exam 2 Flashcards

(134 cards)

1
Q

Example of a DNA virus that replicates in the cytoplasm

A

pox virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

why are cytoplasmic dna viruses more independent

A

don’t rely on cell machinery for replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why do cytoplasmic dna viruses have large genomes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where are the cellular polymerases

A

the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the largest animal virus (other than girius)

A

pox virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why are pox virus morphology complex

A

contains lateral bodies and core

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

vaccinia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

vaccinia is the cousin of small pox virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how many genes does the vaccinia genome have

A

200!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

1st thing to happen in pox virus after uncoating

A

early mrna production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how does pox virus avoid the innate immune response

A

encodes 10 proteins specifically for that (early proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what happens in intermediate transcription

A

make a bunch of mrnas that support last transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what kind of proteins impact the host cell in pox viruses

A

intermediate proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

define IMV

A

intracellular mature virion, brought to golgi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe variola minor

A

mild

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the causative agent of small pox

A

variola virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what type of vaccine is the smallpox vaccine

A

live attenuated vaccinia virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is better for viruses, treatment or prevention?

A

treatment is difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

why is antiviral treatment difficult

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is passive antibody therapy
normal human igG fraction, heat treated to destroy viruses. creates serum
26
read in text fig 7.23
27
list 3 complication of passive immunization that limit it from being used commonly
fever, difficulty breathing, skin lesions
28
how could you create a perfect vaccine (3)
evoke b and t cell immunity, will not make patient sick, don't need 100% uptake of vaccine to get immunity
29
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
e
30
what are the two types of traditional vaccines
1. live, attenuated 2. killed, inactivated
31
4 steps to producing attenuated vaccines
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
32
list 6 advantages of live attenuated vaccines
strong immune response, long lasting, cross reactive, low cost, quick immunity, don't require -80 for storage
33
what are some disadvantages of live attenuated vaccines
problem if not properly attenuated, can revert to virulence, not possible with all viruses, not recommended for immunocompromised people
34
Viruses that have lost their ability to cause disease are said to be
attenuated
35
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
d
36
How do you produce inactivated viral vaccines
virus is exposed to denaturing agent that results in lost of inefectivity
37
what is formalin
denaturing agent used in inactivated viral vaccines
38
are inactivated viral vaccines able to replicate
no
39
advantages of inactivated vaccines
sufficient humoral immunity, no mutation, little to no risk if inactivated properly because it won't become virulent suddenly, can be used by immunocompromised
40
disadvantages of inactivated vaccines
less effective than attenuated, not possible for all viruses, boosters needed, higher cost, must be tested in monkies
41
list the 5 new approaches to different vaccines
1. recombinant subunit 2. synthetic peptides, 3. naked dna vaccines 4. live recombinant vector vaccines 5. mrna vaccines
42
what approach produces an entire viral protein from plasmid to illicit an immune response
recombinant subunit
43
what approach produces a peptide to illicit an immune response
synthetic peptides
44
what approach uses plasmid dnas injected that contain a gene encoding a viral antigen of interest
naked dna vaccines
45
what approach inserts an antigen of interest into a safe virus and infect with the hybrid virus to illicit an immune response
live recombinant vector vaccines
46
what approach used mrna coated in a lipid shell
mrna vaccines
47
general procedure for creating recombinant subunit hbv vaccine
grow in yeast, put cloned for heb b surface protein into the yeast plasmid, transform the yeast, isolate surface protein
48
how do you produce naked dna vaccines
purify out genetic material that encodes surface protein, incorporate into dna plasmid, forcefully insert it using gene gun into muscle
49
using a recombinant form of vaccinnia, what virus vaccine is dropped in forests to give immunity to animals
rabies vaccine
50
what virus uses live recombinant vector vaccines using reassortment
flu
51
advantages of recombinant subunit vaccines
cheapily manufactured at large quantities, most very stable, can use for wide variety of viruses
52
disadvantages of recombinant subunit vaccines
delivery is hard, post translational modification can be difficult, poor antigenicity
53
how do edible vaccines work
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
54
what 2 unwanted immune responses might a vaccine cause
th2 immunopathogy (all and adeergic inflamatory response) and ADE (virus uses antibodies to aid in infection)
55
stage 1
animal studies
56
stage 2 phase 1
use healthy volunteers and see if they get sick
57
3 ways to visualize virus particles
electron microscope, transmission em, scanning em, x ray crystallography
58
how does negative staining work
molds around virus particle, reveals cavities and internal structures
59
2 types of animal cell culture
1. continuous/immortalized 2. primary cell culture
60
advantages of immortilized cell lines
powerful tool, drug toxicity testing, antibody production
61
what is continuous cell lines bad to use to study
subtle effects of virus infection, differentiated cell function
62
properties of immortalized cells
immortal, grow quick, aneuploidy(wrong number of chromosomes)
63
what is a primary culture
isolated from embryonic fetal tissue and identical to original tissue
64
properties of primary cells
normal chromosome number, require growth factors, cannot grow in suspension, finite lifetime, may survive in animal
65
examples of cytopathic effect (CPE)
cell rounding, cell lysis/apoptosis, accumulation of virus components at site of assembly
66
what does the plaque assay do
determine how many virion particles you're iteratively adding
67
pfu
dilution factor * number of plaques
68
how many pfu in 1 mL of 10^4 dilution given 33 plaques in .1 mL of 10^4 dilution
330 pfu
69
what is the titer concentration given 33 plaques in .1 mL of 10^4 dilution
33*10^5 pfu/mL
70
expected range of pfu and moi
pfu around 10^7, moi less than 100 pfu/cell
71
diffeerence between em and plaque assay
em counts every particle, plaque assay counts infectious particles
72
hybridization techniques for characterization of viral genomes
northern, southern blot. in situ hybridization
73
Hoow big are rna virus genomes
small about 10k nucleotides
74
why is rna genome so small
don't have proofreading and rna sucks
75
what do both positive and negative rna viruses encode
RdRP
76
which viral genome + or - more closely resembles our rna
+ sense
77
why most - rna viruses encode RdRP
genome is complementary to rna so must copy rna first with RdRP
78
does double stranded mrna viruses package a RdRP
yes
79
which types of rna viruses are non infectious
negative and double stranded
80
what is the initial event in the cell for + sense rna virus
translation
81
what is the initial event in the cell for- sense rna virus
transcription
82
structure of polio and + or - ssRNA
non enveloped icosahedral, +ssRNA
83
how to disinfect for polio
chlorine, hydrochloric acid, heat
84
describe the first steps of the polio infectious cycle
1. virus attaches to PVR 2.binding=conformational change in capsid VP4 3. enters cytoplasm through pore
85
what is unique bout polio translation
cap independent (IRES)
86
how does polio create so many proteins
proteases chop it up
87
how does polio use translation inhibition
degrades initiation factors
88
how does poliovirus assemble
assemble pentamers around rna
89
how is polio released
lysis
90
what is an inclusion body related to polio
naked virions become concnetrated near the site of maturation, leading to lysis
91
what vaccines exist for polio
salk (inactivated trvalent), sabin (attenuated strains). don't use salbin anymore to avoid the risk of vaccine polio
92
roadblocks of polio eradication
contagious, ipv in tropical regions is hard, resistance to mass vax, opv can cause polio
93
structure and genome of rubella
+ssRNA, enveloped helical
94
hcv structure and genome
+ ssRNA, enveloped icosahedral
95
examble of rhabdovirus
rabies virus, vsv
96
how do -ssrna virus get in cell
clathrin mediated endocytosis
97
where does replication occur for -ssRNA viruses
cytoplasm
98
strutcure and genome of paramyxovirus
enveloped helical -ssRNA
99
how does paramyxovirus get in cell
fusion
100
role of neuromididase for virion release
stops virions from sticking to each other or the cell theyre budding from
101
how is flu different in regards to rnps
rnps are brought to the nucleus because it relies on cell machinery
102
how does flu use cap scavenging in transcription
takcell recognizes cap and begins transcriptiones host cap and binds it to biral genome,
103
assembly of flu
nucleocapsidis transported to cytoplasm, all the proteins come, bud through plasma membrane
104
antigenic drift is responsible for...
seasonal strains
105
antigenic shift is responsible for
pandemic strains
106
why is antigenic shift a concern
reassortment with a non human host, get new N and H proteins (viral attachment proteins)
107
which strain of flue is more common in non human hosts
influenza a
108
what is the standard flu vaccine
inactivated
109
structure and genome of flu
helical enveloped, -ssRNA
110
does flu or mumps require a rna primer
flu
111
is flu or mumps nonsegmented
mumps
112
what polymerase replicate and transcribe rna nuclear viruses
DdDP and DdRP
113
why is there a risk of dna nuclar viruses integrating into the host chromosme
replicate in nucleus and have dna genome
114
parvovirus structure and genome
ssDNA, nonenveloped icosahedral
115
distinct characteristics of parvovirus
dependent on host cell cycle, must become ds before transcription
116
parvovirus genetics
2 ORFs, 6 rna species
117
structure and genome of papilliomavirus
naked icosahedral, curcular ds dna
118
where is uncoating of papylomovirus
nucleus
119
what is unique about polyomavirus transcritption
there are early promoters and late promoters
120
what is an early promoter in transcritpion
proteins for replication, regulatory proteins, proteins that alter host cell
121
how does late mrna synthesis work
uses same primary transcript with alternative splicing
122
roles of large t antigen
dna replication, increased transcription of late genes, decreaased transcription of early genes, cell transformation
123
where is assembly of polyomavirus
nucleus
124
how is polyomavirus relesased
lysis
125
where does nuclear dna viruses translate mrna
cytoplasm
126
structure and genome of adenovirus
non enveloped icosahedral, dsDNA. not associated with histones
127
how does adenovirus get in cell
endocytosis
128
where does dna get released after uncoating
nucleus
129
immediate early and early proteins of adenovirus
transcription, dna synthesis, interfere with host anti viral defense
130
where does adenovirus assemble
nucelus
131
how is adenovirus different from papillomavirus
encodes its own dna polymerase
132
herpes structure
enveloped icosahedral, dsDNA
133
how does herpes pentrate the cell
fusion, partial uncoating in cytoplasm, fully encoded in nucleus
134
where does herpes replicate
nucleus by viral dndp