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virology exam 1 > exam 2 > Flashcards

exam 2 Flashcards

1
Q

Example of a DNA virus that replicates in the cytoplasm

A

pox virus

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2
Q

why are cytoplasmic dna viruses more independent

A

don’t rely on cell machinery for replication

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3
Q

why do cytoplasmic dna viruses have large genomes

A

must encode DdDp and DdRp, don’t use cell machinery

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4
Q

where are the cellular polymerases

A

the nucleus

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5
Q

what is the largest animal virus (other than girius)

A

pox virus

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6
Q

why are pox virus morphology complex

A

contains lateral bodies and core

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7
Q

what virus causes a localized skin infection and can cause a severe systemic disease in immunocompromised

A

vaccinia

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8
Q

why do we study the structure of vaccinia for understanding small pox

A

vaccinia is the cousin of small pox virus

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9
Q

how many genes does the vaccinia genome have

A

200!

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10
Q

1st thing to happen in pox virus after uncoating

A

early mrna production

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11
Q

how does pox virus avoid the innate immune response

A

encodes 10 proteins specifically for that (early proteins)

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12
Q

what happens in intermediate transcription

A

make a bunch of mrnas that support last transcription

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13
Q

what kind of proteins impact the host cell in pox viruses

A

intermediate proteins

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14
Q

define IMV

A

intracellular mature virion, brought to golgi

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15
Q

which statement regarding pox viruses is incorrect?
a. they are the largest and most complex of all the animal viruses
b. they multiply in the cytoplasm
c. their sites of multiplication within infected cells appear as inclusion bodies
d. they are non enveloped dna viruses
e. none of the above.

A

d

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16
Q

list ways that pox viruses evade the immune response/why is variola so nasty

A

IFN receptor (viroceptor-mimics cell receptor for IFN)
virokine-(mimic chemokines)
chemokine binding protein
dsRNA binding protein (hides it from RIG-I)
homolog to eif-2 (blocks translation)

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17
Q

difference between IEV and CEV

A

IEV-released by fusion, responsible for host to host transmission, uses microtubules
EEV-actin tails push through the PM and transmit cell to cell

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18
Q

4 types of variola major viruses (virus that causes small pox)

A
  1. ordinary-accounts for most cases 30% mortality
  2. vaccine modified
  3. flat or malignant pox, 90% mortality rate
  4. hemorrhagic
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19
Q

describe variola minor

A

mild

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20
Q

what is the causative agent of small pox

A

variola virus

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21
Q

how did we eradicate small pox

A
  1. narrow host range
  2. no carriers (all symptomatic)
  3. no animal reservoirs
  4. effective attenuated vaccine
  5. easy to surveillance
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22
Q

what type of vaccine is the smallpox vaccine

A

live attenuated vaccinia virus

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23
Q

What is better for viruses, treatment or prevention?

A

treatment is difficult

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24
Q

why is antiviral treatment difficult

A

most of the damage to cells occurs early and only a few effective antivirals exist

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25
Q

what is passive antibody therapy

A

normal human igG fraction, heat treated to destroy viruses. creates serum

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26
Q

read in text fig 7.23

A
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27
Q

list 3 complication of passive immunization that limit it from being used commonly

A

fever, difficulty breathing, skin lesions

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28
Q

how could you create a perfect vaccine (3)

A

evoke b and t cell immunity, will not make patient sick, don’t need 100% uptake of vaccine to get immunity

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29
Q

which of the following is true:
a. it is easier to prevent a virus than to treat it
b. the perfect vaccine will invoke a strong immune response
c. the perfect vaccine will not cause disease
d. it is not necessary to get 100% uptake due to herd immunity
e. all of the above

A

e

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30
Q

what are the two types of traditional vaccines

A
  1. live, attenuated
  2. killed, inactivated
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31
Q

4 steps to producing attenuated vaccines

A
  1. pathogenic virus is isolated from host and grown in human cultured cells
  2. cultured virus is used to infect foreign cells
  3. pass to other cells, mutates over time and becomes less virulent
  4. virus no longer grows well in human cells but still looks enough like a pathogen to invoke immune response
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32
Q

list 6 advantages of live attenuated vaccines

A

strong immune response, long lasting, cross reactive, low cost, quick immunity, don’t require -80 for storage

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33
Q

what are some disadvantages of live attenuated vaccines

A

problem if not properly attenuated, can revert to virulence, not possible with all viruses, not recommended for immunocompromised people

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34
Q

Viruses that have lost their ability to cause disease are said to be

A

attenuated

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35
Q

what is one disadvantage of using attenuated vaccines
a. they require fewer doses than other types of vaccines
b. they provide long lasting protection
c. the organisms multiply following vaccination
d. the organisms can mutate back to a virulent form following vaccination

A

d

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36
Q

How do you produce inactivated viral vaccines

A

virus is exposed to denaturing agent that results in lost of inefectivity

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37
Q

what is formalin

A

denaturing agent used in inactivated viral vaccines

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38
Q

are inactivated viral vaccines able to replicate

A

no

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39
Q

advantages of inactivated vaccines

A

sufficient humoral immunity, no mutation, little to no risk if inactivated properly because it won’t become virulent suddenly, can be used by immunocompromised

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40
Q

disadvantages of inactivated vaccines

A

less effective than attenuated, not possible for all viruses, boosters needed, higher cost, must be tested in monkies

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41
Q

list the 5 new approaches to different vaccines

A
  1. recombinant subunit 2. synthetic peptides, 3. naked dna vaccines 4. live recombinant vector vaccines 5. mrna vaccines
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42
Q

what approach produces an entire viral protein from plasmid to illicit an immune response

A

recombinant subunit

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43
Q

what approach produces a peptide to illicit an immune response

A

synthetic peptides

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44
Q

what approach uses plasmid dnas injected that contain a gene encoding a viral antigen of interest

A

naked dna vaccines

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45
Q

what approach inserts an antigen of interest into a safe virus and infect with the hybrid virus to illicit an immune response

A

live recombinant vector vaccines

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46
Q

what approach used mrna coated in a lipid shell

A

mrna vaccines

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47
Q

general procedure for creating recombinant subunit hbv vaccine

A

grow in yeast, put cloned for heb b surface protein into the yeast plasmid, transform the yeast, isolate surface protein

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48
Q

how do you produce naked dna vaccines

A

purify out genetic material that encodes surface protein, incorporate into dna plasmid, forcefully insert it using gene gun into muscle

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49
Q

using a recombinant form of vaccinnia, what virus vaccine is dropped in forests to give immunity to animals

A

rabies vaccine

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50
Q

what virus uses live recombinant vector vaccines using reassortment

A

flu

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51
Q

advantages of recombinant subunit vaccines

A

cheapily manufactured at large quantities, most very stable, can use for wide variety of viruses

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52
Q

disadvantages of recombinant subunit vaccines

A

delivery is hard, post translational modification can be difficult, poor antigenicity

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53
Q

how do edible vaccines work

A

cut leaf, expose leaf to bacteria carrying an antigen gene qne qn antibiotic resistant gene. kill cells that dont have the new gene. grow plant

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54
Q

what 2 unwanted immune responses might a vaccine cause

A

th2 immunopathogy (all and adeergic inflamatory response) and ADE (virus uses antibodies to aid in infection)

55
Q

stage 1

A

animal studies

56
Q

stage 2 phase 1

A

use healthy volunteers and see if they get sick

57
Q

3 ways to visualize virus particles

A

electron microscope, transmission em, scanning em, x ray crystallography

58
Q

how does negative staining work

A

molds around virus particle, reveals cavities and internal structures

59
Q

2 types of animal cell culture

A
  1. continuous/immortalized 2. primary cell culture
60
Q

advantages of immortilized cell lines

A

powerful tool, drug toxicity testing, antibody production

61
Q

what is continuous cell lines bad to use to study

A

subtle effects of virus infection, differentiated cell function

62
Q

properties of immortalized cells

A

immortal, grow quick, aneuploidy(wrong number of chromosomes)

63
Q

what is a primary culture

A

isolated from embryonic fetal tissue and identical to original tissue

64
Q

properties of primary cells

A

normal chromosome number, require growth factors, cannot grow in suspension, finite lifetime, may survive in animal

65
Q

examples of cytopathic effect (CPE)

A

cell rounding, cell lysis/apoptosis, accumulation of virus components at site of assembly

66
Q

what does the plaque assay do

A

determine how many virion particles you’re iteratively adding

67
Q

pfu

A

dilution factor * number of plaques

68
Q

how many pfu in 1 mL of 10^4 dilution given 33 plaques in .1 mL of 10^4 dilution

A

330 pfu

69
Q

what is the titer concentration given 33 plaques in .1 mL of 10^4 dilution

A

33*10^5 pfu/mL

70
Q

expected range of pfu and moi

A

pfu around 10^7, moi less than 100 pfu/cell

71
Q

diffeerence between em and plaque assay

A

em counts every particle, plaque assay counts infectious particles

72
Q

hybridization techniques for characterization of viral genomes

A

northern, southern blot. in situ hybridization

73
Q

Hoow big are rna virus genomes

A

small about 10k nucleotides

74
Q

why is rna genome so small

A

don’t have proofreading and rna sucks

75
Q

what do both positive and negative rna viruses encode

A

RdRP

76
Q

which viral genome + or - more closely resembles our rna

A

+ sense

77
Q

why most - rna viruses encode RdRP

A

genome is complementary to rna so must copy rna first with RdRP

78
Q

does double stranded mrna viruses package a RdRP

A

yes

79
Q

which types of rna viruses are non infectious

A

negative and double stranded

80
Q

what is the initial event in the cell for + sense rna virus

A

translation

81
Q

what is the initial event in the cell for- sense rna virus

A

transcription

82
Q

structure of polio and + or - ssRNA

A

non enveloped icosahedral, +ssRNA

83
Q

how to disinfect for polio

A

chlorine, hydrochloric acid, heat

84
Q

describe the first steps of the polio infectious cycle

A
  1. virus attaches to PVR
    2.binding=conformational change in capsid VP4
  2. enters cytoplasm through pore
85
Q

what is unique bout polio translation

A

cap independent (IRES)

86
Q

how does polio create so many proteins

A

proteases chop it up

87
Q

how does polio use translation inhibition

A

degrades initiation factors

88
Q

how does poliovirus assemble

A

assemble pentamers around rna

89
Q

how is polio released

A

lysis

90
Q

what is an inclusion body related to polio

A

naked virions become concnetrated near the site of maturation, leading to lysis

91
Q

what vaccines exist for polio

A

salk (inactivated trvalent), sabin (attenuated strains). don’t use salbin anymore to avoid the risk of vaccine polio

92
Q

roadblocks of polio eradication

A

contagious, ipv in tropical regions is hard, resistance to mass vax, opv can cause polio

93
Q

structure and genome of rubella

A

+ssRNA, enveloped helical

94
Q

hcv structure and genome

A

+ ssRNA, enveloped icosahedral

95
Q

examble of rhabdovirus

A

rabies virus, vsv

96
Q

how do -ssrna virus get in cell

A

clathrin mediated endocytosis

97
Q

where does replication occur for -ssRNA viruses

A

cytoplasm

98
Q

strutcure and genome of paramyxovirus

A

enveloped helical -ssRNA

99
Q

how does paramyxovirus get in cell

A

fusion

100
Q

role of neuromididase for virion release

A

stops virions from sticking to each other or the cell theyre budding from

101
Q

how is flu different in regards to rnps

A

rnps are brought to the nucleus because it relies on cell machinery

102
Q

how does flu use cap scavenging in transcription

A

takcell recognizes cap and begins transcriptiones host cap and binds it to biral genome,

103
Q

assembly of flu

A

nucleocapsidis transported to cytoplasm, all the proteins come, bud through plasma membrane

104
Q

antigenic drift is responsible for…

A

seasonal strains

105
Q

antigenic shift is responsible for

A

pandemic strains

106
Q

why is antigenic shift a concern

A

reassortment with a non human host, get new N and H proteins (viral attachment proteins)

107
Q

which strain of flue is more common in non human hosts

A

influenza a

108
Q

what is the standard flu vaccine

A

inactivated

109
Q

structure and genome of flu

A

helical enveloped, -ssRNA

110
Q

does flu or mumps require a rna primer

A

flu

111
Q

is flu or mumps nonsegmented

A

mumps

112
Q

what polymerase replicate and transcribe rna nuclear viruses

A

DdDP and DdRP

113
Q

why is there a risk of dna nuclar viruses integrating into the host chromosme

A

replicate in nucleus and have dna genome

114
Q

parvovirus structure and genome

A

ssDNA, nonenveloped icosahedral

115
Q

distinct characteristics of parvovirus

A

dependent on host cell cycle, must become ds before transcription

116
Q

parvovirus genetics

A

2 ORFs, 6 rna species

117
Q

structure and genome of papilliomavirus

A

naked icosahedral, curcular ds dna

118
Q

where is uncoating of papylomovirus

A

nucleus

119
Q

what is unique about polyomavirus transcritption

A

there are early promoters and late promoters

120
Q

what is an early promoter in transcritpion

A

proteins for replication, regulatory proteins, proteins that alter host cell

121
Q

how does late mrna synthesis work

A

uses same primary transcript with alternative splicing

122
Q

roles of large t antigen

A

dna replication, increased transcription of late genes, decreaased transcription of early genes, cell transformation

123
Q

where is assembly of polyomavirus

A

nucleus

124
Q

how is polyomavirus relesased

A

lysis

125
Q

where does nuclear dna viruses translate mrna

A

cytoplasm

126
Q

structure and genome of adenovirus

A

non enveloped icosahedral, dsDNA. not associated with histones

127
Q

how does adenovirus get in cell

A

endocytosis

128
Q

where does dna get released after uncoating

A

nucleus

129
Q

immediate early and early proteins of adenovirus

A

transcription, dna synthesis, interfere with host anti viral defense

130
Q

where does adenovirus assemble

A

nucelus

131
Q

how is adenovirus different from papillomavirus

A

encodes its own dna polymerase

132
Q

herpes structure

A

enveloped icosahedral, dsDNA

133
Q

how does herpes pentrate the cell

A

fusion, partial uncoating in cytoplasm, fully encoded in nucleus

134
Q

where does herpes replicate

A

nucleus by viral dndp

virology exam 1 (3 decks)

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