
Q

What components of (-) RNA continue on to infect the next cell?

A

RNA polymerase,

62
Q

Retrovirus are (+/-) RNA

A

+

63
Q

How does a retrovirus affect cells?

A

It integrates into host DNA

64
Q

What enzyme does a DNA virus use to transcribe viral genes?

A

RNA pol III

65
Q

How do small DNA viruses signal transcription enzymes?

A

Encode viral gene promoters to redirect host RNA pol II

66
Q

What enzyme does a large DNA virus use to replicate viral genes?

A

its own DNA pol (target for antiviral drugs)

67
Q

What enzyme does a small DNA virus use to replicate viral genes?

A

host DNA pol

68
Q

“Hole” in a confluent monolayer of cells left after cell lysis

A

Plaque

69
Q

Plaque

A

“Hole” in a confluent monolayer of cells left after cell lysis

70
Q

Lysate

A

Suspension of virions in culture medium that results from unrestricted growth of the virus on a monolayer of cells

71
Q

Suspension of virions in culture medium that results from unrestricted growth of the virus on a monolayer of cells

A

Lysate

72
Q

Biological assay of infectivity, measured in pfu/mL lysate

A

Plaque Assay

73
Q

What is determined by a plaque assay?

A

Number of infectious viruses in a suspension

74
Q

Particle to pfu ratio

A

Number of particles compared to the number of INFECTIOUS virions (assumes that not all viruses are capable of infection)

75
Q

Multiplicity of Infection

A

ratio of infectious particles to number of target cells to be infected

76
Q

What does a low particle to pfu ratio demonstrate?

A

Most of the cells are capable of infection

77
Q

What does an MOI of 5-10 signify?

A

All cells are infected

78
Q

2 reasons that viruses have high mutation frequencies:

A

1) Large number of genome copies

2) High error rate among RNA polymerases

79
Q

Complementation

A

Protein sharing among viruses (such as sharing a functional protein with a virus lacking that functional protein)

80
Q

One way to repair a defective DNA virus.

A

Recombination

81
Q

Reassortment

A

In segmented RNA viruses, segments of RNA can exchange (AABB + aabb –> AaBb + aAbB)

82
Q

Common example of reassortment

A

Especially virulent strands of the flu virus

83
Q

How does reassortment affect viral immunity?

A

The virus may have different epitopes, unfamiliar to immune system

84
Q

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?

A

Coinfection (such as complementation) is necessary to produce progeny (virus cannot leave cell if 1 defective virus infects the cell)

85
Q

Most common route for viral infection

A

respiratory

86
Q

Two ways for localized spread

A

1) Release of progeny and infection of surrounding cell

2) Syncytia

87
Q

Synctia

A

Fusion of infected cell and uninfected cells, forming a large multinucleated cell; does not require release and reentry

88
Q

Viremia

A

Viruses within bloodstream

89
Q

Viruses spread in the body via:

A

bloodstream and lymphatics

90
Q

Methods for viruses gaining access to CNS:

A

1) circumventing the BBB
2) CSF
3) direct uptake in peripheral nerves (polio)

91
Q

Acute phase

A

symptomatic phase

92
Q

Viral genome remains in cell indefinitely, but virus particles are not produced unless activated

A

Latent viral infection

93
Q

Virus is produced at low levels throughout persistent infection

A

Chronic viral infection

94
Q

Viral genome integrates into cellular DNA and changes cells, i.e. cancer

A

Transforming (oncogenic) viral infection

95
Q

First immune defense against viruses

A

NK cells and IFN

96
Q

Induced by viral PAMPS binding to Toll-like receptors and PRRs

A

IFN

97
Q

Three pathways induced by IFN

A

PKR, 2-5A system, Mx pathway

98
Q

Inactivates/phosphorylates translation initiation factor eIF-2, which inhibits viral AND cellular protein translation

A

Protein kinase pathway

99
Q

Activates RNase L, which cleaves RNA and destroys the genome or inhibits viral transcription

A

2-5A System

100
Q

PKR

A

Inactivates/phosphorylates translation initiation factor eIF-2, which inhibits viral protein translation

101
Q

2-5A System

A

Activates RNase L, which cleaves RNA and destroys the genome or inhibits viral transcription

102
Q

Mx Pathway

A

GTPase proteins inhibit RNA polymerase activity

103
Q

GTPase proteins inhibit RNA polymerase activity

A

Mx Pathway

104
Q

Antigen specific imune responses:

A

CD8+ cytotoxic cells and Neutralizing antibodies

105
Q

What activates PKR pathway?

A

dsRNA

106
Q

Immune Mechanisms of viruses:

A

Infection of neural cells (no MHC I), cytokine homologs, inhibition of antigen presention, antigen variation

107
Q

When may a vaccine be impractical?

A

1) If many disease-causing strains exist

2) Variation exhibited in dominant antigen structure (epitope)

108
Q

Antibody responses from live vaccine.

A

IgG and IgA

109
Q

Vaccine form that does not require injection

A

Live

110
Q

Vaccine form with a single dosing that results in long term immunity

A

Live

111
Q

Non-heat labile vaccine form

A

Inactivated

112
Q

Benefit of IgA antibodies against a virus.

A

The virus is inactivated in the gut, so it is not shed/spread to others

113
Q

Form of vaccine that may revert to virulence

A

Live

114
Q

Derived from only ONE viral protein expressed in yeast so it cannot cause disease (but requires multiple injections)

A

Subunit vaccine (HBV and HPV)

CMD Block 2 (38 decks)

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