exam 1 Flashcards
(138 cards)
1
Q
What is penetration by fusion
A
Attachment has envelope associated with plasma membrane of the host. plasma membrane fuses to lipid envelope
2
Q
2 types of penetration for enveloped viruses
A
entry via endosomes, fusion with plasma membrane
3
Q
what is entry via endosomes
A
particle brought in via endocytosis
4
Q
acidification to allow for fusion in entry via endosomes is created by
A
proton pumping
5
Q
how does influenza penetrate cell
A
gets inside with receptor mediated endocytosis. all 8 segments of genome go striaght into the cytoplasm. endosome gets close to nuclear pore, uncoats
6
Q
from a one step growth curve where protein comes up first, what type of virus is that
A
positive sense because the rna virus genome can be read into proteins since it looks the same as our rna
7
Q
how long is the infectious cycle of polio (picornavirus)
A
8 hours
8
Q
how long is infectious cycle of herpes virus
A
> 40 hours
9
Q
describe what type of virus polio is
A
+ ssRNA
10
Q
name the 8 basic steps of the infectious cycle
A
attachment/adsorption, penetration, uncoating, replication, genome expression, assembly, release
11
Q
what is adsorption
A
virus develops an attachment protein that can bind to the cell receptor
12
Q
tropism
A
ability of a virus to replicate in particular cells or tissues
13
Q
what two factors control tropism
A
- how the virus gained entry 2. interaction of a virus attachment protein with a specific cell receptor molecule
14
Q
true or false, adsorption is temperature and energy independent
A
true
15
Q
what is the cell receptor for poliovirus
A
ICAM-1
16
Q
why is influenza called a recycling virus
A
it detaches from the cell in a hydrolysis reaction which allows it to leave the cell
17
Q
what are the HIV attachment proteins
A
gp 120 and gp 41
18
Q
how is adsorption different from penetration
A
penetration is energy dependent
19
Q
how does HIV penetrate cell
A
fusion with the plasma membrane
20
Q
how do naked viruses usually penetrate the cell
A
receptor mediated endocytosis and membrane pore formation
21
Q
how does polio penetrate the cell
A
pore formation. vp1 interacts with cell receptor, when ph is low theres a conformational change, virion enters cell
22
Q
name 2 unusual ways naked viruses can penetrate the cell
A
-entry across plasma membrane, -direct puncture of cell membrane
23
Q
purpose of uncoating
A
makes genome available
24
Q
what happens after uncoating
A
degradation of the capsid and genome is transported to site where transcription and replication will occur
25
what two events must occur for a virus to infect a cell
1. synthesis of viral nucleic acid 2. synthesis of viral protein
26
where to dna viruses release their genome to rely on cellular machinery for transcription
nucleus
27
what do + rna viruses encode and package
RdRP, does not package it
28
what do - rna viruses encode and package
RdRP must package it
29
which rna virus looks like our mrna
+ sense
30
example of dsDNA
hsv, adenovirus, human pap
31
describe how ssdna viruses create protein
reverse transcriptase creates dsDNA, dsDNA creates ssRNA intermediate, reverse transcription back in -ssDNA, dna polymerase creates + ssDNA
32
are +ssRNA segmented
no they are unsegmented
33
examples of + ssRNA viruses
poliovirus, west nile, rhinovirus
34
What kind of genome does -ssRNA viruses have
segmented or nonsegmented
35
examples of -ssRNA viruses with nonsegmented genomes
rabies, ebola
36
examples of -ssRNA viruses with segmented genomes
influenza
37
how does HIV replicate
uses dsDNA intermediate, ssRNA is reverse transcribed into dsDNA
38
what is assembly
components are assembled into a particle
39
what stage does a virus become infectious
maturation
40
how do enveloped viruses leave the cell
budding
41
how do non enveloped viruses leave the cell
lysis
42
when does HIV go through maturation
viral protease cleaves budding and matures after leaving cell
43
what happens when a virus damages a cell or kills it
cell death can cause paralysis or death or increase mucus secretion
44
what stage of the infectious cycle is targeted by antiviral intervention
any!
45
what enzymes does chemotherapy often target
nucleic acid polymerase, protease, integrase, neuraminidase
46
what step would be targeted if the antiviral targets polymerases
replication
47
what drugs block were tested to see if they block RdRP during transcription
Remdesivir
48
how does covid penetrate cell
viral host membrane fusion or endocytosis
49
how does covid replicate
creates a -ssRNA with RdRP, transcribes this copy into + RNA
50
what might chloroquine do for covid
blocks cell receptor, might stop endosomal acidification and prevent formation of clathrin complexes
51
how might chemotherapy affect attachment
agents block cell receptors
52
explain how hiv could be blocked at attachment
add extra receptor
53
how might chemotherapy block penetration
block low pH needed for endosome membrane fusion
54
how might chemotherapy block uncoating
block ion transport
55
how might chemotherapy block replication
take advantage of high specificity of polymerases to block reverse transcription
56
example of drug action that blocks replication
azt looks like thymidine and gets incorporated into RT by rna polymerase and then stops transcription
57
what RdRp drug is used against flu
favipiravir
58
what are the targets for the best drugs to treat HIV
block maturation by targeting the proteases that clips the bud
59
how might chemotherapy block release
a neuraminidase can block the release of viral proteins
60
schemes for classifying viruses
host range, tissue infected, mode of transmission. now use basic structure and molecular biology
61
who names viruses
international committee of taxonomy of viruses
62
what are the ictv properties for classifying viruses
1. order 2. family 3. subfamily 4. genus
5. common names
63
Several different criteria have been used to classify a virus. Which of the following is NOT among these criteria.
a. the type of nucleic acid that constitutes the viral genome.
b. the nature of the disease caused by the virus.
c. the metabolic activity of the virus outside of its host cell.
d. the replication strategy of the viral genome.
e. the mode of transmission of the virus.
c
64
why must the skin be breached in order for it to be considered a place of entry
top layers are dead so there is no virus replication in dead cells
65
what kind of inhibitory mechanism prevent viruses from infecting the respiratory tract
cilliated epithelium, mucus secretion, lower temepratre
66
why is the gi tract a difficult place of entry
hostile environment
67
why are the eyes an easy target for viral entry
easy to access and unprotected
68
examples of viruses that enter through the skin
pap virus, HSV
69
examples of viruses that enter through respiratory tract
rhinovirus, coranovirus, flu
70
viruses that infect gastrointestinal tract
rotavirus, norovirus
71
where do viruses most often cause symptoms
at the point of entry
72
define latrogenic induction
infections generated by a physician
73
type of virus that replicates at site of infection
localized infection
74
type of virus that moves to another site in the host
systemic infection
75
example virus of systemic infection
poliovirus, herpesvirus
76
what are 3 mechanisms for spread
bloodstream (viremia), nervous system, lympthatic system
77
how do viruses shed
usually leave through routes of entry
78
what does a productive infection mean
entry into permissive cells followed by virion formation
79
what does abortive infection mean
entry into non permissive cell, does not create virion
80
restringent or restrictive infection means
transiently permissive and some virus is produced
81
what type of infection is HSV
restringent
82
why are persistent infections bad
1. epidemic importance
2. virus reactivation
3. can act as precursor for another disease
4. can cause cancer
83
is rhinovirus persistent or non persistent and why
non persistent, gets completely cleared
84
example of chronic infection
hiv
85
example of slow infection
TSE
86
what does it mean when a virus is in latency
there is no infectious virus present
87
how does HSV latency work
HSV enters epithelial cell, then enters nerve cell, decides to just hang out there
88
describe the model for establishin latency
1.virion attaches and penetrates the neuronal cell
2. loss of tegument proteins on axonal transport
3. enters viral genome by uncoating and circularizes
4. does not transcribe
5. forms chromatin
6. forms latent rna
89
describe how hsv-1 starts as acute infection
1. enters skin cell and uncoats
2. genome enters nucleus
3. viral mrna creates viral genome
4. viral genome repackages and buds out
5. goes up trigeminal ganglion
90
advantages of being in a neuron
1. no good immune surveillance
2 non dividing
3, pathway of axon allows virus to get back to epithileal cells
91
what happens to t cells in aids
they all die
92
what kind of virus is hep b and why is it improtant
dsDNA, chronic human infection
93
3 conditions required for viral persistence
1. infect some host cells without cytopathology
2. mechanism for long term maintenance of viral genome
3. must avoid detection of host defense systems
94
explain what it means for viral persistence to require no viral cytopathology
-infection of non permissive cells
-infection of small number of permissive cells
-infection by virus variant that are less cytopathic
95
explain what it means for viral persistence to require maintenance of viral genome
dna: integration into host chromosome
rna: continuous low level replication
96
explain what it means for viral persistence to require escape from host defense system
-limited viral gene expression to avoid detection
97
Which of the following are required for viral persistence?
a. Infect some host cells without cytopathology
b. Mechanism for long term maintenance of viral genome in host cells
c. Virus must avoid detection by host defense systems
d. All of the above
d
98
what host changes can produce disease
age, immunity, immune supression
99
what viral agent changes can produce disease
survival in environment, mode of transmission, evasion of host immunity
100
what environment changes can produce disease
population density, climate, water
101
what affects severity of infection
1. virus genotype
2. ammount of innoculum delivered to host
3. host immune competence
102
name some physical innate immunity
1. skin
mucous
acid pH
103
describe the virus specificity, time frame, range of effect, and general mode of action of interferons
specificity: non specific
time frame: within minutes or hours
range of effect: localized
mode of action: induce antiviral state to affect protein synthesis
104
describe the virus specificity, time frame, range of effect, and general mode of action of antibodies
specificity: virus specific antiviral
timeframe: 7-10 days
range of effect: systemic
general mode: neutralize virus entry and destroy virus infected cells
105
describe cellular altruism
when virus infects first cell, blocks protein synthesis and stops host from makign the repressor that silences interferon formation. then it sends the interferon signal to neighboring cells.
106
what is considered the inducer for the interferon system
dsRNA (either enters virally like that or is an intermediate during ssRNA replication)
107
what receptors binds to dsRNA to send off signal for interferons
rig-I or mda5
108
how do you create an antiviral state
blcoking translation
109
what 3 pathways create the antiviral state
oligoA intiviral response, PKR, RNAse L
110
how does rnase L contribute to an antiviral state
kills infected cells by apoptosis and destroys viral mrna
111
how does pkr contribute to the antiviral state
inhibits translation by phosphorylating a kinase rgar phosphorylates the initiation factors
112
other examples of non specific defense
nk cells, phagocytes
113
how are nk cells activated
activated by interferons
114
examples of active evasion
adenovirus and hsv
115
what does active evasion do
viral protein mediates blockage
116
what molecule use immunosuppression as active evasion
HIV
117
how does HIV evade the immune response
kills t cells via apoptosis
118
how does ebola avoid the interferon response
virus attaches, penetrates, uncoats. dsRNA is made as replicative intermediate. this should signal interferon response, but vp35 binds to the ds rna and blocks it from rig I
119
how does inhibition of cytokines work for active evasion
inhibits cytokine transcription, translation, and function
120
how does a viroceptor block chemokines in active evasion
-competitively binds to chemokine and blocks signaling
121
how does vck block chemokines in active evasion
mimincs cellular cytokine and blocks cytokine receptor
122
how does vCkBP block chemokines in active evasion
binds to cellular chemokine to stop it from binding to receptor
123
2 types of passive evasion
antigenic drift (mutation accumulate to make changes in the part of rna the immune system recognized), internal sanctuaries
124
name several ways covid evades ifn response
blocks activation of rig-I, inhibits nfkb, blocks a lot. in neighboring cells, blocks transcription factors
125
what type of virus is covid
+ ssRNA
126
structure of covid
enveloped helical
127
VAP and receptor of covid
spike protein and ace2 receptor
128
how does covid produce a lot of proteins
ribsomal frame shifting, polyprotein, subgenomic rna
129
what type of virus is HIV
+ssRNA
130
structure of HIV
enveloped icosahedral
131
what type of virus is VSV
-ssRNA
132
what type of virus is polio
+ssRNA
133
structure of polio
nonenveloped icosahedral
134
how does polio enter the cell
pore formation
135
structure of HSV
enveloped icosahedral
136
what type of virus is flu
-ssRNA
137
all viruses that -ssRNA are what structure
enveloped helical
138
how does flu avoid the immune response
binds to reim25 and stops rig-i from starting interferon response
