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Virology > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What is emerging disease

A

Newly recognized or evolved

expansion in an area, host, or vector

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2
Q

Relies totally upon the host cell for energy and synthesis of structural components

A

Virus - no ribosomes, mitochondria

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3
Q

Progeny infectious virus particles are called

A

Virions

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4
Q

formed by denovo assembly from components within the host cell

A

virions

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5
Q

vehicle for transmission of viral genome to next host

A

viron

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6
Q

transmission strategies

A

close contact - enveloped
resistant to environment - naked
uses arthropod
vertical - infects fetus

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7
Q

3 parts to virion

A

Nucleic Acid - RNA or DNA
Capsid - outer shell
Envelope

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8
Q

Capsid is the outer shell of a virus comprised of repeating protein subunits called

A

capsomeres

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9
Q

the nucleic acid protein assembly packaged in the viron is called

A

neucleocapsid

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10
Q

2 types of capsids

A

icosahederal or helical

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11
Q

purpose of capsid

A

cover & protect

conserve energy

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12
Q

Where is virus envelope dervirved from

A

host cell membrane

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13
Q

glycoproteins important for attachment to host cell are called

A

peplomeres

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14
Q

process where envelope is acquired is called

A

budding

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15
Q

Viral glycoportiens that project through envelope

A

spikes or peplomeres

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16
Q

fibers that project from naked virions

A

pentons

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17
Q

what is sensitive to heat, drying, detergents, and acid

A

virus envelopes

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18
Q

what are non-enveloped virus called

A

naked

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19
Q

enzymes needed for NA replication and proteins that allow take over of host cell

A

non-structural

made 1st

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20
Q

proteins that form the capsid and package the NA genome

A

structural

made last

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21
Q

3 properties of viral propagation

A

viron mediate transmission of viral NA from host to host
viral genome contains the info for initiation and completing and infectious cycle
all virus are able to establish in a host population so they can survive

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22
Q

What does the nature of viral disease depend on

A

effects of replication on host cells
response of host defense system
ability of virus to spread

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23
Q

what effects do virus have on cells

A

lysis
establish a persistent infection
transformation - neoplasia

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24
Q

viral genome always present but virons not always produced

A

latent infection

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25
Q

virions always being produced

A

chronic infection

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26
Q

Since enveloped virus are sensitive to dry,heat, detergent, acid

A

close contact required
can spread w/o killing cell
host has to have both humoral and cell-mediated response to inactivate

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27
Q

naked virus capsids are resistant to dry,heat, acid, and detergents

A

survive in environment
fomite transmission
released by lysis of infected cells
humoral antibody response

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28
Q

examples of enveloped virus

A

influenza A - helical

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29
Q

examples of naked virus

A

parvovirus
adenovirus
both icosahederal

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30
Q

T or F Viruses are acellular, small, and simple

A

True

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31
Q

T or F Viruses can contain both DNA and RNA

A

True but not both at same time

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32
Q

T or F Viruses are obligate intracellular parasite

A

True - they depend on host cells to produce viral proteins

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33
Q

2 general types of viral proteins are:

A

Structural - building blocks Later physical structure

Non-structural - Functional EARLY

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34
Q

What does viral replication depend on

A

release of the genome from the viron

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35
Q

What is the range of size of viruses

A

Pox (300nm)

Parvo (20nm)

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36
Q

What is required for the viral life cycle

A

genetic information in the viral genome

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37
Q

what do viral genomes produce

A

messenger RNA (+) or sense strand

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38
Q

where do DNA viruses replicate

A

nucleus of the infected cell

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39
Q

Where do poxviruses (DNA virus) replicate

A

Cytoplasm

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40
Q

Where do RNA viruses replicate

A

Cytoplasm

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41
Q

Which is smaller DNA or RNA genomes

A

RNA is smaller

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42
Q

Where do retroviruses replicate

A

RNA virus with DNA intermediate which replicates in Nucleus

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43
Q

Viral genomes encode minimal info bc:

A

1- genome replication and packaging
2- produce viral proteins
3 - subversion of cellular function to produce new virons

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44
Q

What are the 2 arrengments of viral nucleic acid

A

Monoparite - single NA molecules

Segmented - reassort rapidly

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45
Q

What do viral genomes encode

A 
gene products for replication of the viral genome
assembly and packing of genome
regulation of replication
evasion of host defense
spread to other cells and new host
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46
Q

what do viral genomes NOT encode

A

ribosomal RNA or RNA translation proteins
genes involved in energy metabolism or membrane synthesis
telomeres
centromeres

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47
Q

The synthesis of RNA molecules by RNA viruses is a unique process that …

A

has no parallel in the cell

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48
Q

RNA viruses encode a _____ to synthesize new RNA genomes

A

RNA-dependent RNA polymerase

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49
Q

retroviruses genome have 4 coding regions

A

gag - group specific antigen (maxtrix protein, nucleoprotein, capsid)
Pro - Protease
Pol- Reverse Transcriptase and RNaseH
env - envelope and receptor binding

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50
Q

What are the effects of infection with retrovirus

A

latent infection
active infection with production of new virons
cell transformed and oncogensis occurs

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51
Q

What are the steps of replicative intermediates

A

+ parental strand serves as a template for the transcription of of many (-) RNA strands that can be used as templates for production of new (+) stranded genomes

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52
Q

T or F If a virus contains a + strand RNA genome they are directly infectious to host cell

A

True - immediately translated

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53
Q

why are RNA viruses with (-) RNA genomes NOT directly infective

A

b/c the viron must first be acted upon by a polymerase

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54
Q

Poxoviruses use cytoplasmic factories that result in the formation of…

A

intracytoplasmic inclusion bodies

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55
Q

DNA viruses that mutiply in the nucleus use ____ for transcription

A

DNA-dependent RNA polymerase

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56
Q

T or F Replication of viral DNa is conserative

A

FAlse - semi-conserative with symmetrical both stands being replicated

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57
Q

Why are most DNA viruses potentially oncogenci

A

they contain genes capable of transforming cells

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58
Q

In the replication cycle a large mRNA called _____ is produced

A

pg-RNA )pre-genomic RNA

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59
Q

a cDNA copy of the pgRNA is made by

A

reverse transcriptase called viral RNA-dependent DNA polymerase

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60
Q

What type of protein is envelope glycoproteins that are attachment between viron and cell

A

Structural

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61
Q

What makes up the capsid

A

capsomers that are identical protein subunites

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62
Q

What is the capsid in non-enveloped virus

A

external layer of the viron

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63
Q

What is the envelope composed of

A

lipid bilayer from budding of the host cell membrane

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64
Q

virus envelope glycoproteins function to

A

intial attachment of virion to target cell
penetration
fusion
cell to cell spread

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65
Q

T or F Budding or forming the envelope can result in cell death of host cell

A

True

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66
Q

What is the primary criteria for delineating the main viral taxa

A

type and character of viral genome
strategy of viral replication
structure of the viron (size,shape)

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67
Q

How are animal viruses differentatied and classified

A 
physical and chemical properties
genetic and antigenic relatedness
host range
cytopathology
site of replication
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68
Q

A persistent infection of a cell in which the complete viral genome is continually present, but no infectious virus is produced except during periodic reactivations

A

Latent infection

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69
Q

chemical or physical agents that increase the mutation rate of DNA

A

mutagens

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70
Q

A state wherein the particular virus in question is permitted to replicate by the cell and produce progeny virus

A

Permissive

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71
Q

An infection of a cell by a virus that results in the production of progeny virus particles

A

Productive Infection

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72
Q

a measure of the sensitivity of the host cell to infection by presence or abscence of receptors

A

Susceptibility

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73
Q

The natural virus used as reference strains no mutations or variants

A

Wild Type

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74
Q

What are the steps of viral replication

A 
attachment
penetration
uncoating
Transcription of mRNA viral proteins
Translation of viral proteins
replication of progeny genomes
maturation and assembly of virions
release of progeny virus
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75
Q

Attachment occurs by

A

ligand on the virus and receptor on the host cell

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76
Q

Can viral infection occur without attachment

A

NO

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77
Q

The receptor for Foot and Mouth and Bovine Herpes 1 is

A

Heparin sulfate

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78
Q

The receptor for HIV is

A

CD-4 molecule on human T-lymphocytes

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79
Q

Receptor for rabies is

A

Acetylcholine receptor

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80
Q

How are viruses uptaken

A

Receptor mediated endocytosis
fusion of the viral envelope with plasma membrane
Capsid interacts with cell receptors in non-enveloped virus

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81
Q

How are fusion proteins activated

A

cleavage by a cellular protesase or by a drop in the pH of the enviroment

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82
Q

What are the steps in Uncoating

A

removal of capsid
endocytic vacuole or cytoplasm
requires pH drop or enzyme
inhibited by antibody or modulation of pH
genome ready for replication cycle or integration

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83
Q

In order for the virus to complete its replication cycle the genome needs to produce 2 major categories of products

A

proteins to make up its capsomeres and its envelope glycoprotiens
New genome

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84
Q

What is produced and translated into viral proteins

A

messenger RNA

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85
Q

What mechanisms do viruses use to direct the machinery of the host cell to synthesize viral products instead of host cell products

A

viral mRNA takes over host cell translation machinery and viral mRNA is translated instead of the host cells

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86
Q

What happens to the host cells metabolism and protein synthesis during viral RNA synthesis

A

they are both shut down and only viral products are made

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87
Q

T or F Viruses have the capablility to switch genes on and off

A

TRUE called gene regualtion

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88
Q

how does gene regulation occur in large DNA viruses and retroviruses?

A

sequential waves

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89
Q

What are the 3 classes of gene expression

A

intermediate-early
early
late

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90
Q

What are early proteins

A

Large regulatory enzymes

Polymerases and transcriptional activators

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91
Q

What are large proteins

A

proteins to form the viron structure

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92
Q

T or F Replication of viral RNA is a thing unique to only viruses

A

TRUE

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93
Q

Explain the replication of viral RNA

A

transcription of RNA from an RNA template requires RNA-dependent RNA polymerase, a virus encoded enzyme that is not found in uninfected cells

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94
Q

WHat is the maturation and release of non-enveloped viruses

A

structural proteins of simple icosahedral viruses associated spontanoulsy to form capsomeres than capsids. More complex viruses have a packaging sequence encoded at the end of thier DNA

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95
Q

what is the maturation and release of enveloped viruses

A

all mammalian viruses with helical nucelocapsids mature and acquire an envelope by budding through host cellular membranes.

96
Q

How is the viron released in non-enveloped viruses

A

the cell must die and lost its membrane integerity

thousand of progeny virions are released by host cell death and lysis

97
Q

how is the viron released for enveloped viruses

A

plasma membrane is not breached hence thousand of virions can be shed over several hours or days without significant cell damage
many are persistent infections

98
Q

Where do exterior influenza virus shed from

A

apical membrane

99
Q

where do persistent infections (retroviruses) bud from

A

baso-lateral membrane

100
Q

What is unique about the viral life cycle

A

there are many steps that can be blocked

101
Q

What are the stages of Multiplication or Replication

A

Eclipse - where the virus is taken up by cells
Latent
Yield
Cellular

102
Q

T or F Viruses don’t like mutations

A

FALSE - they actually rely on mutations to live and die

103
Q

Which strands of viruses replicate faster

A

virulent strands

104
Q

What happens when high titer viremia is achieved during infection

A

likelihood of transmission to additional uninfected hosts is increased

105
Q

Arboviruses use high titers as a strategy to infect new arthopod hosts who co-evolved mechanisms to what

A

tolerate the viral load

106
Q

What is important for completion of viral transmission cycle, with many viruses demonstrating tropism for specific host receptors

A

Capacity to replicate in key tissues

107
Q

how do viruses envade the host immune response

A

encoding proteins that interfere with specific host antiviral activities

108
Q

mutations in nucleotide sequence are usually lethal for the virus but

A

sometimes mutation causes a survial advantage and a mutant strain is able to propgate

109
Q

what are the common types of mutations

A

single nucleotide substitution called point mutations

110
Q

What type of viruses are more stable

A

DNA are more stable than RNA bc they have proofreading

111
Q

DO RNA viruses have proofreading ability

A

NO only DNA

112
Q

what are host range mutations

A

a species jump
parvo in dogs was parvo in cats 1st (1980)
flu from swine to humans
equine flu infects dogs now

113
Q

what are conditional lethal mutations

A

replicate under specific conditions

temperatute-sensitive mutations

114
Q

what are deletion mutations

A

results from a loss of nucleotides

115
Q

what is antigenic shift

A

Large change due to a novel gene or change in existing one

116
Q

what is antigenic drift

A

small change resulting from accumulation of point mutations (single base subsutitions)

117
Q

T or F Antigenic changes can have changes at the phenotypic level

A

TRUE

118
Q

What are the ways viruses interact with eachother

A 
complementation - 1 deficient
recombination - chromosomes
reassorment - viral segments
reactivation - nonnon-infectious
phenotypic mixing - non genetic interaction
119
Q

What is a cytocidal viral infection

A

lysis of host cells

120
Q

what is a productive viral infection

A

production and release of new virons

121
Q

what is non-productive viral infection

A

new virons cant be produced

122
Q

what are permissive host cells

A

they support complete replication of a particular virus

123
Q

what is non-permissive host cells

A

they block viral replication

124
Q

What type of interactions are persistent and latent infection

A

non-productive virus cell interactions

125
Q

What are the 4 types of changes virus have on host cell

A

cytocidal - death or lysis, apoptosis
cytopathology - distrupt functions of specialized cells
malignant changes
no alteration

126
Q

syncytium formation allows the plasma membrane to

A

fuse with neighboring cells

127
Q

what are multinucleated giant cells

A

synctia that envades the host cell defense system

128
Q

What happens with cell membrane fusion

A

fusion proteins found in enveloped viruses
glycoproteins
FP - are inactive but become activated by pH or protease

129
Q

how is a syncytial recgonized

A

focal clusters forming like in measles and herpes

130
Q

WHat is it called with virus absorb red blood cells

A

hemadsorption/hemagglutination

131
Q

What is it called when virus distrupts the cytoskeleton leaving a rounded up apperance

A

cytoskeleton distruption

132
Q

Name 3 viruses that have inclusion bodies

A

hepres - intranuclear
adeno - multiple intranuclear
pox - large intra cytoplasmic

133
Q

WHat is a negri body

A

neuron infected with rabies

134
Q

DNA viruses associated with oncogenesis are

A 
marek disease (Herpes)
Papilloma
135
Q

WHat phase is turned on in oncogenesis

A

S - phase = rapid multiplication or uncontrolled growth

136
Q

what RNA viruses associated with oncogenesis

A

avain leukossi
feline luk
Retrovirade - provirus
integrade thier genome into host chromosome

137
Q

What are the 2 ways retroviruses can cause onogenesis

A

enoding oncogenes

altering expression of proto-oncogenes by inserting their chromosomes

138
Q

what are the 3 types of persistent infections

A

steady state infection - virus production
carrier state - lysis produce new virus
interference with specialized function of high differentiated cells - hormones, or immune

139
Q

What does pathogenic mean

A

capable of inducing disease or lesion

140
Q

WHat is virulence

A

measure of ability to produce disease in the host

141
Q

What are the sources of virus infections

A 
diseased animals
persistently infected animals
animal products
environment
reservior host and vectors
142
Q

how are viruses transmitted

A

horizontal - between animals
Direct contact - cohabition
indirect contat - formites
vectors

143
Q

What is vertical transmission

A 
parent to offspring
in germplasm - retroviruses
through egg
across placenta - non-immune dams
milk
144
Q

what are the 2 portals of entry for viruses

A

respiratory tract and fecal oral

145
Q

where are virus shed

A 
respiratory route
oral route
fecal
milk
skin
urogential
146
Q

Respiratory tranmission

A 
Flu CDV - aerosolized
mucocillary clearance
phagocytosis
immunosuprission
receptor - entry into cell
impair clearence - macrophage
147
Q

Alimentary tract transmission

A

VM - CPV, Rota
ingested in contaminated food or water
low pH stomach and high pH of SI mucous and persitaltic action prevent entery and remove virus

148
Q

Skin transmission

A

Tramua
Insect bit
animal bite
instruments

149
Q

Transmission genital tract

A

veneral infections

herepesviruses

150
Q

placental transmission

A 
infertility if embryo killed early
mummy is fetus killed kid-gestation
abortion if fetus killed late gestation
stillbirth if fetus is dead at term
congential abnormal at term
persistant tolerant infections if infected early in pregancy
normal is fetus is immune
151
Q

virus - host interactions

A 
inapparent or subclinical - parvo in adults
local - equine flu
generalized - systemic
sequale of primary infection - distemper
persistant infection
152
Q

mechanisms of disease production by virus

A

direct cell damage with loss of organ function
cell transfomation, tumor production
inflammatory response
Immunosupression destorys lympocytes, and macrophages
immune mediated antigen antibody accumulation

153
Q

what determines severity of disease

A 
location (swelling in brain vs skin)
function (what does target cell do )
Regeneration ability (nureons cant)
154
Q

local virus replication

A

entry, replication, lesions, shedding in organ system

155
Q

what determines if virus stays local or spreads

A

presence of susceptible cells in other tissues

outcome of encounter between immune system and the virus

156
Q

sytemic virus replication

A

entry, spread to other systems, shedding in several secretions and excretions

157
Q

pathogenesis of acute viral infection

A

after entry at one surface virus is able to penetrate into tissue under and multiply
virus spreads via lymphatics to infect regional lymph nodes - primary amplification
virus spreads to blood no clinical signs
virus gets to central organs
spleen mass replication - fever systemic symptoms
secondary virema
replication in susceptible cells

158
Q

localized infections

A

very rapid, immune system prevents re-infection
by time of fever, sheeding is large and disease signs appear, take samples early
wait days after fever to take post infection samples

159
Q

recovery from virus

A

depletion of susceptible cell population

immune response - cell mediated cytotoxic response

160
Q

control of virus infections

A

viral epi - study in a population
helps prevent or interrupt spread of disease
life cycle of virus requires excretion from animal

161
Q

quarantine procedures

A

restrict movement
testing of imported animals
quarentine during epidemics
closed herds

162
Q

sanitation procedures

A

slaughter and disposal by burn or bury
disposal of bedding, food, manure
disinfection of housing
heat treatment of animal material for feed

163
Q

wildlife control of spread

A

reduce risk of exposure to domestic animals

housing, fencing, removal of wildlife and vaccination

164
Q

vector control

A

reduce the spread of infection
insect control in barns
dipping or spraying animals
destruction of breeding sites for insects

165
Q

susceptibility is usually correlated with ___

A

increased levels of replication in the tissues

166
Q

What is a major factor in determine the outcome of infection

A

genetic background but specific factors are not known

167
Q

What determines resistance to different viruses

A

genes

168
Q

WHat is associated with the presence of absence of a host cell receptor on target cells

A

susceptibility

169
Q

What are some exapmples of host cell determinantes

A

transcription factors
DNA replication enzymes
host cell proteases

170
Q

The immune system determines the level of susceptibility of animals to a virus by

A

the antiviral action of OFN or CMI

171
Q

Does age have an effect of viruses production

A

yes some viruses produce more severe infections in young animals = maturation of the immune system or of specific cells

172
Q

what role does fever play

A

fever inhibits the replication of many viruses and enhances the inflammatory reaction which aids in clearance of virus

173
Q

Virus and immune systems are both shaped by the constant pressure of

A

the immune system to eliminate the virus

174
Q

what drives the evolution of viruses

A

effort of the virus to envade the immune response - virus cant afford to be eliminated

175
Q

how does a host change to fight off infection

A

host become better able to survive infection and those genes are selected for

176
Q

Non antigen receptors influence the outcome of infection examples

A

interferon
NK cells
muco-cillary response

177
Q

what 2 things play a vital role in inhibiting viral replication

A

interferons and cytokins

178
Q

T or F viruses can turn on and off cytokins

A

TRUE = this enables them to direct the immune system that best suits its needs for replication

179
Q

WHat cells are important in the clearance and inactivation of most viral pathogens

A

macrophages = also major target cell and resivor

180
Q

What is importatn in preventing the inital entry of virus

A

Ab bc it decreased teh inital load of virus in blood

181
Q

why is cell mediated immunity importatn in recovery

A

lysis of virus infected cells prevents further replication and leads to clearance from host

182
Q

how do viruses avoid immunity

A

immune privelaged sites - neurons
down regulation of protein expression
infects cells lacking MHC to envade T-cell reponse
integration of viral genome into host chromosome DNA
infection of lymphocytes and macrophages
non-neitralizing Ab
induction of Ab which enhances infection by attaching to virus and aiding infection of macrophages

183
Q

What is antigenic drift

A

mutation of viral genes by HA and N function

subtle changes but give replication advantage

184
Q

what is antigenic shift

A

reassortment of viral genome

severe epidemics

185
Q

what is virus induced immune mediated inflammatory disease

A

viral anitgen persits and there is continued immune response at the site of viral infection causing more extensive damage to surronding tissues

186
Q

What is immunosuppression

A

viruses destroy lymphocytes resulting in immunosupression and predisposing the host to develop opportunitics infections

187
Q

what is modular mimicry

A

viral anitgens does not remian but primes the immune response to produce autoimmune disease

188
Q

What is persistant viral infection

A

virus remains for long time killing cells without being eleminated by host cell defence
usually requies a specialized cell type to set up persistent infection

189
Q

Examples of persistent infections

A 
canine distemper and herpes
feline luke, FIV, herpes, peritonitis, calici
equine herpes, EIA, arteritis
bovine herpes BVD, Luke
PRS cholera, PRRS, circo
blue tounge, visna
caprine arthrisits encephalitis
Mareks disease
190
Q

what is important about persistant infections

A

can be source in population infecting new animals
can reactivate and cause acute disease
immunopathologic diaseas
neoplasms

191
Q

what are the general features of persistant infections

A

natural selection pressures
minimal tissue damage
difficult to control by vaccination

192
Q

What are the 2 types of persistant infections

A

chronic - persistant shedding

latent - only periodic shedding or none

193
Q

chronic virus infection

A

virus replicates in host to a degree then persist over time
clinical disease patterns are variable
shedding to enviroment ocurs

194
Q

how do chronic infections damage the host

A

cytopathic effects of the virus on the cell

immunopathologic tissue damage

195
Q

WHat is the objective of vaccination

A

prevent animal from developing disease if exposure to the pathogen occurs

196
Q

T or F Vaccination prevent infection

A

FALSE - only primes the host immune system to respond to pathogen exposure

197
Q

WHat is the overall objective of vaccination

A

Immunize as many as possible
vaccinate no more than necessary
vaccination only against risky pathogens

198
Q

What is sterilizing Immunity

A

vaccine gives complete protection for clinical disease

No viral replication or shedding to other animals

199
Q

What has to happen for a vaccine to be the most effective

A

generate the type of immune response that the natural infection would

200
Q

What can block spread of the virus from blood and also prevent clinical disease

A

Serum IgG

201
Q

what can be a reasonable estimate for the level of protection like CDV, CPV2

A

serum IgG

202
Q

When is CMI more important that systemic antibody

A

if virus is intracellular or persistant infection

203
Q

When do serum IgG levels NOT correlate to protection

A

in intracellular or presistant infections like Herpes, retroviruses, and calicli

204
Q

What % vaccinations immunize the target species

A

65-98%

205
Q

Does contagious viruses with high amounts of shedding have better protection from vaccines

A

Yes those vaccines protect about 98% of the time

206
Q

Viruses that are latent infections or have sporadic shedding have high levels of vaccine protection

A

NO - actually have low levels of protection

207
Q

What age animals are the target of vaccine programs

A

Young animals bc their are most susceptible to disease
immune system matures months after birth
also clinical disease is worse

208
Q

T or F Themorulation is import when vaccinating neonates

A

TRUE - hypothermia permits replication of viruses that would be inhibited at normal tempature
Especially Canine Herpes in puppies

209
Q

What is the Window of susceptibility

A

When colostral antibody declines and neonate is exposed to virulent virus

210
Q

Why do we vaccinate neonates multiple times

A

presence of colostral antibodies blocks the development of adaptive immune response and neonates remain vulnerable despite prior vaccinations

211
Q

What makes Live viruses so different

A

they actually replicate in the host so they see the live virus

212
Q

What are the 5 types of Live Viruses

A 
1 - MLV or Attenuated
2 - Cold-adapted, temp sensitive
3 - recombinant vectored vaccine
4 - deletion mutant vaccine
5 - Chimera
213
Q

What are the 4 types of killed vaccines

A

1 - Whole virus
2 - subunit
3 - Nucleic Acid
4 - Peptide

214
Q

Why are MLV the best type of vaccine, Most common and effective

A

they activate both arms of the adaptive immunity the CMI and humoral

215
Q

How are MLV derived

A

passaging a pathogenic virus in tissue cultures or another species

216
Q

If MLV are adminstered on the epithelial or mucosal surfaces they can initate

A

Local secretory IgA

217
Q

What vaccine can overcome materal antibodies blockade

A

MLV

218
Q

What are temp-sensitive vaccines

A

only replicate when temp is lower than core body temp

219
Q

How are Recombinant vector virus derived

A

genes associated with protective antigens of a pathogenic virus is inserted into another virus that is NOT a pathogen but will express the pathogen virus

220
Q

T or F Vectored vaccines will replicate in mammals

A

FALSE - they do NOT

canary-pox vectored vaccine for WN, distemper, FELV, Avipox

221
Q

Why would poxviruses be particulary attractive for use in live agent recombinate vector vaccines

A

They replicate in the cytoplasm
They are large DNA virus so there is room to insert genes
They are not natural to mammals so they can’t replicate to form a super pathogen

222
Q

Advantages of Vectored Vaccines

A

can NOT revert to virulence or cause disease
can induce robust immune response, with live non-replicating live virus (Ab&CMI)
overcomes maternal antibodies
Diagnostic can differentiate between natural infection and vaccine induced response

223
Q

What is a deletion mutant recombinate vaccine

A

delete or inactive a gene that is required for virulence while leaving the capability to replicate intact

224
Q

What is used to distinguish vaccinated animals from natural infections

A

Marker vaccines or DIVA test (distinguished from infected animal)

225
Q

What type of vaccine is used in eradication programs

A

Deletion mutant recombinant vaccine

226
Q

WHat is a chimeric vaccine

A

recombinatnt vaccine that contains at least one functional gen from a pathogenic closely-related virus

227
Q

How are chimeric vaccines made

A

inserting a structural protein gene from a pathogenic virus into non-path vaccine strain

228
Q

What are the advantages of live vaccines

A

robust immunity (CMI - sees virus)
decreased potential for allergic reactions bc antigenic load is small and adjuvants are not needed
long duration
recombinate can overcome materal antibodies
one injection gets immunity

229
Q

when are live vaccines indicated

A

sistuations where antibody levels do not correlate with protection and where induction of anitbody may block effective imunological response or contribute disease

230
Q

Disadvantages of Live vaccines

A

Can replicate in host
- overt disease in vacc animals
- acquire mutations and revert to virulence
-teratogenic and/or abortions
- transmitted to others
very susceptible to inactivation - handle, mix store carefully

231
Q

What are the 3 types of inactivated vaccines

A

non infectious whole agent - Killed
Genetic vaccines - DNA plasmids, RNA mRNA
Purified subunit vaccine

232
Q

T or F inactivated viruses replication occurs in the host

A

FALSE - no reversion to virulence

no sheddign

233
Q

why do inactivted killed and non-infectiour vaccines require higher antigen mass and adjuvants

A

hypersenstitivity reactions
injection site reactions
sarcomas in cats

234
Q

Which type of vaccines are stable to store and safer for pregant and immune supporesed animals

A

inactivated or killed

235
Q

What are the disadvantages of killed vaccines

A

require multiple doses, very frequent
can NOT overcome maternal antibodies
Short duration
NO CMI

Virology (4 decks)

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