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Virology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

List 6 ways that viruses impact domestic animals, humans, and science

A
  1. Common agents of Dz that you may encounter with some frequency
  2. High economic impact diseases
  3. Zoonotic diseases
  4. Viruses induce cancer in animals
  5. Newly emerging disease
  6. Tools for cell biology, gene therapy, vaccines
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2
Q

What is a virus

A

an infectious agent comprised of one or more molecules of DNA or RNA surrounded by a protein coat, and sometimes a lipid envelope

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3
Q

Replication
Bacteria vs Viruses

A

Bacteria: binary fission
Viruses: assembly line

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4
Q

Genetic Material
Bacteria vs Viruses

A

Bacteria: Both RNA and DNA
Viruses DNA or RNA

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5
Q

Protein production?
Bacteria vs Viruses

A

Bacteria: Yes
Viruses: No

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6
Q

Energy production?
Bacteria vs Viruses

A

Bacteria: Yes
Viruses: No

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7
Q

Requirement for Repro?
Bacteria vs Viruses

A

Bacteria: can replicate/divide on their own

Viruses: requires a cell

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8
Q

Susceptible to abx?
Bacteria vs Viruses

A

Bacteria: Yes
Viruses: No

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9
Q

List the 5 major primary sources of virus that affect animals

A
  1. Transiently infected animals
  2. wildlife
  3. environment
  4. persistently infected animals
  5. arthropods
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10
Q

Ways to mitigate transmission of a virus

A

sanitation
vaccination
flea/tick prevention
quarantining

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11
Q

define Virion

A

the intact, complete, physical infectious virus particle

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12
Q

virus genome structure

A

linear or circular
single stranded or double stranded

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13
Q

define capsid

A

protein that surrounds the viral genome

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14
Q

capsid proteins are encoded by the ?

A

viral genome

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15
Q

2 fundamental patterns of capsid proteins

A

icosahedral and helical

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16
Q

which capsid pattern is common in spherical viruses

A

icosahedral

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17
Q

which pattern is the most efficient way of forming a capsid shell?

A

icosahedral

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18
Q

the more icosahedral capsule produced, the (smaller/larger) the virus

A

larger

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19
Q

which capsid pattern is seen in all rod-shaped animal viruses?

A

helical

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20
Q

viral genome forms a spiral in the capsid (icosahedral or helical)

A

helical

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21
Q

describe an evelope

A

lipid and proteins that surround the capsid
(lipid bilayer and glycoproteins)

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22
Q

all animal viruses that are helical are (naked/enveloped)

A

enveloped

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23
Q

the lipid bilayer portion of an envelope is acquired by ?

A

budding through a host cell membrane (usually the plasma membrane)

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24
Q

another name for glycoproteins within an envelope

A

spikes or peplomers

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25
Q

matrix

A

inner layer of envelope used to protect rigidity

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26
Q

nucleocapsid

A

additional layer surrounding the genome

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27
Q

tegument

A

“packing” between the capsid and envelope of herpesviruses

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28
Q

(enveloped/non-enveloped) viruses are more fragile

A

enveloped

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29
Q

5 ways that inactivate an enveloped virus

A
  1. more heat labile
  2. more vulnerable to oxidation
  3. more susceptible to freezing and thawing
  4. more susceptible to dessication
  5. inactivated at low pH
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30
Q

capsid proteins (are/are not) highly conserved

A

are

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31
Q

Function of the capsid

A
  1. mediated binding to cell membrane for entry
  2. promotes uncoating after entry
  3. packages genome during assembly
  4. facilitates exit from the cell
    • mRNA is translated by capsid proteins
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32
Q

Functions of the envelope

A
  1. carry glycoproteins that are important for interaction with the host cell
  2. binding to host cell receptors
  3. fusion with cell membrane for entry
  4. important in uncoating for some viruses
  5. facilitate exit from host cells
  6. viral GPs are often protective or neutralizing agents
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33
Q

define serotype

why is it important?

A

a set of viruses that can be distinguished from other viruses in the same species on the basis of antigenic properties.

important for understanding neutralizing properties

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34
Q

3 major viral characteristics/critera for classification of viruses

A
  1. type of viral genome (RNA, DNA, +, -)
  2. virion structure (enveloped or not, capsid symmetry)
  3. strategy of replication
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35
Q

describe virus attachment

A

binding and attachment of the virion to the host cell

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36
Q

the viral attachment protein is on the (host cell/virion)

A

virion

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37
Q

the virus receptor is on the (host cell/virion)

A

host cell

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38
Q

describe penetration

A

normal cellular process for uptake of macromolecules via a specific receptor

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39
Q

penetration is used by (enveloped/naked/both)

A

both enveloped and naked viruses

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40
Q

can a naked virus undergo fusion?

A

no, requires an envelope

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41
Q

cells without appropriate receptors (are/are not) susceptible to infection by the virus

A

are not

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42
Q

what does penetration provide/facilitate

A

provides an environment that promotes fusion or uncoating

facilitates intracellular trafficking

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43
Q

how do naked viruses penetrate a cell membrane

A

membrane puncture

direct penetration (perforation or lysis)

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44
Q

how to enveloped viruses penetrate cell membranes?

A

membrane fusion using fusion proteins in the virus envelope

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45
Q

how do fusion proteins work?

A

they contain hydrophobic domains (fusion peptides) that are inserted into the cell membrane. the inactive fusion peptide needs to be activated by a conformational change

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46
Q

how is a fusion protein activated? what follows activation?

A

it is cleaved by a host protease at the cleavage site -> activation and membrane fusion

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47
Q

describe uncoating

A

removal of capsid, release of the viral genome (DNA or RNA)

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48
Q

is uncoating independent of penetration?

A

can occur simultaneosly or independent of penetration

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49
Q

describle biosynthesis

A

synthesis of mRNAs recognized nby the cell translation machinery - makes proteins for replication

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50
Q

goal of biosynthesis

A

replicate the viral genome! new genomes for packing into virions

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51
Q

describe assembly

A

virus proteins and genomic nucleic acid must co-localize and assemble into a functional virus particle

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52
Q

how are non-enveloped viruses released?

A

generally requires cell lysis

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53
Q

how are enceloped viruses released

A

may or may not require cell lysis.

can undergo budding which is not lethal to the cell

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54
Q

Viral Growth curve: What is A?

What steps of viral replication does this step match with?

A

Virus Absorption

Attachment and Penetration

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55
Q

Viral Growth curve: What is B/D?

What steps of viral replication does this step match with?

A

Eclipse Period
Virus uncoating and sythesis of genome and proteins

Uncoating and biosynthesis

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56
Q

Viral Growth curve: What is C?

What steps of viral replication does this step match with?

A

Virus assembly, maturation and virion release

Assembly and Release

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57
Q

Viral Growth curve: What is happening at E?

A

virus accumulating intracellularly

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58
Q

Viral Growth curve: What is happening at F?

A

virion begins to accumulate extracellularly

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59
Q

Viral Growth curve: What is happening at G?

A

large increase in extracellular virus - a lytic virus will burst

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60
Q

describe the eclipse period

A

there are no full virus particles. The virus has opened its capsid or envelope so the parts are disassembled. No detectable virions at this stage

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61
Q

What does the viral growth curve tell us about a virus?

A
  1. virus production is step wise (not linear or exponential)
  2. the replicating entity is actually a virus (only viruses have an eclpise phase)
  3. how fast the virus replicates
  4. how many progeny particles are pruduced per cell (burst-size or yield)
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62
Q

what is the primary determinant of host cell specificity?

A

the appropriate receptor

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63
Q

What steps of virus replication can Ab interfere in?

A

Attachment and penetration (neutralizing Abs)

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64
Q

Change in a receptor can result in?

A

expansion of tissue tropism, host range, and emerging disease

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65
Q

How can Protease cleavege site and distribution of cellular proteases affect a virus

A

they can affect tissue distribution and pathogenicity (Ex: low pathogenic vs high pathogenic avian influenza)

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66
Q

What is involved in viral biosynthesis for DNA viruses?

A

DNA viruses usually use host cell proteins and enzymes to make additional DNA that is transcribed to messenger RNA (mRNA) by DNA-dependeent RNA-polymerase , which is then used to direct protein synthesis.

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67
Q

What is involved in viral biosyntheses for RNA viruses?

A

RNA viruses use their own polymerase (RNA-dependent RNA-polymerase) to transcribe their genome into mRNA

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68
Q

both RNA and DNA viruses must be transcribed into (?), then to viral proteins

A

(+) mRNA

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69
Q

why must replication of all viruses result in production of positive sense mRNA?

A

all viruses must make mRNA that can be recognized by the host translational machinery

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70
Q

two strategies that RNA viruses employ to produce positive sense mRNA

A

use virus encoded enzymes (polymerases) for replcation

(-) RNA –RdRp–> (+) RNA –> protein

or use a reverse transcriptase

RNA –RT–> DNA –> (+) RNA –> protein only retroviruses can do this

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71
Q

(DNA/RNA) viruses are more prone to developing genomic mutations

A

RNA

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72
Q

Why are RNA viruses more prone to developing genomic mutations?

A

lack of proofreadinf functions leads to a higher rate of error during RNA virus genome replication

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73
Q

why are viral encoded polyproteins and polymerases excellemt targets for developing antiviral therapeutics?

A

the pathways are not normally found in mammalian cells and are necessary for viral reproduction

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74
Q

Where does cell assembly occur for RNA viruses?

A

in the cytoplasm of the cell (they bring their own enzymes! don’t need access to the nucleus)

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75
Q

Where does cell assembly occur for DNA viruses?

A

in the nucleus of the cell

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76
Q

How is location of viral cell assembly useful in indentifying viral infection in cells?

A

the site of assembly is often where diagnostic inclusion bodies are seen by light microscopy

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77
Q

what is a susceptible cell

A

the cell is sensitive to infection by a particular virus. largely a function of presence or absence of receptors

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78
Q

what is a permissive cell

A

the cell is able to support complete replication of a particular virus. this is a function of the interal biochemistry of the cell.

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79
Q

for an infection to be successful, the cell has to be (permissive/submissable)

A

both!

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80
Q

Cytolitic infections: CPE?

A

Yes

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81
Q

productive persistent infections: CPE?

A

little to none

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82
Q

latent persistent infections: CPE?

A

usually no effects on cell

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83
Q

Cytolytic infections: continued cell division?

A

cell death

84
Q

productive persistent infections: metabolic change?

A

little metabolic change

85
Q

latent persistent infections: metabolic change?

A

usually no effect on cells

86
Q

cytolytic infections: alter cell specialized functions?

A

inhibition of protein, RNA and DNA synthesis

87
Q

productive persistent infections: alter cell specialized functions?

A

loss of some specialized functions

88
Q

productive persistent infections: continued cell division?

A

cells continue to divide

89
Q

cytolytic infections: viral productivity?

A

produces virus

90
Q

productive persistent infections: viral productivity?

A

virus produced

91
Q

latene persistent infections: viral productivity?

A

no virus produced, but can be induced

92
Q

define cytopathic effects (CPE)

A

morphologic changes observed in cell culture due to virus infection

93
Q

What does CPE tell you about a sample submitted to a diagnostic lab?

A

often, CPE is a characteristic of a particular virus and can be useful in prelimiary diagnostics

94
Q

Types of Cytolytic CPE

A
  1. cell shape changes
  2. cell lysis
  3. formation of Syncytial or “giant” cells
  4. viral inclusion bodies
95
Q

define viral latency

A

virus infection where the viral genome is maintained but new viral gene products are not made and no virus is produced

96
Q

it there a dianostic test for a latent virus?

A

No, but PCR can tell you if infection is present (just cant tell you if its latent or productive)

97
Q

What diagnotic test can you use to confirm a productive virus?

A

ELISA for Ag on whole blood, or PCR for viral genome on whole blood (v-RNA)

98
Q

define proto-oncogene

A

Normal cellular gene whose product promotes cell growth (growth factors, growth factor receptors, proteins for signal transduction, transcription activators, cell cycle regulators)

99
Q

define oncogene

A

cellular gene that produces autonomous cell growth in cancer cells (due to mutation or overexpression)

100
Q

define viral oncogene

A

mutant of overexpressed version of a proto-oncogene carred by a virus

101
Q

What kind of virus typically carries viral oncogenes?

A

retroviruses

102
Q

define viral transforming gene

A

viral gene that mimics a cellular oncogene but evolved independently and is genetically distinct

103
Q

define oncoprotein

A

protein that is constitutively active to promote autonomous cell growth

104
Q

What produces oncoproteins

A

transcription of oncogenes, viral oncogenes and viral transforming proteins produce oncoproteins

105
Q

define transduction

A

transfer of genetic material from one cell to another cell by a virus (retroviruses)

106
Q

3 ways that DNA viruses promote tumor development

A
  1. inactivation of tumor suppressor genes
  2. bind growth factor receptors and activate signaling pathways
  3. produce oncoproteins that drive or limit transcription
107
Q

how do retroviruses transform cells?

A

by making mistakes in replication and producing oncogenic products

108
Q

describe insertional cis-activation of cellular proto-oncogenes

A

retrovirus genome integrates near a cellular proto-oncogene.

the expression of c-onc is under the control of the virus LTR

LTR contains the viral promoter - where transcription factors bind and promote transcription. this is why all retroviruses have the potential to become neoplastic

109
Q

describe transactivation by virus encoded proteins

A

during replication, cellular proto-oncogene is mistakenly acquired by the retrovirus genome. Genes are no longer under control of the cell, but are under control of the virus LTR.

The oncogene can be transferred from one cell to another by the virus

110
Q

define pathogenicity

A

ability of the virus to cause Dz (YES OR NO). contributed by both the host and the virus

111
Q

define virulence

A

the relative measure of pathogenicity (the DEGREE of damage) a propety of the virus.

112
Q

management strategies to keep majority of infections resulting in inapparent Dz

A

vaccinate, provide good nutrition, manage dose (environmental)

113
Q

changes in virulence are responsible for….

A

emergence and re-emergence of viruses, host range expansion, and overcoming the host immune response

114
Q

how can a highly virulent virus shift the “iceberg”?

A

highly virulent viruses often establish infection in a greater number of hosts than they cause disease

115
Q

3 principle factors that determine the outcome of viral infection and severity of disease

A
  1. genetic features of virus
  2. route and dose of inoculum
  3. host factors
116
Q

What factors at the individual host level can influence disease outcome?

A

immunity (Vx or not), nutrition, age, sex, breed…

117
Q

what is DEED and how does it influence the risk of viral transmission

A

Dose, Envelope or not, Environment, Distance

  • Envelope matters when considering disinfection
  • enviro: cold, wet and windy environments tend to increase the risk of transmission
  • distance between infected individuals
118
Q

transient infection duration

A

generally short

119
Q

are transient infections cleared?

A

the virus is eventually eliminated from the host

120
Q

(transient/persistent) infections may be self-limiting, and/or controlled by innate or adaptive immune responses

A

transient

121
Q

are persistent infections cleared?

A

no

122
Q

persistent infection Dz patterns

A

variable - from subclinical to progressive

123
Q

5 mechanisms that viruses use for persistent infection in a host

A
  1. immunological tolerance
  2. latency
  3. infection of immune cells
  4. infection of tissues in immunologically privilaged sites
  5. escape from competent adaptive immune response (antigenic variation)
124
Q

3 major anatomic portals that diseases use to enter/exit a host

A

mucosal (GI, resp, urogenital, conjunctiva), skin, veritcal transmission

125
Q

barriers at mucosal surfaces

A
  1. mucociliary clearance
  2. acid, bile, proteaes
  3. rapid turnover
  4. peristalsis
126
Q

how do viruses enter skin

A

via abrasions or penetrations (injuries, mechanical insults, arthropod vectors)

127
Q

what is vertical transmission

A

without passage through the environment - usually refers to transmission prior to birth (in germ line of fert. eggs, across the placenta, during passage through the birth canal)

128
Q

consequences of vertical transmission

A

abortion, congenital Dz, persistent infection, neoplasia

129
Q

portals of exit

A

may or may not be the same sites of entry. include resp droplets/aerosol, feces, saliva, skin, feather follicle, urine, semen and milk

130
Q

portals of exit for localized infections

A

typically the same as site of entry

131
Q

describle immunological tolerance and give an example

A

virus continually divides but the viral antigens are recognized as self. Ex: BVD

132
Q

describe latency

A

allows the virus to persist in animal populations (silent carriers) for life without showing clinical signs

133
Q

what are some immunologically privilaged sites?

A

gonads, brain, (protected)

GI tract, resp, skin (commonly present with antigens, have a high threshold for immune activation)

134
Q

3 ways that viruses escape from a competent adaptive immune response

A
  1. ineffective non-neutralizing Ab (animals make Ab but against the wrong Ag)
  2. change neutralizing Ag (antigenic variation)
  3. interfere with antigen presentation (blocks pathways of Ag presentation by MCH I and II)
135
Q

how does restricted viral gene espression aid in viral persistence

A

evades the immune system through the “trojan horse” model
absence (or minimal) viral protein production allows virus to hide from immune effector molecules

136
Q

localized viral infection: site of replication?

A

at or near th body surface through which they entered

137
Q

localized viral infection: incubation period?

A

usually short

138
Q

localized viral infection: where does lesion formation and shedding occur?

A

in the same organ as viral entry and replication

139
Q

localized viral infection: spread

A

cell to cell

140
Q

localized viral infection: viremia?

A

no

141
Q

localized viral infection disease severity vs systemic disease severity

A

cannot compare. localized does not mean less severe

142
Q

systemic viral infection: virus spread, shedding

A

viruses spread from the entry site through lymphatic and hematogenous dissemination to cause generalized infections in specific organs. sites of entry, the ‘target’ organ, and shedding site may or may not be the same.

143
Q

systemic viral infection: incubation period

A

longer than localized

144
Q

systemic viral infection: when is peak viremia?

A

second viremia

145
Q

primary viremia

A

the first viremic period (transient and subclincal)

146
Q

secondary viremia

A

large amounts of virus in bloodstream. Peak viremia, Very detectable

147
Q

4 factors that govern whether a virus remains localized or spreads sytemically

A
  1. directional release - how a virus enters/exits a cell
  2. availability of susceptible and permissive cells in deeper tissues
  3. macrophage/monocyte susceptibilty and permissivity
  4. temperature range of the virus
148
Q

release from apical surface of cell (Localized or Systemic)

A

localized

149
Q

release from baslolateral surface of the cell (Localized or Systemic)

A

Systemic

150
Q

virus-macrophage infection (Localized or Systemic)

A

Systemic

151
Q

virus can’t replicate at higher body temps - (Localized or Systemic)

A

Localized to cooler areas (resp/oral, mucosa, skin)

152
Q

what type of immune cell is KEY in a lot of systmic infections?

A

macrophages

153
Q

2 major factors that contribute to the termination of an active viral infection

A
  1. depletion of susceptible cells
  2. the immune response
154
Q

depletion of susceptible cells in more important for (localized/systemic) infections

A

localized

155
Q

the innate immune response is more important for (localized/systemic) infections

A

localized

156
Q

the adaptive immune response is more important for (localized/systemic) infections

A

systemic

157
Q

peak viral replication occurs prior to febrile response and other clinical signs in (localized/systemic) infections

A

both!

take samples early for both types of infection.

158
Q

how does the innate immune system detect viral infections?

A

PRRs (TLRs and RLRs) recognize PAMPs on the virus

159
Q

Type I IFNs are produced by

A

produced and secreted by virus infected cells

160
Q

Type I IFN repsonse time to infection

A

rapid! within 3-4 hours

161
Q

role of Type I IFNs

A

protects neighboring, uninfected cells - upgregultes IFN-stimulated genes which leads to enhanced defenses against viral invasion and replication

162
Q

Type I IFNs (are/are not) specific to a particular virus

A

are not

163
Q

What causes fever during viral infection and how does it benefit the host?

A
  • pro-inflammatory cytokines!
  • elevated temperature inhibits viral replication
  • increased rate of chemical/enzymatic reactions
  • increased blood flow to inflamed areas
  • increased speed of inflammatory processes
164
Q

Phagocytes and NK cells are actived by

A

pro-inflammatory cytokines

165
Q

Phagocytes and NK cells (are/are not) anitgen specific

A

are not

166
Q

Phagocytes and NK cells target what type of cell

A

mostly infected cells

167
Q

Phagocytes and NK cells time to response

A

48-72 hours

168
Q

role of NK cells in infection

A

kill infected cells

169
Q

role of phagocytes in infection (macrophages, neutrophils)

A
  • phagocytose and degrade virus infected cells or debris
  • relase vasoactive substances that increase speed and intensity of immune response
  • secrete cytokines important in induction of the adaptive immune response
170
Q

role of APCs in infection

A

capture, process, and present Ag on their surface to T-cells

171
Q

Humoral immunity: extracellular or intracellular viruses

A

extracellular

172
Q

Cell-mediated immunity (CMI): extracellular or intracellular viruses

A

any viruses, but more effective against intracellular

173
Q

3 types of Ab mediated host defense mechanisms

A
  1. neutralization
  2. opsonization
  3. ADCC
174
Q

describe Ab neutralization

A

Ab binds to virions and blocks infection by preventing attachment, penetration, uncoating or release

175
Q

describe opsonization - what is a downfall to this?

A

Abs bind to virus and assist phagocytic cells with update and intracellular destruction of viruses

**some viruses take advantage of this to enhance entry into host cells (ADE - Ab dependent enhancement of infectivity) - can increase Dz severity

176
Q

describe ADCC (Ab-dependent cell-mediated cytotoxicity)

A

Ab binds to virus infected cells expressing surface Ag and assists immune effector cells in recognizing and killing infected cells

177
Q

describe Ab neutralization mechanisms

A
  1. steric hinderance (physically interferes with virus ligant attachment to receptors)
  2. interfering with fusion (enveloped) or stablizing the capsid (non-enveloped)
  3. lysis of the virion before it can infect a cell
  4. Ab-mediated aggregation
178
Q

How to CTLs help clear infections. When are they most important?

A
  • Activated CTLs release granzymes/perforin and kill virus-infected cells through apoptosis
  • CTL does a better job controlling the spread of viruses after they gain entry. They are most important in recovery from established infection.
179
Q

how can the immune response contribute to the pathogenesis of viral diseases like FIP?

A

excessive immune response can lead to depletion of things like T-cells, macrophages… etc

180
Q

goal of vaccination

A

Prevent or reduce disease, not necessarily to prevent infection.

181
Q

Viral Vx prevent or modify disease (with/without) preventing infection

A

without

182
Q

most common form of live virus vx?

A

modified live

183
Q

goal of modified live Vx?

A

The goal is to reduce virulence but maintain induction of protective immunity (And stimulation of natural immune pathways)

184
Q

how to develop attenuated virus strains?

A

genetically enginerred, temperature sensitive, empirically derived

185
Q

define DIVA

A

Differentiating Infected from Vaccinated Animals

186
Q

define replication competent virus vectors

A

usually, large DNA viruses are used as the vector. Can undergo replication (cause an “infection”) within the vaccinated animal, but generally non-pathogenic

187
Q

define replicaton defective virus vectors

A

can only undergo a single round of replication. Do not produce infectious virus, Less chance of virus transmission, but more Vx needed. (boosters)

188
Q

types of replicating viruses

A
  1. live
  2. modified live
  3. virus-vectored (replicating)
189
Q

types of non-replicating viruses

A
  1. inactivated
  2. virus vectored (non-repliacting)
  3. virus component (protein subunit Vx, virus-like particle Vx, Nucleotide Vx)
190
Q

what is a protein subunit Vx

A

composed of individual protective protein subunit of the virus

191
Q

What is VLP Vx

A

Virus-like partice. non-infectious. lack nucleic acids (empty capsid). Morphologically resemble the real virus

192
Q

what is a nucleotide Vx

A

viral DNA or mRNA. Does not insert into the host genome, but stimulates an immune response

193
Q

define adjuvant

A

chemicals or other compounds added to a Vx to heighten/enhance the immune response

194
Q

adjuvant is especially important for what types of Vx?

A

inactivated/non-replicating Vx

195
Q

Adjuvant mechanisms of action

A
  • Induce cytokine/chemokine responses
  • Enhance recruitment of innate immune cells -> adaptive immune cells
  • Enhance Ag uptake and presentation
  • Enhance Ag transport to LNs
  • Alter quality and quantity of immune response
196
Q

(replicating/non-replicating) Vx are more effective

A

replicating

197
Q

(replicating/non-replicating) Vx are safer

A

non-replicating

198
Q

(replicating/non-replicating) Vx are more stable (storage)

A

non-replicating

199
Q

(replicating/non-replicating) Vx stimulate a longer lasting immune response

A

replicating

200
Q

(replicating/non-replicating) Vx spreads across mucosal surfaces during replication better, thus timulating a greater mucosal immunity

A

replicating

201
Q

(replicating/non-replicating) Vx yield greater anigenic mass because of the amplifyig effect

A

replicating

202
Q

(replicating/non-replicating) Vx have concern for return to virulence

A

replicating

203
Q

(replicating/non-replicating) Vx are more dangerous to pregnant animals

A

replicating

204
Q

barriers to producing antiviral drugs in vet med

A
  • Early detection is challenging as animals are often brought to the vet after the viral infection has progressed.
  • clincial symptoms usually later in infection = missed opportunited for Tx
  • antivrial drugs are specific - determining the specific virus responsible for the disease takes time
205
Q

2 modes of action for antiviral drugs

A

prevent infection - prophylaxis/pre-exposure prophylaxis (PrEP)

stop/limit infection (Therapeutic)

206
Q

Why is there a limited repertoire of antivirals?

A
  1. saftey/efficacy issues
  2. specificity of viral agent
  3. insufficent knowledge base/challenges of in vitro replication
  4. cost (low profits for pharmaceutical companies)
207
Q

main 4 mechanisms of action of antiviral drugs

A
  1. block uncoating
  2. block genome synthesis
  3. block protein synthesis
  4. block release

Virology (5 decks)

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