Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Virology Michelle > Exam One > Flashcards

Exam One Flashcards

1
Q

Virion

A

complete extracellular infective form of a virus

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

Virus

A

includes the virion of inactivated virus particle, or viral nucleic acid and protein in the infected cell

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

Viriod

A

infectious particle smaller than viruses, agent of some plant dzs

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

Where will viral attachment proteins be found

A

envelope or capsid (if the virus is naked)

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

Nucleocapsid

A

nucleic acid + capsid

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

Incomplete virion

A

empty capsid

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

Defective virus

A

Can’t replicate due to mutations or errors, needs helper virus

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

Episome

A

extra-chromosomal genetic element

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

Provirus

A

viral DNA is integrated into host cell chromosome (can be transmitted to daughter cells)

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

Cubic Symmetry/Icosahedral

A

12 corners/verticies, 20 facets (triangula faces and 30 edges.

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

Helical structure

A

capsomeres + nucleic acids self-assemble, impossible for incomplete virions to form (all helical viruses are enveloped)

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

Complex structure

A

Made up of several parts w/ seperate shapes and symmetries. Think Pox Virus

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

Capsid functions

A 
structural symmetry
nucleic acid production
attachment of naked viruses
contains enzymes (reverse transcriptase)
Detemines antigenic characteristics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is the envelope/lipid bilayer acquired?

A

budding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do Glycoprotein peplomeres/spikes do?

A

receptor binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do fusion proteins do?

A

Viral entry/release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do matrix proteins do?

A

recognition site and add rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How can the lipid bilayer be disrupted?

A

Drying, acid, heat
Solvents (ether or chloroform)
Detergents (sodium deoxcholate)

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

T/F all viral genomes are haploid

A

true, only contain 1 copy of each gene

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

Monopartitie

A

all genes in 1 choromosome (all DNA viruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Multipartitie/segmented

A

genes distributed among several chromosomes and can undergo genetic reassortment

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

Which sense RNA strand is infectious if injected into host cell? (+/-)

A

+

- sense RNA not infectious

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

Which is more stable, naked or enveloped viruses?

A

Naked

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

Viral proteins are denatured at what temp?

A

55-60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

T/F acid leads to reversable dissassembly of the capsid

A

F, can also be irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hematogenous spread/Viremia

A

Virus reaches bloodstream via lymphatics or direct innoculation and replicates in endothelial cells or subepithelial blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Passive viremia

A

direct innoculation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Active viremia, primary

A

progeny viruses released from initial site of infection into the blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Active viremia, secondary

A

Release of the virus from a localized area of secondary multiplication of the virus in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cell associated viremia

A

viruses not cleared by Ab and tend to cause prolonged viremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How can viruses be transported via neural spread?

A

axons
endoneural space
perineural lymphatics
infected Schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Centripedal movement

A

towards the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Centrifugal movement

A

CNS to body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Macule

A

flattened, red and inflammed, virus replicating in the dermis noninfectious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Papule

A

raised and reddened, local inflammation, noninfectious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Vesicle

A

fluid filled and raised, contains infectious virions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pustule

A

Pus filled vesicle, can lead to scar formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Infection of the GIT causes

A

enteritis, diarrhea, usually infect undifferentiated cell of villi
rapid destruction of enterocytes then replacement by cubiodal cells (self limiting infections)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Viral infectious of Resp tract can cause

A

Ciliostasis
Loss of mucus layer
Destruction of epithelial cells
Depressed alvelor macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Neurotropic viruses cause

A

neuronal necrosis
nonsupprative encephalitis
perivascular infiltration of mononuclear cells (perivascular cuffing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Infection of vascular epithelium leads to

A

activation of intrinisic pathway of clotting
edema and petechial hemorrhage
Disseminated Intravascular Coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

T/F Most viral infections of the dam have no effect on the fetus

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Inapparent Viral Infection

A

Doesn’t cause noticeable illness

Most viruses are this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Acute viral infection followed by clearance

A

Short clinical course, virus cleared by host immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Persistant infections

A

Host immune response can’t clear the virus

carrier animals can continouly or intermitently shed the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Persistant infection type I

A

virus persists in a non infective form with intermitent periods of reactivation and shedding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Persistant Infection Type II

A

Chronic infection
Virus continually shed
host immune system can’t eliminate the virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Persistant Infections Type 3

A

Slow infections, prolonged incubation periods

slow, progressive lethal dz (think prions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Cytopathic effect

A

Virus damage/death to host cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Inclusion bodies

A

Intracellular structures produced in cells by some viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Proto-oncogenes

A

Code for proteins that control normal cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Oncogenes

A

genes coding for transformation of normal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Tumor suppresor genes

A

genes that code for proteins that control cell proliferation, arrest in G1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Rb protein

A

stops entry into S phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

unphosphorylated Rb protein

A

active- stops replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

phosphorylated Rb protein

A

inactivates- replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

p53

A

arrests cell cycle and apoptosis when cell is damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Oncogenic viruses

A

Mostly DNA viruses

Usually integrate into host genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Lysins

A

hydrolytic enzymes that cleave cell walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Retroviral integrase

A

enables retrovirus genome to be integrated into host DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Reverse transcriptase

A

generate cDNA from RNA template

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Nucleic acid polymerase

A

viral genome replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Neuraminidases

A

cleaves glycosidic bonds allowing release of viruses from host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Antigenic drift

A

point mutations within genes that code for antibody binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Silent mutation

A

no change in a.a.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

nonesense mutation

A

stop codon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

missense mutation

A

change in aa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Genetic recombination

A

exchange of nucleotide sequences between 2 viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Genetic reassortment

A

Exchange of genome segments b/w related

viruses (happens faster than recombination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Defective interfering mutants

A

deletion mutation, lacks one or more functional genes needed for virus replication
Need help of wild type virus, can be persistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Viral interference

A

multiplication of virus is inhibited by an infective virus already in the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Pseudotype

A

related viruses infect the same cell and they swap genomes in their capsids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Pseudovirion

A

capsid encloses host nucleic acid, look like normal viruses but cannot replicate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is a primary monolayer?

A

Cells taken directly from humans/animals
Heterogenous/Same chromosome #
Max 20 subcultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is a diploid cell line?

A

single cell type derived from human embryonic tissue or subcultures of a primary culture.
Can be subcultured 100 timesq

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is a continuous/immortal cell line?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How do you prepare a monolayer?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How do you prepare from Rapid Cell Culture System

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What grows on CAM

A

herpes and pox viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the color change in Growth medium?

A

Phenol red turns orange with cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Virus Titration

A

quantitative determination of viral activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Virus Titer

A 
# of infectious units/ml of sample
lowest concentration of virus that still infects cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Physical Quantification

A 
measures the exact # of virus in sample
TEM
Flow cytometry (virus counter 2100)
Hemagglutination assay- Ag conc
PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Biological Assay- Monolayer Plaque Assay

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Biological Assay- Pock Assay

A

Titration of viruses on the CAM of the chick embryo, pock forming units/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Biological Assay- Transformation Assay

A

Same as monolayer but for oncogenic visues
Viruses transform cells so that they lose contact inhibition, observe mound (focus) of cells
focus forming units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Quantal Assay

A

No number only presence or absence of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

TCID50

A

tissue culture infectivity dose

89
Q

ELD50

A

Embryo lethal dose

90
Q

PD50

A

Paralytic dose

91
Q

Permissive Cell

A

productive infection in cell, virus hijacks cell machinery to replicate

92
Q

Non-permissive cell

A

non productive infection, virus can’t replicate

93
Q

Multiplicity of infection

A

of infectious viruses inoculated per cell

94
Q

Eclipse period

A

time b/w uncoating and appearance of first progeny virions inside cells

95
Q

Latent period

A

time from uncoating to just prior to the first release of viruses outside cells (for enveloped viruses- eclipse=latent period)

96
Q

Burst size

A

height of curve= # of virions released

97
Q

Where do most DNA viruses replicate?

A

Nucleus

98
Q

Where do most RNA viruses replicate?

A

cytoplasm

99
Q

In virus replication, how to viruses attach to a host cell?

A

VAPs bind to receptors on host cells

100
Q

Ways a virus can have trouble with attachment

A

Abs can bind to VAP

Virus doesn’t have VAP to fit cell receptors

101
Q

Explain virus penetration via receptor mediated endocytosis

A

Virions move into clathrin coated pits which form vesicles and fuse with lysosomal vesicles to form endosomes

102
Q

How are enveloped viruses released from the endosome in receptor mediated endocytosis?

A

acidic enviroment in endosome

103
Q

How are naked viruses released from endosome in receptor mediated endocytosis?

A

virion surface proteins are activated at low pH causing lysis of endosome and release of nucleocapsid

104
Q

Explain virus penetration via surface fusion

A

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
Q

Explain virus penetration via pore mediated

A

non enveloped viruses inject their genome into the host cytoplasm by making a pore in the host cell membrane

106
Q

Explain virus penetration via antibody mediated

A

Viruses infect wbc’s, Ab binds to the virus and WBC engulfs the virus resulting in infection

107
Q

What is virus uncoating?

A

Seperation of viral nucleic acid from envelope/capsid
Point at which the virus loses infectivity
(Enveloped viruses begins simultaneously with penetration)

108
Q

When in the virus replication cycle will the virus not be detected?

A

Eclipse period

109
Q

What does mRNA need for transcription?

A

5’ cap for stabilization and alignment on ribosomes

Poly A tail for signal transport and binding to ribosome

110
Q

Polycistronic translation of proteins

A

one gene codes for a polyprotein and with protease makes more than one functional protein

111
Q

Monocistronic translation of proteins

A

one gene codes for one protein

112
Q

What enzymes are required for replication of viral DNA

A

helicase, ssDNA binding proteins, DNA polymerase, DNA ligase

113
Q

dsDNA what type of replication?

A

semiconservative

114
Q

ssDNA what type of replication?

A

needs replicative intermediate

115
Q

Retroviruses need ______ for replication

A

DNA intermediate

116
Q

What % of virions are infectious?

A

1-10%

117
Q

How are naked viruses released?

A

lysis

118
Q

How are enveloped viruses released?

A

bud from plasma membrane, ER, golgi, or nuclear membranes

119
Q

Type I Viral Spread

A

Extracellular

Most common

120
Q

Type II Viral Spread

A

Intercellular
Spread through desmosomes after cell fusion
Usually persistent infections

121
Q

Type III Viral Spread

A

Nuclear

Viral genome is integrated into host genome, replicated and passed on to daughter cells

122
Q

How are mucous membranes defended?

A

IgA and virucidal proteins

123
Q

What are some protective mechanisms of the GIT

A

HCl, proteolytic enzymes, bile salts

124
Q

What is the most common portal of entry for viruses?

A

Respiratory tract, via aerosol (coughing/sneezing)

125
Q

What defends the Respiratory tract from viral infection?

A

Mucocilliar apparatus and cooler temp of URT

126
Q

Local spread

A

on epithelial surfaces at site of entry->infect neighboring cells

127
Q

Subepithelial invasion and lymphatic spread

A

virus breaches the basement membrane and reaches lymph nodes

128
Q

Hematogenous spread/Viremia

A

Virus reaches bloodstream, presence of virus in bloodstream

129
Q

Passive viremia

A

direct inoculation into bloodstream

130
Q

Active viremia (primary)

A

progeny viruses released from initial site of replication to blood stream

131
Q

Active viremia (secondary)

A

release of virus from localized area of secondary multiplication of the virus in the bloodstream

132
Q

Which causes a longer viremia, free in plasma or cell-associated?

A

Cell Associated

Free in plasma is neutralized by ab

133
Q

How can viruses have neural spread?

A 
Transported 
in axons
endoneural space
perineural lymphatics
infected schwann cells
134
Q

Centripedal movement

A

towards brain

135
Q

Centrifugal movement

A

CNS to body

136
Q

How are most viruses spread to the CNS?

A

Viremia

137
Q

Rash

A

temporary skin eruption

138
Q

Macule

A

flat and reddened, virus replicating in the dermis + host inflam respons, noninfectious

139
Q

Papule

A

raised and reddened, local inflam, noninfectious

140
Q

Vesicle

A

fluid filled and raised, infectious

141
Q

Pustule

A

pus filled vesicle, neutrophils, can lead to ulceration/scab formation

142
Q

Where do GIT viruses normally infect? What is the result?

A

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
Q

Viral infection of resp tract can cause

A

ciliostasis
loss of mucus layer
destruction of epithelial cells
depressed alveoloar macrophages

144
Q

Neurotopic viruses cause

A

neuronal necrosis
nonsuppurative encephalitis
perivascular infiltration of mononuclear cells (perivascular scuffing)

145
Q

Infection of endothelium leads to

A

activation of intrinsic pathway of clotting
edema and petechial hemorrhage
DIC (disseminated intravascular coagulation)

146
Q

T/F most infections of the dam have no harmful effect on the fetus

A

t

147
Q

Inapparent viral infection

A

asymptomatic, doesn’t cause noticeable illness

most viruses fall under this category

148
Q

Acute viral infection

A

followed by viral clearance

short clinical course, virus cleared by immune system

149
Q

Persistant Infection Type 1

A

Latent infection
virus persists in a a noninfectious form with intermittent periods of viral reactivation and shedding
Viral genome maintained in the cell

150
Q

Persistant Infection Type 2

A

Chronic infection
Virus continually shed
Immune system can’t eliminate the infection

151
Q

Persistant Infection Type 3

A

Slow infection
prolonged incubation period
Slow progressive lethal dz
(think prions type dz)

152
Q

Cytopathic effect

A

damage/death to host cell

usually secondary effect, host can’t keep up w/ metabolic needs

153
Q

Noncytocidal viruses

A

don’t cause immeadiate host cell death

often cause persistant infections

154
Q

Inclusion bodies

A

intracellular structures produced in cells infected by some viruses, can be pathognomonic

155
Q

Proto-oncogenes

A

gens coding for proteins that control normal cell growth

156
Q

Oncogene

A

gene coding for proteins that transform normal cells

157
Q

Tumor suppressor genes

A

encode proteins that inhibit cell proliferation

holds cell at G1

158
Q

Rb protein

A

stops entry into S phase

159
Q

When phosphorylating Rb protein

A

inactivates it- replication

160
Q

When unphosphorylating Rb protein

A

active- stops replication

161
Q

p53 protein

A

arrests cell cycle and apoptosis when DNA is damaged

162
Q

Oncogenic viruses

A

only dna viruses

integrate into host cell genome

163
Q

permissive cells

A

allow viruses to complete its replication cycle

164
Q

non-permissive

A

virus can’t replicate, viral proteins end up causing transformation of host cell

165
Q

Acute transforming viruses v-onc +

A

host cell proto-oncogene incorporated into viral genome= defective virus, can’t replicate

166
Q

Chronic transforming viruses v-onc -

A

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
Q

What are some characteristics of transformed cells?

A

spindle shaped
lose contact inhibition
express tumor antigens in cell membrane (FOCMA)

168
Q

Type 1 Interferons

A

no viral specificity
stable at pH 2
Stimulate production of MHC1 protems and proteosome proteins
IFNa and IFNb

169
Q

IFN a secreted by

A

virus infected leukocytes (macrophages)

not host specific

170
Q

IFN-b secreted by

A

virus infected fibroblasts and epithelial cells

host species specific

171
Q

Type 2 IFN

A

IFN-y
labile at pH 2
Host specific
Enhances expression of MHC 1 and 2

172
Q

IFN-y secreted by

A

stimulated T and NK cells

173
Q

Type 3 IFNs

A

IFN gamma 1,2,3

immunoregulation

174
Q

Internal viral ag stimulate ________response

A

cell mediated

175
Q

Surface viral Ag stimulate _________response

A

humoral (ab) + cell mediated

176
Q

Viruses provoke what immune cells?

A

lymphocytes and monocyte/macrophages

177
Q

During what stage of virus infection are Ab effective?

A

extracellular stage

178
Q

Ab virus neutralization

A

inhibits viral attachment, penetration or uncoating

179
Q

Viral ab opsonization

A

coat virions w/ IgG- phagocytozed by macrophages

180
Q

Ab against viruses can

A

clump viruses
activate complement
ADCC

181
Q

What is the major mechanism for virus infected cell destruction?

A

Cytotoxic T cells, recognize MHC1 proteins w/ viral Ag

182
Q

Antigen multiplicity

A

ag w/ little-no cross reactivity

183
Q

Antigen plasticity

A

rapidly changing surface antigens

184
Q

T/F Most RNA viruses replicate w/i the cytoplasm of infected host cells

A

true

185
Q

t/f ether decontaminated naked viruses

A

false

ether breaks down lipid but not capsid

186
Q

Which viruses have a double layered capsid?

A

Reoviruses

187
Q

According to Baltimore classification, DNA +/- without reverse transcriptase is

A

Class I

188
Q

According to the Balitmore System, DNA + w/o reverse transcriptase is

A

Class II

189
Q

According to the Baltimore Sytems, RNA +/- w/o reverse transcriptase is

A

Class III

190
Q

According the Baltimore system, RNA + w/o reverse transcriptase

A

Class IV

191
Q

According the Baltimore system, RNA - w/o reverse transcriptase

A

Class V

192
Q

According the Baltimore system, RNA + w/ reverse transcriptase

A

Class VI

193
Q

According the Baltimore system, DNA +/- w/ reverse transcriptase

A

Class VII

194
Q

ICTV System suffix for Order

A

virales

195
Q

ICTV System suffix for Family

A

viridae

196
Q

ICTV System suffix for Subfamily

A

viridae

197
Q

ICTV System suffix for Genus

A

virus

198
Q

What is Rate Zonal Centrifugation

A

sample is layered on a density gradient (sucrose). Particles of different sizes sediment as discrete bands

199
Q

What is Isopycnic Centrifugation

A

Particles are seperated by Buoyant Density (object has same density of fluid)

200
Q

What is the Isopycnic point?

A

point at which the buoyant density of a partcle=surrounding density of gradient medium (sucrose of cesium chloride)

201
Q

What is high performance liquid chromotography

A

quantification through UV

202
Q

What is single radial immunodiffusion?

A

radial diffusion of purified viral ag and viral particles through agarose gel s/ polyclonal antisera against viral ag

203
Q

How do you determine the titer

A

avg plaque count x reciprocal of the dilution selected

204
Q

Transformation assay

A

quantification of oncogenic viruses, focus forming units

205
Q

How do you calculate the TCID using Reed Munch eq

A

% infection above 50%-50%/infection above 50%-infection below 50%
Add the answer to the dilution next above 50%
Titer = answer/0.1mL

206
Q

Routes of innoculation in eggs

A

o Yolk Sac
o Allantoic Cavity
o Amniotic Cavity
o Chorioallantoic Membrane

207
Q

Typical ELISA

A

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
Q

Direct ELISA

A

Ag immobilized, enzyme conjugated primary ab are used to detect/quantify ag conc. Specificity of primary Ab important.

209
Q

Indirect ELISA

A

o Primary Ab not labeled, but detected instead w/ enzyme conjugated secondary Ab that recognize the primary Ab.

210
Q

Sandwich ELISA

A

Ag bound between a layer of capture Ab and a layer of detection Ab.

211
Q

Competitive ELISA

A

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
Q

Direct Flurescence Ab test

A

labeled Ab are added to Ag. Fluorescence appears at binding sites.

213
Q

Indirect Flurescence Ab test

A

secondary Ab labeld with fluorescent marker that recognizes the primary antibody bound to ag.

214
Q

Immunohistochemistry

A

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
Q

Immunochromotography

A

o Point of care test, can be done in hospital. Ex- pregnancy test. Control band binds anti-antibodies

216
Q

Complement fixation test

A

serum w/ ab binds to ag- no lysis is positive. RBCs lysed is neg

217
Q

Hemadsorption inhibition test

A

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
Q

When is the best time to collect a sample from a patient

A

at the onset of symptoms

Virology Michelle (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions