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virology exam 1 > exam 3 > Flashcards

exam 3 Flashcards

1
Q

define emergence of a virus

A

viral infection whose incidence is humans has increased within the past two decades

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2
Q

list 5 emerging viral diseases

A

hiv, west nile, sars, monkey pox, ebola

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3
Q

Which of the following is (are) reasons why epidemics of infectious organisms continue to occur?
a. continuous evolution of new strains of an organism
b. continuous evolution of new organisms
c. Both a and b are correct.
d. Neither a nor b is correct.

A

c

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4
Q

how do arboviruses spread

A

bites from arthropods (insects)

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5
Q

what type of genome do arboviruses all have

A

rna

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6
Q

west nile virus and yellow fever are examples of what arbovirus

A

flavivirus

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7
Q

name 3 viruses that are classified as arboviruses

A

flavivirus, hantavirus, rift valley fever virus

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8
Q

what accounts for 40-50% of all chronic liver disease

A

hepatitis c virus

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9
Q

how is hcv transmitted

A

blood, needles, std

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10
Q

why is there concern that hcv will be reemerging

A

unknown transmission route, larger reservoir of chronic carriers, significant health risk

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11
Q

give examples of viral factors as an cdc enabling factor

A

evolution (antigenic drift, coinfection)

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12
Q

give examples of human factors as an cdc enabling factor

A

behavior, genetics, age

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13
Q

2 ways coinfection as a viral factor can drive emergence

A

recombination-two viruses infect the same cell and recombine into one (covid)
reassortment-two viruses infect the same host and combine part of each (flu)

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14
Q

list some examples of human factors as an enabling factor for spread of disease

A

human demographics, urbanization, human movement, global economy, occupation

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15
Q

why is close proximity of humans to animals a concern (like free range farming)

A

can lead to viruses crossing the species barrier, potentially leading to reassortment

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16
Q

how can agricultural practices likes deforestation and dam construction lead to emergence

A

exposes farmers to zoonotic diseases, displaced animals

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17
Q

what structural viruses are usually viral contaminant on food due to use of raw human sewage as fertilizer

A

non enveloped icosahedral viruses because they are more stable in the environment

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18
Q

examples of viruses that are viral contaminants on food

A

hep a, noro, enterovirus, rotavirus

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19
Q

list some examples of ecological factors as enabling factors

A

changes in agricultural practices, population movement into new arthropod habitats, travel, livestock transportation

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20
Q

Which of the following contributes to the emergence of new disease
A. rapid transportation systems and the mobility of the population
B. ecological disruption such as loss of predators and/or loss of habitat
C. increased drug usage and sexual promiscuity
D. All of the above can contribute to the emergence of new diseases.

A

D

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21
Q

why won’t some viruses be eliminated

A

-viruses that cause persistent infections, virus that weaken immune system, viruses that have a non human reservoir (like arboviruses)

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22
Q

theory for origin of hiv

A

siv infected chimp was killed for bushmeet, blood entered wounds of hunter, crossed species barrier

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23
Q

how many people has aids killed

A

> 25 million

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24
Q

where is aids most prevalent

A

sub-saharan africa

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25
Q

4 most common ways hiv is transmitted

A

sex, needles, blood transfusions, congenital aids

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26
Q

what happens to cd4 t lympocytes overtime in an hiv patient

A

drops immediately with primary infection, then decreases steadily as you progress towards aids

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27
Q

how does hiv destroy the immune system

A

kills off helper t cells

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28
Q

what is a long term non progressor

A

-infected with hiv but have stable cd4 cells with no symptoms

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29
Q

how can some people be exposed but not infected with hiv

A

mutant co receptor ccr5

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30
Q

what happens if you have a mutant homozygous ccr5

A

no hiv infection

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31
Q

what happens if you have a mutant heterozygous ccr5

A

progress to aids more slowly

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32
Q

what is the theory for where the mutant chemokine co receptor ccr5 originated from

A

mutant ccr5 led to increased survival during small pox outbreaks, and resulted from natural selection

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33
Q

Individuals of genotype CCR5-∆32/ CCR5-∆32 are
A. more susceptible to HIV infection
B. more common in people of European descent
C. more common in people of African descent
D. None of the above

A

B-small pox epidemic in europe in 14th century

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34
Q

why does variola have a secret

A

encodes a protein whose c terminal contains a smallpox virus encoded chemokine receptor

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35
Q

what does the secret domain on variola virus do

A

acts as a chemokine inhibitor, allowing the virus to evade the immune system

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36
Q

what happens if an individual has a defective chemokine receptor for the secret protein

A

resist HIV or variola from evading the immune response

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37
Q

how might a mutation in the chemokine receptor affect the secret domain of variola and viral infection

A

a mutation means that variola cannot bind to the chemokine, therefore not inhibiting it. this means that the immune response will block the infection

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38
Q

what enzyme is packed into retroviruses

A

reverse transcriptase

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39
Q

describe replication of retroviral genome

A

parental rna is reverse transcribed into cDNA, then it is integrated into dna where it uses the host machinery

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40
Q

how do retroviruses transcribe from dna back to rna

A

they bring their own promoters and enhancers

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41
Q

how does the integrated form of retroviruses have more information than genomic rna

A

long terminal repeats-rt starts at u3, transpose over to r, goes all the way down, then goes all the back to u5 (copy and transpose)

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42
Q

what is a provirus

A

integrated dna

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43
Q

if all ltr have termination sequences, how do they not stop at the beginning

A

first termination site is supressed due to secondary structure regions in GAG

44
Q

The HIV virus uses the host cell’s reverse transcriptase to manufacture DNA
True
False

A

False

45
Q

why can’t you use drugs to block translation for hiv

A

it would kill the host because it uses the host cell machienery

46
Q

name 4 targets for hiv antivirals

A

protease inhibitors (blocks it from cleaving to functional proteins, no maturation)
rt inhibitors, entry inhibitors, integrase inhibitors

47
Q

2 types of RT Inhibitors

A

NRTI (inhibits hiv rt) NNRTI (binding non competeitively to rt)

48
Q

what do fusion inhibitors target in hiv

A

blocks fusion of viral gp41

49
Q

name of hiv protease inhibitor

A

saquinavir

50
Q

where does uncoating and rt happen for hiv

A

cytoplasm

51
Q

why was harrt awesome

A

lowered hiv viremia, increased cd4 cells

52
Q

why was harrt bad

A

expensive, people failed to take it correctly, could create resistant mutants if not taken correctly

53
Q

what inhibitors is prep made of

A

nrtis

54
Q

how did covid spread so effectively

A

you can transmit it before you show symptoms

55
Q

what receptor does covid bind to

A

ace-2 in lungs

56
Q

how does covid cause cytokine storm

A

infects cells in the lungs, cytokines released, t cells and macrophages join, positive feedback loop

57
Q

what do monoclonal antibodies do as a treatment for covid

A

block entry into cell by binding to virus

58
Q

types of covid vaccines

A

mrna, inactivated viral vector (janssen), injecting protein from covid, inactive virus

59
Q

how does covid get in cell

A

fusion

60
Q

how does cov make so many proteins

A

ribosomal frameshifting, cleavage of polyproteins (nonstructural), subgenomic rnas (structural)

61
Q

in the latent life cycle of tumor viruses, what is it called when a virus early proteins are expressed that cause cause changes in the properties of host cell

A

virally transformed cell

62
Q

tumor formation results from a failure of regulatory mechanisms which control what boundary in the cell cycle

A

g0/g1 boundary

63
Q

resting phase

A

g0

64
Q

stimulate cell growth, cause cancer when hyperactive

A

oncogene

65
Q

inhibit cell growth, cause cancer when turned off

A

tumor supressor genes

66
Q

dominant or recessive mutation-oncogene, and why

A

dominant, binding is a gain of function, under normal conditions the gene only binds when a signal is recieved to grow but a mutant binds all the time

67
Q

dominant or recessive mutation-tsg, and why

A

recessive, normal gene always binds to control cell cycle, a mutant does not bind and function is lost

68
Q

oncogene transmitted by virus

A

v-onc

69
Q

cellular proto-oncogene

A

c-onc

70
Q

examples of tumor supressor genes

A

rb, p53

71
Q

how does rb control cell cycle

A

binds to e2f to control inappropriate entry into s phase

72
Q

how does p53 control cell cycle

A

stops it if theres damage to the dna

73
Q

what type of virus is rsv

A

retrovirus

74
Q

what happens when a retrovirs has an oncogene instead of its regular gene

A

needs a helper virus for co infecting

75
Q

difference between acute and chronic transforming retroviruses

A

acute has a v-onc, chronic cause cancer on accident

76
Q

difference between cis and trans activation of cellular oncogenes

A

cis happens on the same location, trans can happen on different chromosomes

77
Q

Acutely transforming retroviruses may deregulate cell division by

A. Bringing in a v-onc
B. Insertional mutagenesis
C. Overexpression of a c-onc
D. Destruction of tumor suppressor

A

A

78
Q

Cellular transformation by retroviruses does not involve which of the following events?

A. Expression of a v-onc, which causes deregulated cell growth.
B. The overexpression of c-onc, which causes deregulated cell growth
C. Insertional mutagenesis results in disruption of a cellular tumor suppressor gene.
D. The virus is able to make a DNA copy from its RNA genome using reverse transcriptase, which causes deregulated cell growth.

A

D

79
Q

what type of cell, permissive or non permissive, is more likely to interate into host genome for dna tumor viruses

A

non permissive

80
Q

example of dna tumor virus associated with warts and cancer

A

hpv

81
Q

warts vs cancer of hpv

A

cancer has abnormal differentiation, expresses e6 and e7, genetic damage

82
Q

what does e6 of hpv do

A

degrades p53 so cell does not ever commit apoptosis and there is uncontrolled cell growth

83
Q

what does e7 of hpv do

A

attacks p21 and pRB, releasing e2F to go into s phase

84
Q

hpv genome

A

non enveloped, circular dna genome

85
Q

hpv vaccine

A

empty viral capsid elicits immune response

86
Q

what cancer is adenovirus associated with

A

retinoblastoma

87
Q

e1a and e1b

A

e1a-adenovirus, inactivation of rb function e1b-adeno-blocks activation of p53

88
Q

why does burkitts lymphoma cause cancer

A

translocation to chromosome 14, puts myc gene under the control of a very active promoter

89
Q

Burkitt’s lymphoma is associated with EBV infection. How might this virus promote cell growth, leading to tumor formation.

Herpesviruses tend to cause dsDNA breaks
Translocation of a c-onc
Overexpression of a c-onc
All of the above
None of the above

A

D

90
Q

what does an ideal viral vector look like

A

deliver therapeutic gene, allow good expression, maintain expression, selectively interact with specific tissues

91
Q

what is a concern of using viral vectors and how can we avoid it

A

loss of therapeutic gene expression because virus tries to avoid immune response. add inducible promoter

92
Q

adenovirus as a viral vector advantage

A

effects dividing and non dividing cells

93
Q

adenovirus as a viral vector disadvantage

A

elicits immune response

94
Q

advantage of aav

A

infects dividing and non dividing cells, no negative effects

95
Q

disadvantage of aav

A

needs helper virus, small insert size

96
Q

retroviral vector advantage

A

long term expression, infect non diciding cells

97
Q

retroviral vector disadvantage

A

chronic overexpression, insertional mutagenesis

98
Q

advantage as hsv as a vector

A

potential delivery to neurological tissue, acceps large inserts, latent infection

99
Q

disadvantages of hsv as a viral vector

A

cant replicate in a dividing tumor cell yet

100
Q

vaccinia virus advantage as a vector

A

replicates in cytoplasm so no need to deliver to nucleus, takes the largest genome size

101
Q

ebola genome

A

enveloped, helical

102
Q

how does ebola evade immune response

A

comes on really quickly, virus infects immune cells, cytokine storm damages other cells

103
Q

what mechanism does ebola use to create more proteins

A

frameshifting

104
Q

why is there no interferon response from ebola

A

vp35 binds dsRNA and hides it from RIG-I

105
Q

Ebola is often fatal because the virus kills the host. How does Ebola do this
Blocks the host immune response
Causes a cytokine storm which damages other cells.
Cytokine storm kills endothelial cells which leads to vascular instability/ hypovolemic shock
Patient usually dies before they can make antibodies
All of the above

A

All of the above

virology exam 1 (3 decks)

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