Exam One Flashcards
(218 cards)
1
Q
Virion
A
complete extracellular infective form of a virus
2
Q
Virus
A
includes the virion of inactivated virus particle, or viral nucleic acid and protein in the infected cell
3
Q
Viriod
A
infectious particle smaller than viruses, agent of some plant dzs
4
Q
Where will viral attachment proteins be found
A
envelope or capsid (if the virus is naked)
5
Q
Nucleocapsid
A
nucleic acid + capsid
6
Q
Incomplete virion
A
empty capsid
7
Q
Defective virus
A
Can’t replicate due to mutations or errors, needs helper virus
8
Q
Episome
A
extra-chromosomal genetic element
9
Q
Provirus
A
viral DNA is integrated into host cell chromosome (can be transmitted to daughter cells)
10
Q
Cubic Symmetry/Icosahedral
A
12 corners/verticies, 20 facets (triangula faces and 30 edges.
11
Q
Helical structure
A
capsomeres + nucleic acids self-assemble, impossible for incomplete virions to form (all helical viruses are enveloped)
12
Q
Complex structure
A
Made up of several parts w/ seperate shapes and symmetries. Think Pox Virus
13
Q
Capsid functions
A
structural symmetry nucleic acid production attachment of naked viruses contains enzymes (reverse transcriptase) Detemines antigenic characteristics
14
Q
How is the envelope/lipid bilayer acquired?
A
budding
15
Q
What do Glycoprotein peplomeres/spikes do?
A
receptor binding
16
Q
What do fusion proteins do?
A
Viral entry/release
17
Q
What do matrix proteins do?
A
recognition site and add rigidity
18
Q
How can the lipid bilayer be disrupted?
A
Drying, acid, heat
Solvents (ether or chloroform)
Detergents (sodium deoxcholate)
19
Q
T/F all viral genomes are haploid
A
true, only contain 1 copy of each gene
20
Q
Monopartitie
A
all genes in 1 choromosome (all DNA viruses)
21
Q
Multipartitie/segmented
A
genes distributed among several chromosomes and can undergo genetic reassortment
22
Q
Which sense RNA strand is infectious if injected into host cell? (+/-)
A
+
- sense RNA not infectious
23
Q
Which is more stable, naked or enveloped viruses?
A
Naked
24
Q
Viral proteins are denatured at what temp?
A
55-60
25
T/F acid leads to reversable dissassembly of the capsid
F, can also be irreversible
26
Hematogenous spread/Viremia
Virus reaches bloodstream via lymphatics or direct innoculation and replicates in endothelial cells or subepithelial blood vessels
27
Passive viremia
direct innoculation
28
Active viremia, primary
progeny viruses released from initial site of infection into the blood stream
29
Active viremia, secondary
Release of the virus from a localized area of secondary multiplication of the virus in the bloodstream
30
Cell associated viremia
viruses not cleared by Ab and tend to cause prolonged viremia
31
How can viruses be transported via neural spread?
axons
endoneural space
perineural lymphatics
infected Schwann cells
32
Centripedal movement
towards the brain
33
Centrifugal movement
CNS to body
34
Macule
flattened, red and inflammed, virus replicating in the dermis noninfectious
35
Papule
raised and reddened, local inflammation, noninfectious
36
Vesicle
fluid filled and raised, contains infectious virions
37
Pustule
Pus filled vesicle, can lead to scar formation
38
Infection of the GIT causes
enteritis, diarrhea, usually infect undifferentiated cell of villi
rapid destruction of enterocytes then replacement by cubiodal cells (self limiting infections)
39
Viral infectious of Resp tract can cause
Ciliostasis
Loss of mucus layer
Destruction of epithelial cells
Depressed alvelor macrophages
40
Neurotropic viruses cause
neuronal necrosis
nonsupprative encephalitis
perivascular infiltration of mononuclear cells (perivascular cuffing)
41
Infection of vascular epithelium leads to
activation of intrinisic pathway of clotting
edema and petechial hemorrhage
Disseminated Intravascular Coagulation
42
T/F Most viral infections of the dam have no effect on the fetus
True
43
Inapparent Viral Infection
Doesn't cause noticeable illness
| Most viruses are this
44
Acute viral infection followed by clearance
Short clinical course, virus cleared by host immune system
45
Persistant infections
Host immune response can't clear the virus
| carrier animals can continouly or intermitently shed the virus
46
Persistant infection type I
virus persists in a non infective form with intermitent periods of reactivation and shedding
47
Persistant Infection Type II
Chronic infection
Virus continually shed
host immune system can't eliminate the virus
48
Persistant Infections Type 3
Slow infections, prolonged incubation periods
| slow, progressive lethal dz (think prions)
49
Cytopathic effect
Virus damage/death to host cell
50
Inclusion bodies
Intracellular structures produced in cells by some viruses
51
Proto-oncogenes
Code for proteins that control normal cell growth
52
Oncogenes
genes coding for transformation of normal cells
53
Tumor suppresor genes
genes that code for proteins that control cell proliferation, arrest in G1
54
Rb protein
stops entry into S phase
55
unphosphorylated Rb protein
active- stops replication
56
phosphorylated Rb protein
inactivates- replication
57
p53
arrests cell cycle and apoptosis when cell is damaged
58
Oncogenic viruses
Mostly DNA viruses
| Usually integrate into host genome
59
Lysins
hydrolytic enzymes that cleave cell walls
60
Retroviral integrase
enables retrovirus genome to be integrated into host DNA
61
Reverse transcriptase
generate cDNA from RNA template
62
Nucleic acid polymerase
viral genome replication
63
Neuraminidases
cleaves glycosidic bonds allowing release of viruses from host cells
64
Antigenic drift
point mutations within genes that code for antibody binding sites
65
Silent mutation
no change in a.a.
66
nonesense mutation
stop codon
67
missense mutation
change in aa
68
Genetic recombination
exchange of nucleotide sequences between 2 viruses
69
Genetic reassortment
Exchange of genome segments b/w related
| viruses (happens faster than recombination)
70
Defective interfering mutants
deletion mutation, lacks one or more functional genes needed for virus replication
Need help of wild type virus, can be persistant
71
Viral interference
multiplication of virus is inhibited by an infective virus already in the cell
72
Pseudotype
related viruses infect the same cell and they swap genomes in their capsids
73
Pseudovirion
capsid encloses host nucleic acid, look like normal viruses but cannot replicate
74
What is a primary monolayer?
Cells taken directly from humans/animals
Heterogenous/Same chromosome #
Max 20 subcultures
75
What is a diploid cell line?
single cell type derived from human embryonic tissue or subcultures of a primary culture.
Can be subcultured 100 timesq
76
What is a continuous/immortal cell line?
capable of indefinite propagation in vitro
derived from tumor cells or by mutating primary or diploid cell lines
Do not resemble cells of origin, abnormal chromosome #
FDA prohibits their use in vaccine production
77
How do you prepare a monolayer?
1. Treat tissue with a protease like trypsin
2. Put in polystyrene container allowing anchorage
dependent growth and add growth medium
3. Incubate at optimal temperature for that species
78
How do you prepare from Rapid Cell Culture System
Rapid Cell Culture System
1.Grow a monolayer on a cover slip of a shell
vial [1-dram]
2.Add the clinical sample to the monolayer and centrifuge
3.Stain the monolayer with horseradish peroxidase or
antibodies to detect the virus
79
What grows on CAM
herpes and pox viruses
80
What is the color change in Growth medium?
Phenol red turns orange with cell growth
81
Virus Titration
quantitative determination of viral activity
82
Virus Titer
```
# of infectious units/ml of sample
lowest concentration of virus that still infects cells
```
83
Physical Quantification
```
measures the exact # of virus in sample
TEM
Flow cytometry (virus counter 2100)
Hemagglutination assay- Ag conc
PCR
```
84
Biological Assay- Monolayer Plaque Assay
Cells are incubated as a monolayer and infected with a virus
Cells are placed in agar and the virus will kill infected cells
Counter stain so cells are clear against a red or purple background
determine titer as plaque forming units/ml
85
Biological Assay- Pock Assay
Titration of viruses on the CAM of the chick embryo, pock forming units/ml
86
Biological Assay- Transformation Assay
Same as monolayer but for oncogenic visues
Viruses transform cells so that they lose contact inhibition, observe mound (focus) of cells
focus forming units
87
Quantal Assay
No number only presence or absence of infection
88
TCID50
tissue culture infectivity dose
89
ELD50
Embryo lethal dose
90
PD50
Paralytic dose
91
Permissive Cell
productive infection in cell, virus hijacks cell machinery to replicate
92
Non-permissive cell
non productive infection, virus can't replicate
93
Multiplicity of infection
of infectious viruses inoculated per cell
94
Eclipse period
time b/w uncoating and appearance of first progeny virions inside cells
95
Latent period
time from uncoating to just prior to the first release of viruses outside cells (for enveloped viruses- eclipse=latent period)
96
Burst size
height of curve= # of virions released
97
Where do most DNA viruses replicate?
Nucleus
98
Where do most RNA viruses replicate?
cytoplasm
99
In virus replication, how to viruses attach to a host cell?
VAPs bind to receptors on host cells
100
Ways a virus can have trouble with attachment
Abs can bind to VAP
| Virus doesn't have VAP to fit cell receptors
101
Explain virus penetration via receptor mediated endocytosis
Virions move into clathrin coated pits which form vesicles and fuse with lysosomal vesicles to form endosomes
102
How are enveloped viruses released from the endosome in receptor mediated endocytosis?
acidic enviroment in endosome
103
How are naked viruses released from endosome in receptor mediated endocytosis?
virion surface proteins are activated at low pH causing lysis of endosome and release of nucleocapsid
104
Explain virus penetration via surface fusion
Only enveloped viruses do this, the viral envelope fuses with the cell membrane via fusion proteins and the nucleocapsid immediately enters the cytoplasm of the cell. Virions can promote fusion b/w adjacent cells= syncytium. Viral proteins stay on the host cell membrane and can be a target for ADCC and complement.
105
Explain virus penetration via pore mediated
non enveloped viruses inject their genome into the host cytoplasm by making a pore in the host cell membrane
106
Explain virus penetration via antibody mediated
Viruses infect wbc's, Ab binds to the virus and WBC engulfs the virus resulting in infection
107
What is virus uncoating?
Seperation of viral nucleic acid from envelope/capsid
Point at which the virus loses infectivity
(Enveloped viruses begins simultaneously with penetration)
108
When in the virus replication cycle will the virus not be detected?
Eclipse period
109
What does mRNA need for transcription?
5' cap for stabilization and alignment on ribosomes
| Poly A tail for signal transport and binding to ribosome
110
Polycistronic translation of proteins
one gene codes for a polyprotein and with protease makes more than one functional protein
111
Monocistronic translation of proteins
one gene codes for one protein
112
What enzymes are required for replication of viral DNA
helicase, ssDNA binding proteins, DNA polymerase, DNA ligase
113
dsDNA what type of replication?
semiconservative
114
ssDNA what type of replication?
needs replicative intermediate
115
Retroviruses need ______ for replication
DNA intermediate
116
What % of virions are infectious?
1-10%
117
How are naked viruses released?
lysis
118
How are enveloped viruses released?
bud from plasma membrane, ER, golgi, or nuclear membranes
119
Type I Viral Spread
Extracellular
| Most common
120
Type II Viral Spread
Intercellular
Spread through desmosomes after cell fusion
Usually persistent infections
121
Type III Viral Spread
Nuclear
| Viral genome is integrated into host genome, replicated and passed on to daughter cells
122
How are mucous membranes defended?
IgA and virucidal proteins
123
What are some protective mechanisms of the GIT
HCl, proteolytic enzymes, bile salts
124
What is the most common portal of entry for viruses?
Respiratory tract, via aerosol (coughing/sneezing)
125
What defends the Respiratory tract from viral infection?
Mucocilliar apparatus and cooler temp of URT
126
Local spread
on epithelial surfaces at site of entry->infect neighboring cells
127
Subepithelial invasion and lymphatic spread
virus breaches the basement membrane and reaches lymph nodes
128
Hematogenous spread/Viremia
Virus reaches bloodstream, presence of virus in bloodstream
129
Passive viremia
direct inoculation into bloodstream
130
Active viremia (primary)
progeny viruses released from initial site of replication to blood stream
131
Active viremia (secondary)
release of virus from localized area of secondary multiplication of the virus in the bloodstream
132
Which causes a longer viremia, free in plasma or cell-associated?
Cell Associated
| Free in plasma is neutralized by ab
133
How can viruses have neural spread?
```
Transported
in axons
endoneural space
perineural lymphatics
infected schwann cells
```
134
Centripedal movement
towards brain
135
Centrifugal movement
CNS to body
136
How are most viruses spread to the CNS?
Viremia
137
Rash
temporary skin eruption
138
Macule
flat and reddened, virus replicating in the dermis + host inflam respons, noninfectious
139
Papule
raised and reddened, local inflam, noninfectious
140
Vesicle
fluid filled and raised, infectious
141
Pustule
pus filled vesicle, neutrophils, can lead to ulceration/scab formation
142
Where do GIT viruses normally infect? What is the result?
ingested viruses normally infect undifferentiated cells of villi. Result in rapid destruction of enterocytes and replacement by immature cuboidal cells that are resistant to viral infection- self limiting infections.
143
Viral infection of resp tract can cause
ciliostasis
loss of mucus layer
destruction of epithelial cells
depressed alveoloar macrophages
144
Neurotopic viruses cause
neuronal necrosis
nonsuppurative encephalitis
perivascular infiltration of mononuclear cells (perivascular scuffing)
145
Infection of endothelium leads to
activation of intrinsic pathway of clotting
edema and petechial hemorrhage
DIC (disseminated intravascular coagulation)
146
T/F most infections of the dam have no harmful effect on the fetus
t
147
Inapparent viral infection
asymptomatic, doesn't cause noticeable illness
| most viruses fall under this category
148
Acute viral infection
followed by viral clearance
| short clinical course, virus cleared by immune system
149
Persistant Infection Type 1
Latent infection
virus persists in a a noninfectious form with intermittent periods of viral reactivation and shedding
Viral genome maintained in the cell
150
Persistant Infection Type 2
Chronic infection
Virus continually shed
Immune system can't eliminate the infection
151
Persistant Infection Type 3
Slow infection
prolonged incubation period
Slow progressive lethal dz
(think prions type dz)
152
Cytopathic effect
damage/death to host cell
| usually secondary effect, host can't keep up w/ metabolic needs
153
Noncytocidal viruses
don't cause immeadiate host cell death
| often cause persistant infections
154
Inclusion bodies
intracellular structures produced in cells infected by some viruses, can be pathognomonic
155
Proto-oncogenes
gens coding for proteins that control normal cell growth
156
Oncogene
gene coding for proteins that transform normal cells
157
Tumor suppressor genes
encode proteins that inhibit cell proliferation
| holds cell at G1
158
Rb protein
stops entry into S phase
159
When phosphorylating Rb protein
inactivates it- replication
160
When unphosphorylating Rb protein
active- stops replication
161
p53 protein
arrests cell cycle and apoptosis when DNA is damaged
162
Oncogenic viruses
only dna viruses
| integrate into host cell genome
163
permissive cells
allow viruses to complete its replication cycle
164
non-permissive
virus can't replicate, viral proteins end up causing transformation of host cell
165
Acute transforming viruses v-onc +
host cell proto-oncogene incorporated into viral genome= defective virus, can't replicate
166
Chronic transforming viruses v-onc -
viruses lack v-onc genes, weakly oncogenic, viral gene promoter/enhancer may be integrated into the host genome near a proto-oncogene- enhanced expression
167
What are some characteristics of transformed cells?
spindle shaped
lose contact inhibition
express tumor antigens in cell membrane (FOCMA)
168
Type 1 Interferons
no viral specificity
stable at pH 2
Stimulate production of MHC1 protems and proteosome proteins
IFNa and IFNb
169
IFN a secreted by
virus infected leukocytes (macrophages)
| not host specific
170
IFN-b secreted by
virus infected fibroblasts and epithelial cells
| host species specific
171
Type 2 IFN
IFN-y
labile at pH 2
Host specific
Enhances expression of MHC 1 and 2
172
IFN-y secreted by
stimulated T and NK cells
173
Type 3 IFNs
IFN gamma 1,2,3
| immunoregulation
174
Internal viral ag stimulate ________response
cell mediated
175
Surface viral Ag stimulate _________response
humoral (ab) + cell mediated
176
Viruses provoke what immune cells?
lymphocytes and monocyte/macrophages
177
During what stage of virus infection are Ab effective?
extracellular stage
178
Ab virus neutralization
inhibits viral attachment, penetration or uncoating
179
Viral ab opsonization
coat virions w/ IgG- phagocytozed by macrophages
180
Ab against viruses can
clump viruses
activate complement
ADCC
181
What is the major mechanism for virus infected cell destruction?
Cytotoxic T cells, recognize MHC1 proteins w/ viral Ag
182
Antigen multiplicity
ag w/ little-no cross reactivity
183
Antigen plasticity
rapidly changing surface antigens
184
T/F Most RNA viruses replicate w/i the cytoplasm of infected host cells
true
185
t/f ether decontaminated naked viruses
false
| ether breaks down lipid but not capsid
186
Which viruses have a double layered capsid?
Reoviruses
187
According to Baltimore classification, DNA +/- without reverse transcriptase is
Class I
188
According to the Balitmore System, DNA + w/o reverse transcriptase is
Class II
189
According to the Baltimore Sytems, RNA +/- w/o reverse transcriptase is
Class III
190
According the Baltimore system, RNA + w/o reverse transcriptase
Class IV
191
According the Baltimore system, RNA - w/o reverse transcriptase
Class V
192
According the Baltimore system, RNA + w/ reverse transcriptase
Class VI
193
According the Baltimore system, DNA +/- w/ reverse transcriptase
Class VII
194
ICTV System suffix for Order
virales
195
ICTV System suffix for Family
viridae
196
ICTV System suffix for Subfamily
viridae
197
ICTV System suffix for Genus
virus
198
What is Rate Zonal Centrifugation
sample is layered on a density gradient (sucrose). Particles of different sizes sediment as discrete bands
199
What is Isopycnic Centrifugation
Particles are seperated by Buoyant Density (object has same density of fluid)
200
What is the Isopycnic point?
point at which the buoyant density of a partcle=surrounding density of gradient medium (sucrose of cesium chloride)
201
What is high performance liquid chromotography
quantification through UV
202
What is single radial immunodiffusion?
radial diffusion of purified viral ag and viral particles through agarose gel s/ polyclonal antisera against viral ag
203
How do you determine the titer
avg plaque count x reciprocal of the dilution selected
204
Transformation assay
quantification of oncogenic viruses, focus forming units
205
How do you calculate the TCID using Reed Munch eq
% infection above 50%-50%/infection above 50%-infection below 50%
Add the answer to the dilution next above 50%
Titer = answer/0.1mL
206
Routes of innoculation in eggs
o Yolk Sac
o Allantoic Cavity
o Amniotic Cavity
o Chorioallantoic Membrane
207
Typical ELISA
Ag in well, Ab tagged with enzyme, Ag binds to enzyme tagged Ab, wash excess unbound Ab, add substrate, enzyme tagged to Ab will change color of substrate. More color=more positive rxn
208
Direct ELISA
Ag immobilized, enzyme conjugated primary ab are used to detect/quantify ag conc. Specificity of primary Ab important.
209
Indirect ELISA
o Primary Ab not labeled, but detected instead w/ enzyme conjugated secondary Ab that recognize the primary Ab.
210
Sandwich ELISA
Ag bound between a layer of capture Ab and a layer of detection Ab.
211
Competitive ELISA
Ag of interest and Purified immobilized Ag compete from binding to the capture Ab. A decrease in signal w/ purified Ag alone indicated presence of Ag in sample.
212
Direct Flurescence Ab test
labeled Ab are added to Ag. Fluorescence appears at binding sites.
213
Indirect Flurescence Ab test
secondary Ab labeld with fluorescent marker that recognizes the primary antibody bound to ag.
214
Immunohistochemistry
Ab tagged w/ enzyme (horserasish peroxidase). Enzyme reacts w a substrate to produce a color you can see w/ a light microscope.
o Direct- Primary enzyme binds to Ag
o Indirect- Enzyme bound to secondary Ab that is specific against primary Ab.
215
Immunochromotography
o Point of care test, can be done in hospital. Ex- pregnancy test. Control band binds anti-antibodies
216
Complement fixation test
serum w/ ab binds to ag- no lysis is positive. RBCs lysed is neg
217
Hemadsorption inhibition test
Glycoproteins are inserted into host cell membrane at sites of budding enveloped viruses. Monolayer cells adsorb RBCs on their cell membranes. Ab bind to glycoproteins, wash excess Ab, incubate monolayer with RBCs, RBC binding is inhibited.
218
When is the best time to collect a sample from a patient
at the onset of symptoms
