Virology Flashcards

(139 cards)

1
Q

What is an obligate intracellular parasite that replicates by self-assembly of individual components?

A

Virus.

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2
Q

Can viruses make energy or proteins independent of a host cell?

A

No.

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3
Q

Can a viral genome be made of both RNA and DNA?

A

No: they either have RNA or DNA but not both.

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4
Q

What is the name of a virus particle?

A

Virion.

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5
Q

What 4 characteristics are used to classify viruses?

A
  1. Size
  2. Morphology
  3. Type of genome
  4. Mechanism of replication
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6
Q

+RNA genomes are what in regards to mRNA?

A

Same sense.

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7
Q

-RNA genomes are what in regards to mRNA?

A

Opposite sense.

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8
Q

T or F. DNA genomes are larger than RNA genomes.

A

T: b/c of DNA polymerase proofreading.

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9
Q

Virus genomes are packaged into what?

A

Protein shells called capsids.

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10
Q

Are capsids rigid?

A

Yes.

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11
Q

Can capsids withstand environmental conditions?

A

Yes.

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12
Q

What are capsids the result of?

A

Self-assembly of virally-encoded capsomeres.

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13
Q

What are the 3 forms of capsids?

A
  1. Helical (concerted assembly)
  2. Icosahedral or spherical (sequential assembly)
  3. Complex
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14
Q

T or F. The shape of the capsid is determined by the capsomeres that self-assemble, not by the shape of the genome.

A

T.

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15
Q

What is a nucleocapsid?

A

Genome plus capsid.

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16
Q

What is the virion for a naked virus?

A

Nucleocapsid.

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17
Q

Can some viral nucleocapsids be surrounded by a lipid envelope?

A

Yes.

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18
Q

Where is the lipid envelope derived from?

A

Cellular membranes.

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19
Q

What do virally-encoded glycoproteins do?

A

Insert in membrane. Serve as virus attachment proteins and membrane fusion proteins.

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20
Q

What is the virion for an enveloped virus composed of?

A

Nucleocapsid plus membrane.

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21
Q

T or F. Enveloped viruses are more stable than naked viruses.

A

F.

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22
Q

Why are enveloped viruses more stable than naked viruses?

A

The envelope is mostly lipid: more susceptible to drying, sensitive to detergents and alcohols, cannot survive in GI tract.

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23
Q

How do enveloped viruses spread?

A

Large droplets, secretions, organ transplants, and blood transfusions.

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24
Q

Are enveloped viruses always in some form of liquid?

A

Yes.

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25
What are the 8 major steps of virus replication?
1. Attachment 2. Penetration 3. Uncoating 4. Early transcription and synthesis of nonstructural proteins 5. Genome replication 6. Late transcription and synthesis of structural proteins 7. Assembly of virus particles 8. Relese of virus particles
26
What types of viruses can use endocytosis for penetration?
Enveloped and non-enveloped.
27
Is endocytosis a pH-dependent event?
Yes.
28
What types of viruses can use membrane fusion for penetration?
Enveloped only.
29
Is membrane fusion a pH-dependent event?
No.
30
In early transcription, do RNA viruses use host RNA polymerase?
No: use a virally-encoded RNA-dependent RNA.
31
In early transcription, do DNA viruses use host RNA polymerase?
Yes (except poxviruses).
32
Where does genome replication take place for RNA viruses?
Cytoplasm.
33
Where does genome replication take place for DNA viruses?
Nucleus.
34
Where does assembly take place for RNA viruses?
Cytoplasm.
35
Where does assembly take place for DNA viruses?
Nucleus (except poxviruses and hepadnaviruses).
36
What are 2 mechanisms for release of virus particles?
Cell lysis and budding.
37
T or F. Budding is only a mechanism of enveloped viruses.
T.
38
What are the 6 types of viral cytopathogenesis?
1. Inhibition of cell protein synthesis 2. Inhibition and degradation of cellular DNA 3. Alteration of cell membrane structure 4. Disruption of cytoskeleton 5. Formation of inclusion bodies 6. Toxicity of virion components
39
+RNA virus genomes function as what?
mRNA.
40
T or F. +RNA virus genomes are immediately translated by cellular ribosomes.
T.
41
Are +RNA virus genomes translated as a polyprotein that must be cleaved to individual proteins?
Yes.
42
What does RNA-dependent RNA polymerase do?
Transcribes -RNA strands from the +RNA genome.
43
Where does the RNA-dependent RNA polymerase come from?
Cleaved from the translated polyprotein.
44
T or F. -RNA strands serve as templates to make many copies of the +RNA genome.
T.
45
T or F. +RNA copies are used as mRNA to make structural proteins.
T.
46
Are +RNA copies encapsidated to produce nucleocapsids?
Yes.
47
Can -RNA virus genomes be used as mRNA?
No: must first be used as a template to transcribe a +RNA strand.
48
How is the -RNA genome transcribed?
Incoming virus particles carry a RNA-dependent RNA polymerase with it.
49
What type of polymerase do retroviruses carry with them?
RNA-dependent DNA polymerase (aka reverse transcriptase).
50
What does reverse transcriptase do?
Reverse transcribes the retrovirus +RNA genome into dsDNA.
51
Where do retrovirus genomes integrate once it has been reverse transcribed?
Into the host genome.
52
What produces retrovirus proteins and the retrovirus +RNA genome?
Host enzymes.
53
What type of polymerase transcribes DNA virus genomes?
Host DNA-dependent RNA polymerase.
54
Do many DNA viruses have a host shut-off mechanism that degrades host mRNA?
Yes.
55
Do many DNA viruses use specific transcription factors that redirect host polymerases to viral genes and away from cellular genes?
Yes.
56
In larger DNA viruses, what does viral genome replication depend on?
Virally-encoded DNA-dependent DNA polymerases.
57
In smaller DNA viruses, what does viral genome replication depend on?
Smaller viruses use host DNA polymerase.
58
What is a plaque?
The hole in a confluent monolayer of cells resulting from the virus lysing the infected cells.
59
What is a lysate?
Suspension of virions in culture medium that results from unrestricted growth of the virus on a cell monolayer.
60
Are all virus particles produced in a lysate infectious?
No.
61
What does the particle-to-pfu ratio measure?
The number of physical particles compared to the number of infectious virions.
62
What do plaque assays measure?
The number of infectious virions in a given volume of lysate.
63
What units are plaqe assays in?
Plaque-forming units (pfu) per mL of lysate.
64
T or F. Plaque assay is a biological assay of infectivity.
T.
65
What is the Multiplicity of Infection (MOI)?
Ratio of number of infectious particles to the number of target cells to be infected.
66
An MOI of 1 will infect what percentage of cells in a monolayer?
60%.
67
What value of MOI is needed to ensure all cells are infected?
MOI between 5 and 10.
68
What 2 periods can a single-cycle growth curve be divided into?
Eclipse period and latent period.
69
T or F. The eclipse period is the post-penetration phase until the virus can be detected intracellularly.
T.
70
What stages of virus replication are included in the eclipse period?
Uncoating, early transcription, and genome replication.
71
At what stage does the eclipse period end?
Virus assembly stage.
72
T or F. The latent period is the post-penetration phase until the virus can be detected extracellularly.
T.
73
Does the latent period include the eclipse period?
Yes.
74
What stages of virus replication are included in the latent period?
Uncoating, early transcription, genome replication, virus assembly, and virus release.
75
Do viral mutations occur at a high frequency? Why?
Yes. Large number of genome copies produced in every cell. Polymerase errors (especially RNA viruses b/c RNA polymerases are sloppy).
76
What 3 things can virus genomes undergo within a single cell?
1. Complementation 2. Recombination 3. Reassortment
77
What is complementation?
An exchange of proteins.
78
If a lethal mutation arises within a virus genome, can it infect a second cell? If so, will it be able to replicate in the second cell?
Yes: by using wild-type copies for functional purposes. No: b/c it still contains the lethal mutation.
79
What is recombination?
An exchange of genetic material on the same segment of genome.
80
Can RNA viruses undergo recombination?
No: only DNA viruses.
81
T or F. RNA viruses can exchange genetic material in a way that resembles recombination.
T: it is not true recombination though.
82
What is reassortment?
An exchange of genetic material on different segments of genome.
83
T or F. Reassortment is unique to viruses.
T.
84
Is reassortment the mechanism behind emerging new strains of flu?
Yes.
85
What is required for reassortment?
Two segmented viruses infect the same cell.
86
When does the reassortment take place?
During virus assembly.
87
What are the 5 points of virus-host interactions?
1. Route of entry/transmission 2. Secondary spread 3. Incubation period 4. Acute vs. persistent infection 5. Control
88
What are the 6 routes of virus entry/transmission?
1. Fecal-oral 2. Respiratory 3. Blood-borne 4. Sexual transmission 5. Maternal-neonatal 6. Animal reservoir or arthropod vector
89
What is the most common route of virus entry/transmission?
Respiratory.
90
How do viruses enter?
Through breaks in the skin or through mucosa.
91
What is characteristic of the cells where initial replication takes place?
They express viral receptors and contain appropriate cellular factors for replication.
92
What are the 2 mechanisms of localized spread of virus?
1. Release of virus from an infected cell and subsequent infection of surrounding cells 2. Some enveloped viruses can fuse an infected cell with uninfected cells to directly spread to surrounding cells (termed synctia formation)
93
How do viruses achieve secondary spread?
Gain access to the bloodstream or lymphatic system.
94
How do viruses gain access to the CNS?
By circumventing the BBB, through CSF, or by direct uptake in peripheral nerves.
95
What is viremia?
Presence of virions in the blood.
96
What is the incubation period?
The period post-infection prior to the onset of symptoms.
97
How long is a short incubation period?
1-2 days.
98
Do viruses with short incubation periods require secondary spread to elicit symptoms in the patient?
No.
99
How many days is the incubation period for viruses that require secondary spread?
12-14 days.
100
Can some viruses have incubation periods of months to years?
Yes: ex. HIV.
101
Can patients be infectious during the incubation period?
Yes.
102
What is the acute phase of an infection?
The symptomatic phase.
103
Which patient population has an increased risk for persistent virus infection?
Immunocompromised patients.
104
What are the 3 forms of persistent infection?
1. Chronic 2. Latent 3. Transforming
105
What is the chronic form all about?
Virus is produced at low levels but may not continue to cause disease symptoms (ex. Hepatitis B).
106
What is the latent form all about?
Virus genome remains in the cells indefinitely but virus particles are only produced upon reactivation (ex. herpes).
107
What is the transforming form all about?
Intact or partial virus genome integrates into cellular DNA or is otherwise maintained in the cell. Immortalizes the cell and alters its growth properties. Ex. oncogenic viruses.
108
What is the main viral PAMP?
dsRNA.
109
What are other examples of viral PAMPs?
Unmethylated DNA and 5' modified ssRNA.
110
What does the protein kinase pathway do?
Inactivates translation initiation factor eIF-2 thus inhibiting viral protein translation.
111
What does the 2-5A system do?
Activates RNase L which cleaves RNA thus destroying RNA genomes or inhibiting viral transcription.
112
What does the Mx pathway do?
GTPases inhibit RNA polymerase activity.
113
What is the major cellular response to primary viral infections?
CTL's.
114
What role do Ab's serve in fighting off viruses?
Neutralize virus binding or facilitate lysis of enveloped viruses with complement.
115
T or F. Viruses evolve to evade immune defense mechanisms.
T.
116
How do viruses escape humoral responses?
Antigen variation.
117
How do viruses escape cellular responses?
Inhibition of antigen presentation.
118
Why do viruses secrete cytokine homologs?
To downregulate or block cellular responses.
119
T or F. Latent infections hide in neurons where there are no MHC Class I molecules.
T.
120
What are flu-like symptoms caused by in a virus infection?
IFN and lymphokines.
121
What cells cause inflammation in virus infections?
T cells, macrophages, and PMNs.
122
What is hemorrhagic disease caused by?
T cells, Ab, and complement.
123
What are the 3 types of antivirals?
1. Vaccines 2. Immune globulin 3. Drugs
124
T or F. Vaccines are active immunization.
T.
125
Are vaccines practical if there are a large number of virus strains that cause a disease?
No.
126
Are vaccines always practical if a virus undergoes a lot of antigenic variation?
Not always practical in this case.
127
What are the 3 basic types of viral vaccines?
1. Live attenuated virus 2. Killed virus 3. Subunit (recombinant DNA)
128
Do attenuated virus vaccines cause subclinical infections?
Yes.
129
What are the advantages of attenuated virus vaccines?
Cheap to produce. Strong response (IgG, IgA, T cell) that is long-lasting.
130
What are the disadvantages of attenuated virus vaccines?
Can be labile in transport. Cannot be given to immunocompromised patients. Can revert to virulence in rare cases.
131
Can a killed virus cause illness?
No.
132
What are the advantages of a killed virus vaccine?
Very stable. Rare side effects. Cannot revert to virulence.
133
What are the disadvantages of a killed virus vaccine?
More expensive to prepare. Shorter term immunity that is mostly limited to IgG.
134
What are the 2 viruses that subunit vaccines are available for?
Hepatitis B virus and HPV.
135
What are subunit vaccines composed of?
Single viral proteins that are expressed in yeast using recombinant DNA technology.
136
What are the advantages of subunit vaccines?
Cannot cause disease. Are not derived from blood.
137
What are the disadvantags of subunit vaccines?
Requires multiple injections.
138
Immune globulin is what type of immunization?
Passive immunization.
139
T or F. Immune globulin is used in both pre- and post-exposure prophylaxis.
T.