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Virology > Exam Dos > Flashcards

Exam Dos Flashcards

1
Q

what did Issacs and Lindenmann demonstrate
what year
what virus did they use

A

normal cells produce antivirals
1957
flu

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2
Q

IFNs are chemical messenger proteins called _____

A

cytokines

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3
Q

how many types of IFNs are there

what are they called

A

3

type 1, 2, 3

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4
Q

why interferon type is described and give examples:

  • antiviral & antitumor activity
  • upregulates immune response
  • antiviral activity
A
  • type 1: IFN-a, IFN-b
  • type 2: IFN gamma
  • type 3: IFN lambda
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5
Q

what is the importance of the Type 1 IFN pathway

A

slows down progression of a viral infection

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6
Q

what are the steps to activating the type 1 IFN pathway

A
  1. gene expression of IFN a/b
  2. IFN a/b bind nearby cellular receptors and trigger 2,5 oligo (A) synthase, ribonuclease, protein kinase
  3. cells are in antiviral state
  4. dsRNA activates oligo and kinase
  5. oligo activates ribonuclease
  6. kinase phosphorylates EIF2-p
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7
Q

are the three enzymes produced by the type 1 IFN pathway initially active

A

no

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8
Q

what happens when protein kinase phosphorylates EIF2-p

A

translation is inhibited for the host and virus

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9
Q

are IFNs a part of the adaptive or innate immune response

A

innate

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10
Q

how long does the viral dsRNA need to be to activate the type 1 IFN pathway

A

at least 30 nucleotides

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11
Q

what are the (2) things that IFNs do

A
  1. directly interfere w/ viral replication in host cells

2. upregulate immune response

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12
Q

more than ____ interferon-stimulated genes w/ direct antiviral activity have been indentified

A

20

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13
Q

what type of kinase is PKR

A

serine and threonine kinase

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14
Q

how have some viruses evolved to avoid the IFN1 pathway

A

bind PKR to inactivate it

bind and sequester dsRNA

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15
Q

how did the first IFN medications go

why

A

poorly!! there were lots of unanticipated side effects

there were contaminants

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16
Q

what did Hans Strander do in 1974

A

treated cancer using purified IFN

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17
Q

what bacteria was used to produce purified IFN

A

E. coli

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18
Q

which populations are most vulnerable to infection

A

the elderly and newborns

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19
Q

what type of immunity do deficiencies and malnutrition affect

A

innate and adaptive

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20
Q

t/f: glucocorticoids can suppress the immune response

A

true

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21
Q

t/f: hormone therapies can lead to an increased risk for viral infections

A

true

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22
Q

____% of population is resistant to HIV

A

5

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23
Q

____ is a key co-receptor for HIV

A

CCR5

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24
Q

what is a normal T helper cell titer

A

1000 Th/uL

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25
Q

what is an hallmark of HIV infections

A

opportunistic infections

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26
Q

why do opportunistic infections happen in the midst of an HIV infection

A

because of decreased immunity by decreased Th cells

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27
Q

what is host range

A

the range of cells that can act as a host for virus

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28
Q

what can lead to species resistance

A

virus-receptor interactions (so viruses can’t bind)

incompatible host factors (don’t support viral replication)

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29
Q

_______ ie (______) immunity protects us against any potential pathogen, regardless of the species or type of microbe

A

nonspecific

innate

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30
Q

Name that immunity:

trapping of viruses by mucus and phagocytes in mucosal tract

A

mechanical immunity

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31
Q

Name that immunity:

engulfing and ingesting viruses infected cells

A

phagocytosis

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32
Q

which cells contain pattern-recognition receptors

A

neutrophils
macrophages
monocytes

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33
Q

what do pattern-recognition receptors recognize on viruses

A

pathogen associated molecular patterns

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34
Q

what is the default setting for Natural Killer cells

what is the end result of invoking NK cells

A

to kill unless told otherwise (ie from normal cells)

death

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35
Q

how do NK cells recognize viral infected cells or tumor cells

A

these cells have a declined expression of certain surface molecules

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36
Q

t/f: viruses cannot trigger apoptosis

A

false!

they sure can

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37
Q

when is apoptosis good during an infection

A

when it happens EARLY in infection bc it limits virus production

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38
Q

how can apoptosis be bad during in an infection

A

it can promote release of the virus if it happens later in the infection

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39
Q

how long does it take for specific immunity to kick in

A

days to weeks

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40
Q

what cells are part of the adaptive immune response

A

antibodies/ b cells

t cells

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41
Q

Identify that antibody:

  • found in blood and tissues, high abundance
  • found in mucous and saliva
  • 1st antibody made which indicates a recent or current infection
A

IgG
IgA
IgM

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42
Q

which antibody typically lasts for a very long time

A

IgG

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43
Q

what 2 ways do antibodies help fight viruses

A

-neutralize by binding free virus
-bridge virus particles together in aggregates for easier elimination via WBC
-

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44
Q

what is the key to controlling viruses BEFORE they infect cells

A

antibodies

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45
Q

when is IgM at its highest concentrations

A

around 10 days-2 wks

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46
Q

when do IgG concentrations spike

A

around 15 days into an infection

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47
Q

____ recognize cells that contain foreign antigens and assist other cells

A

T cells

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48
Q

what are the 3 Tcell populations and what do they do?

A

Cytotoxic (killers)
Helper (release cytokines)
Regulatory (control immune response)

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49
Q

cells that process antigens and present them to adaptive immune cells
give an example!

A

antigen presenting cells

dendrites

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50
Q

list the ways viruses can evade immune response (6)

A
  • rapid mutation to escape neutralizing antibodies
  • latency and mimicry
  • excessive soluble viral antigen production
  • inactivating cytokine signals
  • inactivate immune cells
  • block cellular pathways
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51
Q

Vaccines _____ immunization and (are/ aren’t) the same thing

A

cause

aren’t

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52
Q

what are the 2 traditional vaccines

A

live attenuated

inactivated

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53
Q

what are some of the problems with traditional vaccines (6)

A
  • shelf life limitations
  • low yield
  • improper attenuation/activation
  • reversion of attenuated virus
  • not all can be cultivated
  • not all viruses can be prevented
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54
Q

what are the 4 new generation vaccines

A
  • mRNA
  • protein only
  • DNA vaccines
  • virus vectors
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55
Q

what is a virus vector vaccine

A

a significant gene gets genetically engineered into harmless virus

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56
Q

where do enteroviruses typically grow

A

intestines

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57
Q

what type of genome (big or small; envelope or no; rna or dna) does an enterovirus have
how are they transmitted

A

small, nonenveloped, +ssRNA

oral-fecal route

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58
Q

There are over __ human enteroviruses ___ of which don’t cause disease. ___ of them lead to recognizable associated infectious diseases.

A

70
50
20

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59
Q

which dynasty does polio date back to

A

18th

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60
Q

New York City in what year was one of the worst in recorded history for polio
how many deaths

A

1916

6000

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61
Q

What year did Enders, Robbins, and Welter cultivate poliovirus in human tissue

A

1949

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62
Q

what led to polio vaccine production

A

ability to grow in monkey kidney cells

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63
Q

Was it inactivated or attenuated?
1st polio vaccine?
2nd?

A

inactivated

attenuated

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64
Q

what season does polio cases rise

A

summer months

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65
Q

what is the average incubation period for polio

how long does it last in fecal matter

A

6-20 days

3-6 weeks

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66
Q

___% of polio cases are asymptomatic

A

95

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67
Q

t/f:

polio can be shed in feces and transmitted to others via asymptomatic carriers

A

true

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68
Q

what is a hallmark symptom of polio

A

malaise

69
Q

Less than __% of all poliovirus infections lead to major illness like flaccid paralysis, neuron inflammation and destruction

A

1

70
Q

how long is recovery for major polio illness

A

2 year to never

71
Q

what are the three major illnesses associated with polio

A

spinal
bulbar
bulbospinal

72
Q

Name the major polio illness:
asymmetric paralysis (occurs on one side)
lower paralysis in the legs

A

spinal

73
Q

Name the major polio illness:
muscle weakness
inability to talk or swallow
requires iron lung/respirator

A

bulbar

74
Q

Name the major polio illness:

combination of spinal and bulbar paralysis

A

bulbospinal

75
Q

what kind of pressure does the iron lung create on the diaphragm? what pressure does a respirator use? Why is the iron lung better

A

negative
positive
> natural; less stress on the lungs

76
Q
  1. __ - __ % of post poliomyelitis syndrome occurs in individuals that recover from paralytic poliomyelitis
  2. how long does occur after polio infection on average
  3. more common in men or women
A

25-40
36
women

77
Q

what is the hypothesized cause post poliomyelitis syndrome?

how can it be treated?

A

neurons get infected with polio and degenerate and die over a long time period

manage pain/fatigue and physical and occupational therapy

78
Q

what family is polio a member of

genus?

A

picornaviridae

enterovirus

79
Q 
what size is polio virus genome
\+ or - ssRNA
diameter of virus
what is the virus shape?
enveloped or nonenveloped
A 
7-8 kb
\+
30 nm
icosahedral
nonenveloped
80
Q

t/f: polio is an acid-stable virus

A

true

81
Q

what 3 things can inactivate enteroviruses

A

bleach
hydrochloric acid
heat 50 C or 122 F

82
Q

at what temperature do enteroviruses remain stable for several days to weeks

A

4 C or 39.2 F

83
Q

what 6 things are enteroviruses resistant to

A
  • pH lower than 3
  • protease digestion
  • detergents
  • 70% alcohol
  • lipid solvents
  • disinfectants
84
Q

how is polio grown up in labs (4 steps)

A
  1. isolate from poop
  2. replicated in human or monkey kidney cells
  3. detect changes by noting cytopathic effects
  4. determine which serotype it is using neutralization assays
85
Q

similar structure but has different antigens that are attacked by different antibodies

A

serotype

86
Q

how many polio serotypes are there

how can you tell them apart

A

3

they each have different cytopathic effects

87
Q

what are the natural hosts of poliovirus

A

humans and nonhuman primates

88
Q

what two lymphoid tissues are invaded once polio is ingested

A

peyer’s patches

tonsil

89
Q

where does polio replicate and what secondary infection can it lead to

A

peyer’s patch

meninges and blood

90
Q

how does poliovirus attach to host cells

how does it enter the cell

A

poliovirus receptor- CD155

receptor mediated endocytosis

91
Q

describe the poliovirus genome (5’ end, 3’ end, site for ribosome)

A

VPg
poly A tail
tRNA like structures

92
Q

what are the primary viral capsids for polio

A

VP 1-4

93
Q

which end of the terminal houses the structural proteins and which houses the nonstructural proteins for polio

A

5’

3’

94
Q

what is the primer for replication in polio

A

VPg

95
Q

what organelle does polio replicate in

A

vesicles

96
Q

how does polio avoid the type 1 IFN pathway

A

sequester dsRNA inside vesicles

97
Q

What year Dr. Jonas Salk develop an inactive trivalent vaccine?
How did he grow them?
What did he inactivate it with
oral or injected

A

1953
monkey kidney cells
formalin
injected

98
Q

What year did Albert Sabin develop an attenuated trivalent vaccine?
what was a major concern
oral or injected

A

1957
that it would revert back and cause illness
oral

99
Q

which type of vaccine leads to longer lasting immunity and why

A

attenuated

bc it is a living virus that can still replicate an stimulate immune response

100
Q

how do you attenuate the polio virus

A

passage it through monkey testicular cells or intracerebral passages in rhesus monkeys, isolating it from poop, and feeding it back to them

101
Q

what does the oral polio vaccine have the potential to cause

A

vaccine associated paralytic polio

102
Q

There are four dose periods for the IPV. What are they?

A

2 months
4 months
6-18 months
booster @ 4-6 years

103
Q

what was the unrealized goal of WHO in 1988

A

eradicate polio by year 2000

104
Q

t/f: polio has an animal reservoir

A

false

105
Q

does polio withstand mutations well

A

no, one mutation and it attenuates itself

106
Q

t/f: 3 polio serotypes are genetically unstable

A

false

107
Q

respiratory illnesses account for __-__% of enterovirus associated infectious diseases

A

14-21

108
Q

how many serotypes are there of rhinovirus

A

over 100

109
Q

where is rhinovirus replication restricted to

A

cells in the respiratory tract

110
Q

t/f: IPV is inefficient in preventing viral spread

A

true

111
Q

what genera is rhinovirus found in

A

enterovirus C

112
Q

what is the optimal temperature for rhinoviruses

A

33 C

113
Q

rhinovirus causes ___% of colds

A

50

114
Q

what is the incubation period for rhinovirus

what day can it be transmitted

A

12-72 hours

1 day prior, 5 day post symptoms

115
Q

what genus houses Hepatitis A

what family?

A

Hepatovirus

picornaviridae

116
Q

do rhinoviruses come with a fever

A

no!

117
Q

which hepatitis virus is the least serious

A

A

118
Q 
Tell me about Hepatitis A:
acute or chronic?
how is it transmitted?
contagious or nah?
how is it spread?
incubation period?
is death common? what is the cause typically?
A 
acute
fecal-oral
highly contagious
contaminated food and water or raw shellfish
4 weeks
no, it's rare; preexisting liver disease
119
Q

when can you shed Hep A virus

A

up to 2 weeks

120
Q

what is a hallmark symptom of Hep A

A

jaundice

121
Q 
Name that family:
\+ssRNA
naked
icosahedral
VPg on 5' and poly A on 3'
genus: norovirus
A

caliciviridae

122
Q

what is the genome size for caliciviridae

what is the diameter

A

8 kb

35-40 nm

123
Q

cup or goblet

A

calici

124
Q

what cause 1/2 of food-borne gastroenteritis

*give genus and species

A 
norovirus (genus)
norwalk virus (species)
125
Q

where are the 3 most likely places to catch norwalk virus

A

restaurant
nursing homes
cruise ships

126
Q

what is the incubation period for norwalk virus

when does illness set in?

A

12-48 hours

1-2 days

127
Q 
Name that family:
\+ssRNA
5' cap and poly A tail
enveloped w/ spikes
icosahedral
has 1 genus and 1 species
A

matonaviridae

128
Q

what is the size of the matonaviridae capsid? why

what size is the genome

A

70-80 nm
because it has an envelope
10 kb

129
Q

what is the one genus under the family matonaviridae

species?

A

rubivirus

rubella virus

130
Q

how many copies of the spike protein are found on the surface of matonaviridae viruses
is the spike protein a monomer or dimer

A

3

dimer

131
Q

how is rubella virus transmitted

A

via the respiratory system

132
Q

what is a hallmark symptom of rubella

A

rash starting on face that moves downward via the blood

133
Q

what is a serious complication of rubella virus

when can it cause serious fetal defects

A

congenital rubella syndrome

if contracted during 1st trimester

134
Q

what type of vaccine is MMR

A

trivalent live attenuated vaccine

135
Q

how many orf does polio have

how many does rubella have

A

1

2

136
Q 
Name that family:
\+ssRNA
no poly A tail 
5' cap
enveloped
A

flaviviridae

137
Q

what two genera fall under the family flaviviridae

A

flavivirus

hepacivirus

138
Q

what two species fall under flavivirus

A

dengue virus

zika virus

139
Q

what is the genome size of flaviviridae

virus size

A

10-12 kb

40-60 nm

140
Q

is there a vaccine for dengue fever

how is it controlled

A

nope

control the mosquito populations

141
Q

how much of world is at risk of dengue fever infection

A

1/3

142
Q

how many serotypes are there of dengue fever

A

4

143
Q

t/f: you are safe from the other three serotypes if infected with one serotype of dengue

A

false

144
Q

___% of those who recover from dengue fever get dengue hemorrhagic fever. __% of those people then develop DSS which is fatal.

A

0.05

5

145
Q

why is there no dengue fever vaccine

A

because they enhance infection by contributing to antibody-enhanced uptake of the virus

146
Q

when was the first norwalk virus and where

A

1968

norwalk, ohio

147
Q

when was zika discovered
where
when was the first human case

A

1947
zika forest, uganda
1952

148
Q

what did walter reed discover

A

yellow fever transmitted by mosquitoes while building the panama canal

149
Q

what does flavi mean

A

yellow

150
Q

can zika travel across the placenta

when is it dangerous

A

yes

during the first trimester

151
Q

what is a fetal defect caused by zika

A

microencephaly

152
Q

how is zika transmitted (3)

A

mosquitos
sex
blood transfusions

153
Q

when did zika first appear in the US

when was the biggest US outbreak

A

2015

2016

154
Q

what viral species is found under hepacivirus

A

hepatitis C

155
Q

what was hepatitis C originally called

A

non A-non B hepatitis

156
Q

how is Hep C transmitted

A

blood transfusions/sharing needles

157
Q

in the 1970s what percent of blood transfusions were infected with Hep C. What did it drop to when people stopped getting paid to donate blood.

A

21

10

158
Q

what is the most common reason for liver transplants

A

Hep C

159
Q

what are hallmark symptoms of Hep C

A

dark urine

clay-colored stool

160
Q

Hep C can be short lasting but __ to ___ cases are chronic

A

70-85

161
Q

why is it difficult to make a Hep C vaccine?

can it be treated

A

there are 6 genotypes and several subtypes

yes antivirals

162
Q

what do antiviral treatments target and when should they be taken

A

inhibit viral protease OR inhibit RdRp

early

163
Q

t/f: Hep C antivirals protect against re-infection

A

false; they do not

164
Q

what are the 4 coronavirus genera

A

alpha
beta
delta
gamma

165
Q 
Which genera do I belong to:
229E
NL63
--------------
SARS-CoV 1
COV-2
MERS
OC43
HKU1
A

alpha

beta

166
Q

what are 3 main symptoms of coronaviridae

A

respiratory
enter
neurological

167
Q

what are the 5 structural proteins of coronaviridae

A 
spike
membrane
envelope
nucleocapsid
hemmagglutinin-esterase
168
Q

where does replication take place for rubella virus

A

viral factories in endosome membrane surface

169
Q

TALKING CARD:

discuss rubella virus replication

A

see notes

Virology (5 decks)

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