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Medical Virology > Module 1 > Flashcards

Module 1 Flashcards

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USMLE® Step 1 flashcards
1
Q

what is a virus?

A

subcellular, infectious agents, consisting of nucleic acid (DNA or RNA) in a protein coat

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2
Q

what is a virus?

A

obligate intracellular parasites

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3
Q

viruses’ one goal

A

to replicate themselves

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4
Q

viruses

A

type of infectious agent

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5
Q

virions

A

individual virus particles

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6
Q

virus delivery system

A

protein coat

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7
Q

virus payload

A

nucleic acid

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8
Q

why do we study viruses?

A

important pathogens, infect all forms of life, transfer genes between organisms to drive evolution, play a large role in ecological, useful for preventing and curing diseases, providing insight to basic mechanisms

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9
Q

virology is a young science

A

around 120 years old, hippocrates rationalized plagues caused by small organisms

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10
Q

viruses are filtrable agent

A

viruses smaller than bacteria passed through filter, weren’t grown on culture but would infect animals

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11
Q

viruses could …

A

diluted and still cause disease, can regain its strength through replicates, can be passed multiple times

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12
Q

viruses fail to propagate in solutions

A

further study hampered by lack of experimental system

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13
Q

Koch’s postulates

A

virus don’t grow on culture so they don’t follow koch’s postulates

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14
Q

poliovirus replication in cell cultures

A

ender, wellers, and robbins propagate poliovirus in human cell cultures in primary embryonic skin

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15
Q

study of viruses has an impact on molecular and cellular biology

A

gene expression, DNA replication, RNA splicing, cellular oncogenes

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16
Q

smallpox eradication

A

1958-1979, first and only human infectious disease to be eradicated

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17
Q

eradication of rinderpest

A

2nd Virus, 2011, eradicated in cattle

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18
Q

generic viral structure

A

nucleocapsid and envelope

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19
Q

nucleocapsid

A

all viruses have a capsid and nucleic acid

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20
Q

envelope

A

viral proteins embedded, some viruses have envelopes

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21
Q

viruses alive?

A

made of the same material as cells, replicate, evolve, some metabolize

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22
Q

viruses dead?

A

do not have cells, cannot reproduce independently, lack ribosomes, do not typically metabolize

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23
Q

viral genome

A

RNA or DNA contains the information needed to initiate and complete an infectious cycle within a susceptible or permissive host cell

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24
Q

where do viruses package their genomes?

A

inside a protein shell

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25
Q

all viruses can establish themselves in a host population, so as to ensure virus survival

A

true

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26
Q

an infectious cycle includes…

A

attachment, entry/uptake, production of viral mRNA and proteins, genome replication and assembly, release of new particles

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27
Q

how common are viruses?

A

most abundant for of “life,” most common thing that replicates

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28
Q

in seawater?

A

10-50 million phage/ml

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29
Q

viruses play a major role in …

A

carbon and oxygen cycles that regulate the atmosphere

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30
Q

how much oxygen is generated by marine microbes through photosynthesis

A

50%

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31
Q

how many marine microbes are destroyed a day by viruses?

A

20%

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32
Q

human body

A

10 trillion cells are products of 23,000 genes

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33
Q

microbiome

A

100 trillion bacteria, viruses, and fungi and 3 million non-human genes

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34
Q

all cells are infected with viruses

A

true

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35
Q

how much of your DNA is made up of old and new retrovirus genomes

A

8%

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36
Q

are retroviruses passed to human offspring

A

yes

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37
Q

everyone has herpes

A

each of you is infected with at least two types of 9 known herpesviruses, once infected you are infected for life

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38
Q

virus characteristics

A

small, DNA or RNA genome, small genome size (3000 nt - 1.2 million bp), genomes associated with protein, only replicate in living cells

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39
Q

virus particle

A

virion capsid alone or capsid and lipid bilayer envelope

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40
Q

how many rhinoviruses can fit on the head of a pin?

A

9.069 billion

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41
Q

mimivirus

A

kind of metabolize, could have been caused by reductive evolution

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42
Q

how many mimiviruses can fit on the head of a pin?

A

2.27 x 10^7

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43
Q

vertebrate viruses

A

RNA genomes outnumber DNA genomes 2 to 1

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44
Q

viral genomes

A

compact/economical, ~1 protein/1000 nt

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45
Q

mammalian genomes

A

~ 3 billion nt, ~ 1 protein/ 100,000 nt

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46
Q

gene products and regulatory signals for replication of the viral genome

A

encoded in viral genomes

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47
Q

gene products and regulatory signals for assembly and packaging of the viral genome (capsid formation)

A

encoded in viral genomes

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48
Q

gene products and regulatory signals for regulation and timing of the replication cycle

A

encoded in viral genomes

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49
Q

gene products and regulatory signals for modulation of host defenses

A

encoded in viral genomes

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50
Q

gene products and regulatory signals to spread to other cells and hosts

A

encoded in viral genomes

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51
Q

genes for complete protein synthesis machinery

A

not encoded in viral genomes

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52
Q

genes for proteins involved in membrane biosynthesis

A

not encoded in viral genomes

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53
Q

classical centromeres or telomeres

A

not encoded in viral genomes

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54
Q

enzyme systems that produce nucleotides, amino acids, carbohydrates and lipids

A

not encoded in viral genomes

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55
Q

metabolic enzyme systems that generate useable chemical energy

A

not encoded in viral genomes

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56
Q

50-90% of virion mass is made up of?

A

protein

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57
Q

capsid variation

A

limited number of particle design

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58
Q

structure of virion functions

A

protects nucleic acid from nucleases, environment, and shearing, contains elements to recognize target cells, built in system for genome release at correct time and location, includes enzymes essential for infectivity

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59
Q

virions are metastable

A

protection of the genome is stable, coming apart for infection is unstable

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60
Q

virus particles are morphologically diverse

A

true

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61
Q

filamentous viruses

A

helical symmetry, nucleic acid core with 1-2 subunit tube

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61
Q

isometric viruses

A

icosahedral symmetry, 20 faces and 3 axes of symmetry

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61
Q

complex viruses

A

maximalist approach to metastability, round shaped

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62
Q

what percentage of virus taxa have icosahedral capsids?

A

60%

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63
Q

icosahedron characteristics

A

largest ratio of volume to surface area, thermodynamically favorable, maximum enclosed volume for shells

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64
Q

why is icosahedral or helical symmetry beneficial?

A

genetic economy and efficiency and greater stability due to symmetrical arrangement

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65
Q

there are a limited number of ways to achieve icosahedral or helical symmetry

A

true

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66
Q

nonenveloped icosahedral

A

animals, plants, bacteria, and vertebrate viruses

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67
Q

nonenveloped helical

A

plants and bacteria viruses

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68
Q

enveloped icosahedral

A

animals, bacteria, and vertebrate viruses

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69
Q

enveloped helical

A

animals, plants, bacteria, and vertebrate viruses

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70
Q

head tail

A

bacteria virus

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71
Q

complex

A

animals and vertebrate viruses

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72
Q

do viruses have enzyme systems that produce nucleotides, amino acids, carbohydrates and lipids

A

no, acquired from host cells

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73
Q

do viruses have enzyme systems that generate useable chemical energy

A

no, acquired from host cells

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74
Q

do viruses have ribosomes, transfer RNA and enzymes needed for protein synthesis

A

no, viruses are completely dependent on host for protein synthesis machinery

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75
Q

do viruses have membranes to localize and concentrate cellular macromolecules (organic and inorganic ions)

A

no, acquire from host cell membranes

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76
Q

animal viruses classified by…

A

replicative strategy, structure, genome, and host

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77
Q

animal virus classification: structure

A

icosahedral, helical, or complex, enveloped or non-enveloped

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78
Q

animal virus classification: genome

A

DNA or RNA, single or double stranded, positive or negative sense

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79
Q

baltimore classification of viruses

A

basis is pathway from genome to early mRNA, viral genomes must make mRNA that can be read by host ribosomes

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80
Q

class I

A

double stranded DNA

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81
Q

class II

A

single stranded DNA transcribed to double stranded DNA

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82
Q

class III

A

double stranded RNA

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83
Q

class IV

A

positive sense single stranded RNA transcribed to negative sense single stranded RNA

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84
Q

class V

A

negative sense single stranded RNA

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84
Q

class VI

A

single stranded RNA-RT transcribed to DNA or RNA then into double stranded DNA

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85
Q
A
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86
Q

class VII

A

double stranded DNA-RT makes RNA copy and retrotranscribed into DNA

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87
Q

?s for baltimore classification

A

is the genome RNA or DNA
is the genome double or single stranded
if ssRNA, is it positive or negative sense
does the virus use reverse transcription

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88
Q

international committee on taxonomy of viruses classification factors

A

range of characteristics, scheme of order, family, subfamily and genus, concept of species is complex and debated

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89
Q

ICTV classification of characteristics

A

virion morphology and size, nucleic acid type, presence or absence of specific genes, host range, and phylogenetic groupings

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90
Q

order suffix

A

-ales

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91
Q

family suffix

A

-idae

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92
Q

subfamily suffix

A

-inae

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93
Q

genus suffix

A

-virus

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94
Q

type member example

A

measels virus

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95
Q

viral phylogeny

A

align viral sequences of related viruses to interpret relationship

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96
Q

viral phylogeny: root

A

presumed ancestor

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97
Q

viral phylogeny: scale

A

number of changes per length of sequence

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98
Q

viral phylogeny: branches

A

lineages

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99
Q

viral phylogeny: clade

A

branch that represents all viruses with a common ancestor

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100
Q

viral phylogeny: tips or leaves

A

individuals sequenced

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101
Q

viral phylogeny: measure of support

A

probability that sequences cluster together better than other sequences

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102
Q

viral phylogeny: nodes

A

ancestors may be inferred

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103
Q

serotype

A

a system of grouping viruses based on the type of surface antigens present

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104
Q

serotyping is generally determined by …

A

reactivity of viruses with antibodies in serum from individuals infected with specific virus isolates, but this is hard to set up

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105
Q

serotype antibody reactivity

A

measured by virus neutralization, ELIZA, and hemagglutination inhibition

106
Q

serotyping and PCR

A

once system is established, PCR can be used due to known coding sequences

107
Q

origin of viruses: virus early hypothesis

A

start small and acquire genes to gain complexity

108
Q

origin of viruses: regression hypothesis

A

start large and loose genes by relying on other cells for resources

109
Q

origin of viruses: escaped genes hypothesis

A

host genes escape and replicate

110
Q

accepted origin of viruses

A

diversification of replicators and replication strategies from ancestral RRM, acquire protocapsid genes by selfish replicators from primitive cells, evolution of modern cells

111
Q

RRM

A

RNA-recognition motif domain

112
Q

did viruses start out as RNA?

A

RNA originally then transition to DNA based world

113
Q

no single progenitor for origin of viruses

A

some retroviruses are 450 million years old, some may have originated billions of years ago before cells

114
Q

once viruses were formed

A

subject to evolutionary pressures through mutation, recombination, and reassortment. the host provides powerful selective pressure

115
Q

what is the viruses main goal?

A

replication

116
Q

do viruses evolve for virulence?

A

no, they evolve for replication

117
Q

anything that occurs during virus infection is…

A

supportive of virus replication, a side effect of virus replication, or a result of host response to virus infection

118
Q

viruses do not _____

A

divide

119
Q

burst size

A

the number of virions produced from infection of a single cell

120
Q

cellular stages of virus replication cycle

A

enter cell and translocate to the site of replication, replicate genome and produce mRNA, generate viral proteins, assemble pyrogeny virus, emerge from cell

121
Q

extracellular stages of virus replication cycle

A

evade host defenses, disperse and persist in the environment

122
Q

virus replication cycle pathway

A

attachment, entry, uncoating, viral genome expression, replication of viral genome, assembly, maturation, release

123
Q

virus fitness

A

a complex property, the replicative ability of a virus to its environment

124
Q

fitness in vitro

A

determined by comparison of growth rates and viral yields

125
Q

fitness in vivo

A

difficult to measure under natural conditions, infection of complex organisms is large interacting populations

126
Q

relative fitness

A

ratio of fitness between two viral variants

127
Q

relative fitness =1

A

fitness is neutral

128
Q

relative fitness <1

A

reduced fitness

129
Q

relative fitness >1

A

increased fitness

130
Q

what kind of population is required for replicative fitness?

A

a stead state equilibrium population with a large number of virions/genotypes

131
Q

virus evolution is driven by

A

genetic variation and environmental selection

132
Q

genetic variation occurs through

A

mutation, recombination, and reassortment

133
Q

environment selection occurs in

A

the cell, the host, and the environment

134
Q

the _____________ of a viral genotype in a given environment determines viral fitness

A

replicative success

135
Q

genetic variation comes from

A

errors in replication of the viral genome

136
Q

high mutation rate

A

increases the amount of genetic variability available for selection

137
Q

mutation

A

an alteration in the nucleic acid sequence of the viral genome

138
Q

large population size

A

increase the probability of the occurrence of an advantageous genetic change

139
Q

short generation time

A

lessens the time required for advantageous genetics to become selected

140
Q

viruses have high mutation rates

A

true

141
Q

mutation rate

A

genetic changes in individual viruses

142
Q

substitution rate

A

genetic changes within a population (selection)

143
Q

PRRSV virus

A

mutation rate not particularly high, disparity between mutation and substitution rate is likely due to selection

144
Q

effects of single base mutations

A

no effect, (most as far as we know)

145
Q

single base mutations: alter animo acid sequence

A

non-synonymous, codon changes, alternate start/stop, splicing

146
Q

nonsynonymous vs synonymous

A

nonsynonymous does not always have greater effects

147
Q

single base mutations: affect transcript abundance

A

promoter efficiency and message stability

148
Q

single base mutations: influence protein translocation/modification

A

codon usage bias, signal sequence, glycosylation, ubiquitination

149
Q

few mutations, nonsynonymous and synonymous, actually increase relative fitness

A

true

150
Q

nonsynonymous mutations are more _____ than synonymous mutations

A

lethal

151
Q

mutations in viral polymerases that reduce the frequency of errors

A

do not have a selective advantage over wild type, lower mutation rates are neither advantageous nor selected in nature, mutants are often less pathogenic

152
Q

high mutations are ____ during virus evolution

A

selected for

153
Q

mutation is _______ for viral population (within limits)

A

good

154
Q

viral recombination and reassortment

A

requires coinfection of a single cell with two different viruses

155
Q

viral recombination requires

A

coinfection of a single cell with 2 different viruses and sufficient sequence homology

156
Q

recombination are generally random but…

A

hot spots may exist and fitness selects successful recombinants

157
Q

genetic drift

A

polymerase errors lead to nucleotide substitution during genome replication, small changes occurring over time, viral coded polymerase generates a lot of copy errors, may be small changes, but can have big impacts due to large number and short life cycle

158
Q

why do NA virus polymerases generate a lot of copy errors?

A

RNA viruses totally lack proof reading activity and have lower fidelity

159
Q

genetic shift

A

large scale changes due to recombination or reassortment of gene segments between two related viruses, big changes over short periods, requires coinfection of a cell with two dissimilar viruses

160
Q

genesis of the 2009 swine influenza A virus (H1N1)

A

multiple reassortment events, involves three host species, four parental viruses, change antigenic phenoytpe, change virulence

161
Q

effect of genetic drift, bottlenecks and founder effects on genetic diversity

A

the smaller a population is, the greater the effect of genetic drift on genetic diversity

162
Q

viral quasispecies are the _____ in RNA viruses

A

norm

163
Q

quasispecies concept

A

virus populations exist as a dynamic distribution of nonidentical, but related replicons called quasispecies

164
Q

the ability to produce a quasispecies may also virus populations to __________ encountered during spread between hosts, within organs and tissues, and ___________

A

respond to the different environments, and respond to the pressure of the host immune response

165
Q

quasispecies provide …

A

an interpretation for the extensive plasticity, both genetic and phenotypic, displayed by many viruses

166
Q

error prone replication leads to formation of …

A

dynamic mutant distributions

167
Q

viral quasispecies develop due to _________ and are shaped by _________

A

errors in replication, selection

168
Q

non tree like patterns are the result of recombination, represented by

A

a closed lip

169
Q

quasispecies: viral infection in a host consists of initiated by a _________ not a single virus genome

A

population of genomes

170
Q

quasispecies: the large number of pyrogeny are the product of _______________

A

selective forces inside the host acting on the population

171
Q

quasispecies: the survivors that can infect a new host reflect _________________

A

selective forces outside the host acting on the population

172
Q

quasispecies wild type

A

a bunch of different genomes

173
Q

quasispecies act as ________ of mutants for selection to act upon

A

a phenotypic pool

174
Q

quasispecies have _____ and have a record of past genome dominances, ready to readapt to previously experienced selective pressures

A

memory

175
Q

quasispecies memory is reduced by …

A

bottlenecks

176
Q

quasispecies members ______ within the swarm

A

interact

177
Q

how do quasispecies members interact?

A

cooperation, complementation, and interference

178
Q

survival of the fittest

A

a rare genome with a particular mutation may survive a selection event, and this mutation will be found in all pyrogeny genomes

179
Q

survival of the survivors

A

linked but unselected, mutations get a free ride

180
Q

the product of selection after replication is a …

A

new diverse population that shares the selected and linked mutations

181
Q

hepatitis C virus passage in a constant environment

A

mutations accumulate in the population over time

182
Q

dominant

A

high frequency in the virus population

183
Q

frequency of individual mutations in the virus population

A

some persist, others come and go, dynamic

184
Q

error threshold

A

mutation is advantageous but selection and survival balances genetic fidelity and mutation rate

185
Q

error threshold

A

the tipping point between mutation rate and survival

186
Q

exceeding the error threshold results in

A

loss of infectivity, “death”

187
Q

Too far below the error threshold results in

A

viruses inability to produce enough mutations to survive selection

188
Q

RNA viruses evolve ________ the error threshold

A

close to

189
Q

DNA viruses evolve _______ the error threshold

A

far below

190
Q

viruses must achieve a ________

A

balance between mutation and error threshold

191
Q

antiviral ribavirin and poliovirus

A

ribavirin is a guanosine nucleoside analog used to stop viral RNA synthesis and viral mRNA capping. Pairs with uracil or cytosine, including mutations in RNA dependent replication

192
Q

recombination ______ error catastrophe

A

counters

193
Q

poliovirus RdRp L420A

A

recombination defective, exacerbates ribavirin induced error catastrophe, recombination required to counter error catastrophe, reassortment may also accomplish in other viruses

194
Q

reduced bottlenecks

A

causes the accumulation of mutations exceeding error threshold leads to decreased replicative fitness

195
Q

mutations that improve replication lead to

A

increased replicative fitness

196
Q

repeated bottlenecks lead to

A

accumulation of deleterious mutations leading to decreased replicative fitness

197
Q

muller’s ratchet

A

small asexual populations decrease in fitness over time if the mutation rate is high, mutations that exceed the error threshold accumulate during replication and fitness decreases

198
Q

why is fitness reduces?

A

muller’s ratchet, replicating RNA viruses producing many mutations close to the threshold, restricting population growth to serial single founders under otherwise nonselective conditions, so many mutations accumulate exceeding the threshold that decrease fitness

199
Q

sequence space

A

refers to every possible combination of a give sequence

200
Q

sequence space is theoretically a

A

vast multidimensional hypercube connecting all possible combinations

201
Q

sequence space for 400 bases with 4 alleles

A

4^400 = 7 x 10^240 different genotypes

202
Q

fitness landscapes

A

systemic fitness and sequence space

203
Q

fitness landscapes: peak

A

higher rate of survival, will be present in the quasispecies, evolve

204
Q

most changes in genome are …

A

not beneficial

205
Q

fitness

A

the likelihood of a gene, organism, or other unit of study to make it into the next generation

206
Q

virus and prey relationships

A

not antagonistic, one leads and one follows

207
Q

neutral sequence space

A

extent of sequence space in which a sequence change may occur without a fitness cost

208
Q

what defines neutral sequence space?

A

selective pressure from host factors

209
Q

red queen hypothesis

A

infectious agents and their hosts coevolve as one changes the other adapts to that change

210
Q

virus remain _____________ to their host as the host themselves evolve

A

associated and highly adapted

211
Q

viruses infecting new species are …

A

initially poorly adapted

212
Q

what do cells provide for virus replication?

A

building blocks, metabolism to generate energy, protein making machinery, membranes

213
Q

cell building blocks for virus replication

A

nucleotides, amino acids, carbohydrates, and lipids

214
Q

cell metabolism to generate energy for virus replication

A

ATP

215
Q

cell protein making machinery for virus replication

A

ribosomes, transfer RNAs, enzymes

216
Q

cell membranes for virus replication

A

localize replication, concentrate building blocks, supply the lipid bilayer needed for envelopes

217
Q

propagation of viruses in animals

A

originally used laboratory animals and embryonate eggs

218
Q

explants

A

bits of tissue maintained in culture

219
Q

growth of viruses in embryonated eggs

A

used for flu vaccines

220
Q

enders wellers and robbins discovered

A

ability of poliomyelitis viruses to grow in cultures of various types of tissue

221
Q

susceptible cell

A

functional receptor for a given virus, the cell may or may not be able to support viral replication

222
Q

resistant cell

A

no receptor for a given virus, it may or may not be able to support viral replication

223
Q

permissive cell

A

the capacity to replicate a given virus, it may or may not be susceptible, no receptor

224
Q

what is the only cell that can take up a virus particle and support its replication?

A

a susceptible and permissive cell

225
Q

primary cells

A

heterogenous (many cells present), closest to animal cells, technical hassle

226
Q

diploid cell strain cells

A

relatively homogenous, further from animal cells, technically less hassle

227
Q

continuous cell line cells

A

immortal, most homogenous, genetically weird, furthest from animal cells, pretty easy to grow cells

228
Q

primary cell culture technique

A

collagenous treatment of mince tissue, filtered and pellet, harvest supernatant and grow on dish

229
Q

consequences of primary cell passage

A

lose cell population heterogeneity, cell population dies out

230
Q

all continuous cell lines are not ______

A

alike

231
Q

virus induced cytopathic effect (CPE)

A

visible morphological changes in cell cultures caused by viral infections

232
Q

CPE

A

death of cells, rounding up and detachment, swelling and clumping, vacuolization, syncytia, inclusion bodies

233
Q

syncytia formation

A

infected cell fusion into a multinucleated cell

234
Q

viral inclusions

A

aggregates of viral protein in the cell that stain differently

235
Q

types of viral inclusions

A

intranuclear and cytoplasmic

236
Q

hemadsorption

A

for non-cytopathic viruses that produce hemagglutinins (viral proteins that adhere to RBCs)

237
Q

viruses that use hemadsorption

A

influenza, mumps, and parainfluenza

238
Q

focus forming assay for hepatitis C virus

A

uses IHC or IFA instead of CPE to determine endpoint of titration

239
Q

infective assays

A

plaque assay, TCID/CCID, hemagglutination, hemadsorption

240
Q

microscopy methods

A

electron microscopy, immunohistochemistry, in situ hybridization

241
Q

nucleic acid methods

A

PCR and sequencing

242
Q

serologic antibody based methods

A

ELISA and lateral flow

243
Q

detection and quantification of viruses

A

1952, Dulbecco and Vogt developed a plaque assay for animal viruses which transformed animal virology from a descriptive to a quantitative science

244
Q

virus titration - plaque assay

A

mix virus dilution with cells and overlay with agarose to limit virus diffusion, remove agarose stain remaining cells with crystal virus to visualize plaques, virus titer determined by counting plaques and multiplying by the dilution factor, each plaque is the result of infection by one virion

245
Q

tissue culture dose

A

concentration of virus it takes to produce cytopathic effect in 50% of the wells infected with virus

246
Q

virus quantification by TEM

A

add latex beads and virus estimated through electron microscopy

247
Q

TEM advantages

A

can identify type of virus by morphology, does not depend on virus growth, detect viruses in tissue or dirty samples such as feces and urine

248
Q

TEM limitations

A

relatively low sensitivity, sample is dead, cannot differentiate between viable and nonviable virions, expensive equipment

249
Q

TEM detection to viruses in dirty samples

A

can analyze directly from vesicular fluid, feces, and urine

250
Q

TEM identification of virus by morphology

A

size, capsid symmetry, envelope, and other features

251
Q

particule to PFU ratio

A

count virus particles by EM, determine PFU by plaque assay, divide number of particles by number of PFUs, variable is always >1, not all virions are infections

252
Q

immunohistochemistry and immunofluorescence

A

antibody binds to viral antigens, enzyme (IHC) or fluorescent (IFA) label on antibody, cell culture or tissue samples

253
Q

in situ hybridization

A

detects viral nucleic acid, may be direct or indirect

254
Q

PCR

A

geometric amplification of DNA segments, very high sensitivity -1 copy of genome, need to know target sequence, cannot tell if virus is infection

255
Q

sequencing for virus detection advantages

A

no assumptions, sequence info for culture required, can get strain phylogenetic and epidemiologic info directly, can identify previously unknown viruses, may detect multiple pathogens

256
Q

sequencing for virus detection limitations

A

cost is relatively high, low sensitivity compared to PCR, high degree of skill required, no viability info

257
Q

hemagglutination

A

used to estimate titer

258
Q

what does ELISA stand for?

A

enzyme linked immunosorbent assay

259
Q

ELISA

A

relatively fast, high specificity, generally high sensitivity, can be quantitative, lots of different test architectures, used to detect specific antibodies

260
Q

what is important to know about ELISA?

A

how it was done changes the way you interpret it

261
Q

common ELISA test architectures for virus detection

A

direct assay, indirect assay, capture assay sandwich

262
Q

Lateral flow test for virus antigen detection

A

good sensitivity

263
Q

virus one step growth curve

A

every cell in dish synchronously infected

264
Q

multiplicity of infection

A

the ratio of infectious virus to susceptible and permissive cells

265
Q

MOI

A

number of infectious units divided by the number of susceptible cells, infection depends on random collision of virion and cells, infection predicted by a poisson model

Medical Virology (1 decks)

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