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virology exam 1 > exam 3 > Flashcards

exam 3 Flashcards

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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
4 most common ways hiv is transmitted
sex, needles, blood transfusions, congenital aids
26
what happens to cd4 t lympocytes overtime in an hiv patient
drops immediately with primary infection, then decreases steadily as you progress towards aids
27
how does hiv destroy the immune system
kills off helper t cells
28
what is a long term non progressor
-infected with hiv but have stable cd4 cells with no symptoms
29
how can some people be exposed but not infected with hiv
mutant co receptor ccr5
30
what happens if you have a mutant homozygous ccr5
no hiv infection
31
what happens if you have a mutant heterozygous ccr5
progress to aids more slowly
32
what is the theory for where the mutant chemokine co receptor ccr5 originated from
mutant ccr5 led to increased survival during small pox outbreaks, and resulted from natural selection
33
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
B-small pox epidemic in europe in 14th century
34
why does variola have a secret
encodes a protein whose c terminal contains a smallpox virus encoded chemokine receptor
35
what does the secret domain on variola virus do
acts as a chemokine inhibitor, allowing the virus to evade the immune system
36
what happens if an individual has a defective chemokine receptor for the secret protein
resist HIV or variola from evading the immune response
37
how might a mutation in the chemokine receptor affect the secret domain of variola and viral infection
a mutation means that variola cannot bind to the chemokine, therefore not inhibiting it. this means that the immune response will block the infection
38
what enzyme is packed into retroviruses
reverse transcriptase
39
describe replication of retroviral genome
parental rna is reverse transcribed into cDNA, then it is integrated into dna where it uses the host machinery
40
how do retroviruses transcribe from dna back to rna
they bring their own promoters and enhancers
41
how does the integrated form of retroviruses have more information than genomic rna
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)
42
what is a provirus
integrated dna
43
if all ltr have termination sequences, how do they not stop at the beginning
first termination site is supressed due to secondary structure regions in GAG
44
The HIV virus uses the host cell's reverse transcriptase to manufacture DNA True False
False
45
why can't you use drugs to block translation for hiv
it would kill the host because it uses the host cell machienery
46
name 4 targets for hiv antivirals
protease inhibitors (blocks it from cleaving to functional proteins, no maturation) rt inhibitors, entry inhibitors, integrase inhibitors
47
2 types of RT Inhibitors
NRTI (inhibits hiv rt) NNRTI (binding non competeitively to rt)
48
what do fusion inhibitors target in hiv
blocks fusion of viral gp41
49
name of hiv protease inhibitor
saquinavir
50
where does uncoating and rt happen for hiv
cytoplasm
51
why was harrt awesome
lowered hiv viremia, increased cd4 cells
52
why was harrt bad
expensive, people failed to take it correctly, could create resistant mutants if not taken correctly
53
what inhibitors is prep made of
nrtis
54
how did covid spread so effectively
you can transmit it before you show symptoms
55
what receptor does covid bind to
ace-2 in lungs
56
how does covid cause cytokine storm
infects cells in the lungs, cytokines released, t cells and macrophages join, positive feedback loop
57
what do monoclonal antibodies do as a treatment for covid
block entry into cell by binding to virus
58
types of covid vaccines
mrna, inactivated viral vector (janssen), injecting protein from covid, inactive virus
59
how does covid get in cell
fusion
60
how does cov make so many proteins
ribosomal frameshifting, cleavage of polyproteins (nonstructural), subgenomic rnas (structural)
61
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
virally transformed cell
62
tumor formation results from a failure of regulatory mechanisms which control what boundary in the cell cycle
g0/g1 boundary
63
resting phase
g0
64
stimulate cell growth, cause cancer when hyperactive
oncogene
65
inhibit cell growth, cause cancer when turned off
tumor supressor genes
66
dominant or recessive mutation-oncogene, and why
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
dominant or recessive mutation-tsg, and why
recessive, normal gene always binds to control cell cycle, a mutant does not bind and function is lost
68
oncogene transmitted by virus
v-onc
69
cellular proto-oncogene
c-onc
70
examples of tumor supressor genes
rb, p53
71
how does rb control cell cycle
binds to e2f to control inappropriate entry into s phase
72
how does p53 control cell cycle
stops it if theres damage to the dna
73
what type of virus is rsv
retrovirus
74
what happens when a retrovirs has an oncogene instead of its regular gene
needs a helper virus for co infecting
75
difference between acute and chronic transforming retroviruses
acute has a v-onc, chronic cause cancer on accident
76
difference between cis and trans activation of cellular oncogenes
cis happens on the same location, trans can happen on different chromosomes
77
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
78
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.
D
79
what type of cell, permissive or non permissive, is more likely to interate into host genome for dna tumor viruses
non permissive
80
example of dna tumor virus associated with warts and cancer
hpv
81
warts vs cancer of hpv
cancer has abnormal differentiation, expresses e6 and e7, genetic damage
82
what does e6 of hpv do
degrades p53 so cell does not ever commit apoptosis and there is uncontrolled cell growth
83
what does e7 of hpv do
attacks p21 and pRB, releasing e2F to go into s phase
84
hpv genome
non enveloped, circular dna genome
85
hpv vaccine
empty viral capsid elicits immune response
86
what cancer is adenovirus associated with
retinoblastoma
87
e1a and e1b
e1a-adenovirus, inactivation of rb function e1b-adeno-blocks activation of p53
88
why does burkitts lymphoma cause cancer
translocation to chromosome 14, puts myc gene under the control of a very active promoter
89
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
D
90
what does an ideal viral vector look like
deliver therapeutic gene, allow good expression, maintain expression, selectively interact with specific tissues
91
what is a concern of using viral vectors and how can we avoid it
loss of therapeutic gene expression because virus tries to avoid immune response. add inducible promoter
92
adenovirus as a viral vector advantage
effects dividing and non dividing cells
93
adenovirus as a viral vector disadvantage
elicits immune response
94
advantage of aav
infects dividing and non dividing cells, no negative effects
95
disadvantage of aav
needs helper virus, small insert size
96
retroviral vector advantage
long term expression, infect non diciding cells
97
retroviral vector disadvantage
chronic overexpression, insertional mutagenesis
98
advantage as hsv as a vector
potential delivery to neurological tissue, acceps large inserts, latent infection
99
disadvantages of hsv as a viral vector
cant replicate in a dividing tumor cell yet
100
vaccinia virus advantage as a vector
replicates in cytoplasm so no need to deliver to nucleus, takes the largest genome size
101
ebola genome
enveloped, helical
102
how does ebola evade immune response
comes on really quickly, virus infects immune cells, cytokine storm damages other cells
103
what mechanism does ebola use to create more proteins
frameshifting
104
why is there no interferon response from ebola
vp35 binds dsRNA and hides it from RIG-I
105
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
All of the above

virology exam 1 (3 decks)

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