test 1 Flashcards

1
Q

Viruses are composed of _______

A

1) genome composed of ONE type of nucleic acid (DNA or RNA)

2) Protective protein or lipoprotein coat surrounding the genome

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2
Q

where do viruses replicate

A

ONLY inside living cells- viruses are completely dependent on cellular synthetic machinery for replication (no cellular organelles)… Also, viruses cannot capture and store energy

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3
Q

what do viruses use for replication

A

host cell synthetic machinery

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4
Q

can viruses survive and replicate in cell free media

A

NO (only bacteria can)

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5
Q

What is the purpose of the protective coat that surrounds the genome

A

made of proteins or lipoproteins, the coating allows the viruses to survive in the environment. Also, it GIVES THE VIRUS INFECTIVITY- without the glycoproteins attaching to cellular receptors, the virus will not be able to enter the cell

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6
Q

can a naked viral genome infect the cell?

A

NO- the naked viral genome by itself is not infectious

if the naked viral genome is artificially transfected (forced in), then it will be allowed to replicate the virus

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7
Q

what is a virion?

A

a mature virus particle

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8
Q

what makes up a virion?

A

nucleic acid genome (either DNA or RNA) and a capsid

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9
Q

what is a capsid?

A

protein coating that protects the genome, composed of capsomeres

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10
Q

what are capsomeres?

A

proteins that compose the capsid (polypeptides that are held together by non-covalent bonds)

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11
Q

Functions of the viral capsid

A

1) protects the genome from the environment
2) provides structural symmetry… creates stability
3) allows viruses to enter by recognizing and attaching to host cell receptors
4) Aids in virus replication- may contain enzymes necessary for virus replication (i.e. RNA transcriptase)
5) capsid proteins are very immunogenic

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12
Q

what is a nucleocapsid

A

aka the virion- capsid plus the nucleic acid genome

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13
Q

What distinguishes enveloped viruses and non-enveloped viruses

A

an extra outer coat to some viruses (enveloped viruses). Non-enveloped viruses are called NAKED VIRUSES

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14
Q

where is the envelope derived from

A

the host cell membrane (plasma or nuclear), acquired when the virus exits infected cells by budding

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15
Q

when does the virus acquire an envelope?

A

during a process called budding

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16
Q

what happens before budding

A

the virus inserts viral glycoproteins (PEPLOMERS) into the cellular lipid bilayer

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17
Q

where does the lipid bilayer envelope for viruses originate? Where do peplomers originate?

A

Lipid bilayer is of CELLULAR origin

the peplomers are of VIRAL origin

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18
Q

Functions of the viral envelope

A

1) provides structural symmetry
2) allows virus to enter cell (peplomers attach to host cell receptors)
3) may contain enzymes essential for viral replication
4) peplomers are very immunogenic (because they are virally produced)

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19
Q

4 important criteria for viral classification

A

size of the virion
symmetry of the nucleocapsid (icosahedral, helical, or complex)
presence of envelope?
type of nucleic acid

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20
Q

size of the virion

A

most important tool used to classify viruses

Viruses are expressed in NANOMETERS!!!!!!

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21
Q

what term describes the ability to distinguish one object from another?

A

Resolving power
normal eye ~250um
light microscope is 1000X better: ~.250um
electron microscope is 1000X better: ~0.250 nm (but the practical limit of EM is ~2.5 nm)

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22
Q

what is the smallest virus that light microscopy can see?

A

Poxvirus (350 nm)

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23
Q

what are the three types of nucleocapsid symmetries?

A

cubic/icosahedral
helical nucleocapsid
complex symmetry

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24
Q

Symmetry of nucleocapsid: Cubic symmetry

A

AKA Icosahedral

20-sided structure consisting of 20 equilateral triangles, 12 vertices

5:3:2 rotational symmetry

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25
Q

what makes up the triangles of the icosahedral symmetry

A

symmetrical clusters of capsomeres (Pentons and hexons)

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26
Q

What are pentons

A

term describing capsomeres situated at the 12 vertices of icosahedral symmetry nucleocapsids

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27
Q

What are hexons?

A

term describing capsomeres in icosahedral symmetry that are not at the vertices (surrounded by 6 neighboring capsomeres)

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28
Q

What is the significance of helical nucleocapsid?

A

ALL ANIMAL viruses with helical nucleocapsids are ENVELOPED

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29
Q

What is the only known animal virus with complex symmetry?

A

Poxvirus

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30
Q

types of nucleic acids in viruses

A

DNA or RNA
Single stranded or double stranded
linear or circular genome
segmented or non-segmented genome

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31
Q

what are the 2 classifications of RNA virus genomes that are single-stranded

A

positive polarity and negative polarity

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32
Q

if an RNA virus has a positive polarity, how is it translated?

A

it will be translated directly into protein by cellular ribosomes

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33
Q

if an RNA virus has a negative polarity, how is it translated?

A

negative polarity genomes must be transcribed into a COMPLEMENTARY positive strand before it is translated into protein

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34
Q

what enzyme converts strands from negative to positive polarity?

A

polymerase enzyme (ex: RNA dependent RNA polymerase)

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35
Q

for negative polarity RNA viruses, is cellular polymerase sufficient for transcription to its complementary positive strand?

A

NO
we need RNA dependent RNA polymerase (not made by cell)
the viruses bring the polymerase into the cell

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36
Q

Virus replication steps

A

1) attachment of virus to cells
2) entry of virus into cell
3) uncoating of virus
4) Early transcription of viral nucleic acid into viral mRNA
5) translation of early viral proteins (enzymes) from viral mRNA
6) Transcription of parental genomes into progeny genomes (DNA -> DNA; RNA -> RNA)
7) translation of late structural proteins
8) virus assembly within the cell
9) release of virus from the cell (lysis or budding)

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37
Q

Virus attachment or Adsorption into the cell

A

random
nonspecific
reversible

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38
Q

what initiates attachment/adsorption

A

electrostatic attraction

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39
Q

when does the attachment phase become specific?

A

when the capsid proteins (if naked virus) or peplomers (if enveloped virus) recognize complementary cell membrane receptors

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40
Q

what is viral tropism?

A

the affinity of viruses to only specific cells because of the presence of the specific receptors on certain cells

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41
Q

What 2 methods can a virus enter cell?

A

Viropexis: virus is engulfed by the cell membrane, enters the cytoplasm inside a phagocytic vacuole (primary way that most naked icosahedral viruses enter)

Fusion: viral envelope fuses with cell membrane (occurs with many enveloped viruses)

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42
Q

What initiates fusion of the virus envelope with the cell membrane?

A

the peplomers initiate fusion

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43
Q

What is viral uncoating?

A

the physical separation between viral nucleic acid and the viral capsid. Once a virus uncoats, the virus is no longer infectious

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44
Q

if an infected cell is broken up before the virus uncoats, will the virus still be infectious?

A

yes, the virus can still go infect other cells

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45
Q

if an infected cell is broken up after all virus particles have uncoated, is it still an infectious virus?

A

NO, you need a capsid to be infectious

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46
Q

when is viral uncoating complete?

A

when intracellular infectious virus particles cannot be detected in the infected cell, but a viral genome can be detected by PCR

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47
Q

what are the 2 mechanisms for uncoating

A

1) Digestion: digestion of viral protein coat by CELLULAR proteases
2) Conformational changes: changes in polypeptides that make up the capsomeres (due to changes in pH and ion concentration in the cytoplasm–> causes dissolution of the non-covalent bonds)

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48
Q

where do RNA viruses uncoat and replicate?

A

cytoplasm

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49
Q

where do DNA viruses uncoat and replicate?

A

uncoat in the vicinity of the nuclear pores, and uncoated genome will be immediately transported into nucleus for replication

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50
Q

what is the eclipse period?

A

the period where the infectious virus cannot be detected or demonstrated within the cell

begins when uncoating of tyhe virus is complete, ends with the formation of the first infectious virus progeny

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51
Q

what happens during the eclipse period

A

transcription of the viral genome and translation of the structural viral proteins (production of progeny viruses)

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52
Q

How do viruses usually produce the enzymes that are needed for viral replication?

A

the enzymes needed are produced from mRNA created during the early transcription phase of viral genomic nucleic acids into viral mRNA (mRNA is produced to go to the cytoplasm and be translated into these enzymes)

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53
Q

what is the major early protein/enzyme that is made with viruses

A

polymerase enzymes

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54
Q

where are the early proteins produced?

A

in the cytoplasm, using the host cell’s ribosomes

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55
Q

for RNA viruses with positive polarity genomes, does transcription need to occur?

A

NO!!
POSITIVE POLARITY RNA genomes serve as the mRNA, so it directly binds the cellular ribosomes and is translated into the proteins
NO need for transcription for ss(+)RNA viruses

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56
Q

for RNA viruses with negative polarity genomes, does transcription need to occur? How does it occur?

A

YES

the viral RNA must be transcribed into a POSITIVE complementary strand

to do this, the virus needs RNA-dependent RNA-polymerase

PROBLEM: there is no mRNA present yet to produce the polymerase

SOLUTION: negative polarity RNA viruses carry in the RNA dependent RNA polymerase

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57
Q

for DNA viruses, does transcription need to occur?

A

the DNA genome is directly transcribed by CELLULAR DNA dependent RNA polymerase to yield viral mRNA

AGAIN: DNA viruses use host cell polymerase to produce the viral mRNA

the viral mRNA then leaves the nucleus and travels to ribosomes in the cytoplasm for translation of early viral proteins

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58
Q

Where does translation of viral proteins occur?

A

cytoplasm

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59
Q

what early protein is translated in the case for RNA viruses?

A

RNA dependent RNA polymerase

negative polarity RNA strands bring in some of this, but it makes more for faster replication

positive polarity RNA strands do not bring this into the cell, so all of the polymerase for pos. strands is produced this way

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60
Q

What early protein is translated in the case for DNA viruses?

A

DNA dependent DNA polymerase

this is needed for DNA genome replication

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61
Q

other than just polymerases, what is the function of other proteins produced in translation of early viral proteins?

A

disrupt cellular protein translation so that cells focus on making viral proteins

regulate how the viral genome is transcribed

upregulate or down-regulate cellular proteins

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62
Q

Late transcription of the parental genome into progeny genomes: positive polarity RNA genomes

A

VIRAL RNA dependent RNA polymerase transcribes the parent strand (+ ss RNA) into a complementary (-)RNA strand, and then the negative strands are each transcribed into many (+)RNA progeny strands

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63
Q

Late transcription of the parental genome into progeny genomes: negative polarity RNA genomes

A

VIRAL RNA dependent RNA polymerase transcribes the (-)RNA parent strand into a complementary +RNA strand. The positive strand is then transcribed into many progeny (-) RNA strands (using RNA dependent RNA polymerase again)

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64
Q

How many times is RNA dependent RNA polymerase used to produce progeny RNA genomes?

A

twice

1) produces complementary strand
2) takes complementary strand and transcribes progeny strand

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65
Q

for DNA viruses, how is replication of the genome done?

A

the parental ds DNA genome is uncoiled and replicated into many progeny by VIRAL DNA dependent DNA polymerase

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66
Q

where are DNA virus genomes replicated?

A

nucleus

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67
Q

How do retroviruses work?

A

retroviruses carry into the cell a ss RNA molecule

the RNA is copied into a double stranded DNA molecule by reverse transcriptase (brought in by the virus)

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68
Q

what is reverse transcriptase?

A

RNA dependent DNA polymerase

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69
Q

What are the late viral proteins that are translated?

A

structural proteins: polypeptides that will produce capsomeres and peplomers, depending on whether the virus is enveloped or not

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70
Q

what is the mRNA used to translate the late viral proteins?

A

for +RNA viruses, proteins are translated directly from progeny RNA strands

for -RNA viruses, progeny strands are transcribed to a positive polarity strand, and this complementary strand is used to be translated to the proteins

for DNA viruses, late proteins are translated from viral mRNA derived from the progeny DNA genomes

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71
Q

What are the 2 stages of virion assembly?

A

Morphogenesis and encapsidation

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72
Q

What is morphogenesis?

A

process by which the viral capsid polypeptides come together and for assembled capsomeres and intact capsids (with no genome yet)

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73
Q

is morphogenesis spontaneous?

A

yes

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74
Q

what is encapsidation?

A

follows morphogenesis

process where the viral genome is inserted into the already formed capsid

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75
Q

does the capsid form around the genomes?

A

NO!!! the genome gets inserted into pre-formed capsids

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76
Q

What is released with many intact viruses?

A

many non-infectious, empty capsids

not all pre-formed capsids get encapsidated by genomes

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77
Q

where does assembly of the virion take place?

A

where the virus replicates

for RNA viruses, assembly takes place in the cytoplasm

for DNA viruses, assembly takes place in the nucleus

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78
Q

What are the 2 ways that a virus can be released from the host cell?

A

Lysis: physical bursting of the infected cell
Budding: opposite of phagocytosis

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79
Q

where does budding take place?

A

areas of the plasma or nuclear cell membrane that has been modified by the insertion of viral proteins

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80
Q

is budding destructive?

A

no

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81
Q

what is yield?

A

the number of infectious virus particles produced from each cell

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82
Q

replication of Picornavirus (foot and mouth disease)

non-enveloped (+) ssRNA virus with icosahedral capsid

A

1) attaches to specific cell receptors on the cell surface, enter via viropexis and uncoats in cytoplasm
2) +RNA virus, so no transcription needed
3) RNA dependent RNA polymerase translated form parental genome (parental genome serves as mRNA)
4) viral RNA dependent RNA polymerase binds to parent RNA strand and makes complementary negative strands, then does the same to the complementary strands to make progeny viral genomes
5) progeny strands are then translated by cell ribosomes into one long polypeptide strand tha tis then cleaved by viral proteases
6) morphogenesis of progeny occurs in cytoplasm, then encapsidation of progeny genome
7) virus is released via cell lysis

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83
Q

Replication of Herpesvirus

enveloped ds DNA virus with icosahedral capsid

A

1) peplomers bind and attach to cellular receptors, herpesvirus enters by fusion and uncoats in the vicinity of nuclear pores
2) uncoated DNA enters the nucleus before it is digested by cytoplasmic enzymes
3) DNA genome is transcribed into viral mRNA in the nucleus by host DNA dependent RNA polymerase, then the mRNA moves to cytoplasm to be translated into viral DNA dependent DNA polymerase and thymidine kinase… these then go back to the nucleus
4) polymerase and thymidine kinase initiate massive round of viral DNA replication in the nucleus to produce progeny viral DNA genomes
5) mRNA is transcribed from progeny DNA and goes to cytoplasm for translation into viral structural proteins (that move back to nucleus)–> capsomeres and peplomers
6) morphogenesis occurs in nucleus, followed by DNA genome insertion via encapsidation
7) virus leaves cell after viral peplomers are inserted into the nuclear membrane–> then virus leaves cell by budding, acquires envelope from nuclear cell membrane

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84
Q

Replication of retroviruses- what makes them special?

A

enveloped RNA viruses with helical nucleocapsid surrounded by icosahedral capsid
genome is single stranded and diploid

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85
Q

Replication of retroviruses

A

1) peplomers on envelope recognize and attach to CD4 receptors on Th lymphocytes, enter cell by fusion, uncoats in cytoplasm
2) Reverse transcriptase (RNA dependent DNA polymerase) is brought into cell by virus… it binds to uncoated viral RNA in cytoplasm and makes complementary double stranded DNA copy of the RNA genome (viral ds DNA moves to nucleus)
3) the viral ds DNA is then ligated into the cell DNA chromosomes
4) the viral DNA is transcribed into small viral mRNAs, move to cytoplasm, and are translated into viral proteins (peplomers, capsids, RT enzyme)
5) One long mRNA strand is transcribed form the entire DNA genome–> serves as the viral genome
6) morphogenesis occurs in cytoplasm
7) the viral nucleocapsid is encapsidated into the icosahedral capsid ALONG WITH reverse transcriptase
8) viral peplomers are inserted into the PLASMA membrane and virus is released by budding

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86
Q

What is a gene?

A

a nucleotide sequence that encodes for a specific polypeptide or protein

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87
Q

What is a mutation/

A

results from changes in nucleotide sequence within viral genes

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88
Q

what are the types of mutations?

A

substitution mutation: one (point) or several nucleotides are substituted

deletion mutation: one or several nucleotide bases are deleted from the genome

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89
Q

What are spontaneous mutations?

A

occur during normal virus replication

low rate of spontaneous mutations for DNA viruses (10^-8), but high rate of spontaneous mutations for RNA viruses (10^-3)

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90
Q

What are consequences of mutations?

A
  • host range changes: virus adapts to unnatural host
  • increase or decrease in virulence
  • susceptibility to drugs can change (resistance)
  • antigenic makeup of virus changes
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91
Q

What is phenotypic mixing/

A

occurs when 2 closely related viruses infect one cell and produce different progeny viruses

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92
Q

What is a pseudotype?

A

virus progeny that have acquired the genotype of one parent and phenotype of the other parent (A genotype, B phenotype)

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93
Q

What is a mixed phenotype?

A

virus progeny that have acquired the genotype of one parent and phenotype of both parents (A genotype, A and B peplomers/phenotype)

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94
Q

Are pseudotypes and mixed phenotype viruses genetically stable?

A

NO
if one of these infects a cell, they will only be able to produce the phenotype of the genome they have (A genotype can only produce A phenotype)

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95
Q

How does Genetic recombination occur?

A

2 genetically different but related viruses infect the same cell and replicate… And they exchange nucleic acid between parental viruses

progeny viruses are then formed whose nucleic acid is a combination of both parents

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96
Q

In essence, what is a recombinant?

A

part of one virus’ genome in the genome of another virus

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97
Q

When do recombinant viruses occur naturally?

A

when cellular genes are inserted into the viral genome during viral replication in animals

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98
Q

What is reassortment?

A

a type of genetic recombination specific to influenza virus

if a cell is infected with 2 different influenza viruses, progeny viruses have a genome that consists a mixture of segments derived from both viruses

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99
Q

How does influenza form now pathogenic strains?

A

genetic reassortment

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100
Q

Recombinant virus vaccines

A

Insertion of the GENE that encodes for an antigen (ex: G glycoprotein of rabies) into the genome of another virus (Ex: Pox virus). When the vaccine is inoculated into an animal, the rabies gG is translated along with the other pox proteins. The immune system sees the gG, resulting in humoral and cell mediated response to gG

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101
Q

Problems with Antiviral chemotherapy

A

> drugs can be toxic to cells and thus toxic to animals
by the time clinical disease is evident, virus replication has already peaked and the immune response is underway
Resistance to antiviral drugs occur quickly (RNA viruses mutate at high rates)

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102
Q

Strategy of antiviral drugs

A

kill the virus only, not normal cells

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103
Q

Idoxuridine and Trifluridine

A

analogue of thymidine which is incorporated into DNA in place of thymidine

good anti-herpesvirus drug

**Used only as ophthalmic drug to treat for herpes eye infections

converted into IdoxTP (analog of TTP and is inserted into the herpesvirus DNA genome by DNA dependent DNA polymerase–> blocks DNA replication)

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104
Q

Adenine arabinoside

A

nucleotide analog of dATP

inhibits DNA synthesis (inserted into genome by DNA dependent DNA polymerase–> blocks DNA replication)

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105
Q

Acyclovir

A

nucleoside analogue

transported into cells by guanine transporter and then phosphorylated by thymidine kinase into an active metabolite (thymidine kinase is only present in herpesvirus infected cells, so only active in infected cells)

once phosphorylated, it inhibits herpesviral DNA polymerase

ACV is also inserted into DNA terminating DNA synthesis

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106
Q

Amantadine

A

prevents influenza A infection

blocks the uncoating process of influenza by binding M2 protein (which is needed for uncoating)

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107
Q

Azidothymidine (AZT)

A

pyrimidine nucleoside analogue

inhibits reverse transcriptase

100X more affinity for HIV-RT than for DNA polymerase

108
Q

Ribavarin

A

prodrug that is metabolized into nucleotides resembling RNA nucleotides

nucleotides are inserted into viral RNA, causing translation into non-functional viral proteins and non-infectious viral genomes

109
Q

Oseltamivir (Tamiflu)

A

neuramidase inhibitor for Influenza A and B

prevents new viruses from emerging from infected cells

110
Q

Protease inhibitors

A

inhibitor of post-translational proteases (essential for post-translational cleavage of polypeptide sequences)

inhibits the formation of infectious virus

block the late stages of viral replication

111
Q

What are cytopathic effects

A

microscopically visible morphological changes in cell cultures induced by viruses

presence of CPE usually indicate virus replication

112
Q

What causes the visible morphological changes of cytopathic effects?

A

due to cell dying as a result of viral infection

1) cell swelling/rounding/shrinking
2) presence of inclusion bodies within infected cells
3) cell fusion

113
Q

What causes cytopathic effects

A

the shutting down of cellular protein synthesis, which occurs when viruses replicate in permissive cells

this can also occur due to virus infection into non-permissive cells (cells that the virus can’t replicate in)… these effects are caused by direct toxicity of the viral capsid to the host cell

114
Q

What is a viral plaque?

A

In the lab, viruses are grown on a tissue culture monolayer of cells attached to plastic container

when virus replicates in cells, it spreads to surrounding cells-> when the infected cells are killed, they shrink away from the surrounding cells and detach from the plastic. This leaves behind a small denuded area in the cell monlayer called a plaque

115
Q

What are inclusion bodies?

A

intracytoplasmic or intranuclear masses observed in STAINED viral infected cells

seen both in vivo and in vitro

the inclusion bodies are very characteristic of certain viruses

116
Q

do all viruses cause inclusion bodies?

A

no

117
Q

What are the types of inclusion bodies?

A

Intranuclear, intracytoplasmic, or both

DNA viruses cause intranuclear inclusions (Poxvirus is an exception)

RNA viruses cause intracytoplasmic inclusion

118
Q

What are inclusion bodies? (3 part answer)

A

site of virus replication where viral proteins accumulate

aggregate of complete virions (called crystalline masses)

Scars resulting from degenrative changes in the cell

119
Q

Are inclusion bodies specific to certain viruses

A

yes, some viruses will exhibit very distinctive inclusion bodies–> histopathology serves as a very important criterion for diagnosing certain viral infections

120
Q

Rabies inclusion bodies?

A

RV causes intracytoplasmic inclusions called NEGRI BODIES

121
Q

What are Rabies inclusion bodies called?

A

Negri bodies

122
Q

Adenovirus inclusion bodies?

A

Adenovirus causes intranuclear inclusions that are BASOPHILIC (in dogs, mostly in liver)

123
Q

Distemper inclusion bodies?

A

Distemper causes BOTH intracytoplasmic and intranuclear inclusions in the BRAIN

causes mostly intracytoplasmic inclusions in other organs

124
Q

What is a viral syncytium?

A

certain viruses induce a fusion of the plasma membranes of surrounding infected cells

results in formation of a multinucleated giant cell called a synctytia

125
Q

what causes viral syncytium?

A

specific peplomers inserted into the cell membrane during viral replication

126
Q

what viruses induce viral syncytium?

A

parainfluenza virus and herpesvirus

127
Q

What are non-cytopathic viruses?

A

viruses that replicate in cells without dmaging or killing the cell

cause no cytopathology

128
Q

what are the mechanisms of non-cytopathic viruses?

A

persistent infection
latent infection
cell transformation

129
Q

what is a persistently infected cell?

A

cells that are infected and continuously release infectious virus particles while showing no cytopathology

FeLV and feline calicivirus

the non-cytopathic type of bovine viral diarrhea virus causes persistent infections in cattle

130
Q

What is a latently infected cell?

A

cells that have virus in them but the VIRUS IS NOT REPLICATING

131
Q

do latently infected cells produce infectious particles?

A

no, the virus is not replicating

132
Q

when do latently-infected cells stop being latently infected?

A

when the virus begins to replicate and produce Cytopathic effects

133
Q

what is the term for a virus that was in a latently infected cell and is now replicating in that cell?

A

viral recrudescence

134
Q

What causes viral recrudescence?

A

stress, cytokines, irritation, etc.

135
Q

what viruses cause latent infections?

A

retroviruses (HIV, FIV) cause latent infections in lymphocytes

herpesvirus typically causes latent infections in neurons

136
Q

What is a virus transformed cell?

A

a cell that has acquired a different DYSREGULATED growth characteristic as a result of virus infection

137
Q

what do virus transformed cells lead to?

A

virus transformed cells are neoplastic, cause tumors

138
Q

Do cells become virus transformed cells due to infection by DNA or RNA virus infections?

A
BOTH
DNA viruses (herpesvirus, papillomavirus)
RNA viruses (retroviruses)
139
Q

what is expressed due to the virus infection that causes the virus transformed cell?

A

Viruses cause the expression of one of two things:

1) expression of viral oncogene (v-onc) that is carried in by the virus as part of its viral genome. The viral products translated from these oncogenes are the transforming agents
2) expression of cellular oncogenes (c-onc)–> get turned on by the virus when it infects the cell.

140
Q

What do cellular oncogenes cause in the virus transformed cell?

A

one of 4 things is turned on

1) a proto-oncogene, which regulatees cell growth and differentiation
2) a tumor suppressor gene
3) a gene that regulates apoptosis
4) a gene that is necessary for DNA repair

A tumor is thought to arise form the outgrowth of a single cell (monoclonal in origin) that has accumulated multiple genetic mutations in more than one of the above-mentioned oncogenes

141
Q

Are infectious virus particles released from virus transformed cells?

A

if infected with a retrovirus, the virus is replicated

in cells transformed by DNA viruses, the genome of the virus is present in the cell but infectious particles are not detected

in papilloma viruses, infectious particles are only seen in dead cells

142
Q

characteristics of virus-transformed tumor cells

A
  • greater growth potential (immortal and divide indefinitely, lose contact inhibition, increased mitotic rates)
  • cells are altered morphologically and metabolically (serum requirements are less)
  • contain viruses and display viral encoded proteins (cell membranes display new surface proteins)
  • cells have the capacity to produce malignant tumors when injected into immunosuppressed lab animals
  • show chromosomal abnormalities (heteroploidy)
143
Q

What is required for an infection to occur?

A

source of virus/infection
means of virus transmission
source of susceptible animals

144
Q

How do viruses survive outside the host?

A

virus resistance- survive in environment for long time

infection of arthropod vectors (virus replicates in arthropod)

145
Q

What is the extrinsic incubation period?

A

the period of time the vector is infected to the time the virus can be transmitted by the vector

146
Q

How do viruses survive within the host?

A

Establish persistent or latent infections

change antigenic makeup to escape immune response

cause immunosuppression

147
Q

What are enteric viruses (rotavirus and enteroviruses) resistant to?

A

environment, low pH of the stomach, detergent action of bile, and proteolytic digestive enzymes

the enzymatic degradation of the outer capsid wall enhances the infectivity of the irus

148
Q

How are enteric viruses transmitted?

A

typically through contaminated feces or fomites

149
Q

How do respiratory viruses contact the respiratory system?

A

usually via aerosol droplets (droplets 10 um are deposited on mucosa of nasal turbinates)

150
Q

what enhances the transmission of a respiratory virus

A
  • atmospheric conditions (humidity)

- close contact between animals

151
Q

are most respiratory viruses enveloped or non-enveloped?

A

enveloped, so these viruses are usually easily inactivated

152
Q

what do respiratory viral infections predispose the host to?

A

secondary bacterial infections of the respiratory system

153
Q

How do viruses get access to the body through the skin?

A

through a break in the skin (trauma, arthropod bite, needles/iatrogenic)

154
Q

How do viruses gain access to the urogenital system?

A

via sexual relations

the fetus can be infected transplacentally or via the sperm

155
Q

How do viruses enter the body?

A
alimentary system
respiratory system
urogenital tract
conjunctiva (infectious bovine rhinotracheitis virus)
skin
156
Q

What happens after the virus enters the body?

A

viruses may remain localized or they may spread and cause lesions in different organs

157
Q

What are the first cells that the virus encounters? what are the possible outcomes?

A

Macrophages

1) virus can be destroyed by the macrophage
2) replicate in the macrophages and disseminate throughout the body
3) be taken up by the macrophages in organs and spread to adjacent cells and set up an infection in that organ

158
Q

What is viremia?>

A

presence of virus in the blood (virus can be free in the plasma or be cell associated within leukocytes or RBC)

159
Q

Where is the first site of virus replication?

A

at the site of virus entry

160
Q

Mousepox replication

A

site of entry is skin

  • after local replication in skin, virus goes to LN and undergoes another round of replication
  • then invades the blood stream and reaches the liver (primary viremia)
  • after replicating in liver/spleen, it is released in the blood stream in HIGH CONCENTRATIONS (secondary viremia)
  • then goes to skin (target organ), where the virus will replicate again and cause typical mousepox
161
Q

What are the 2 ways viruses can reach the CNS?

A

via peripheral nerves via axon cytoplasm flow

via the bloodstream

  • passive transport between/thru blood vessel endothelium
  • infect vascular endothelial cells and reach the brain parenchyma
  • transport across blood vessels via infected leukocytes
  • infect brain parenchyma via CSF
162
Q

What is perivascular cuffing?

A

small lymphocytes surrounding blood vessels- noted histopathologically in most viral infections of the CNS

163
Q

what causes the CNS lesions during viral infections?

A

immune response to the virus, not direct damage by the virus itself

164
Q

How is a fetus infected via a virus in the dam?

A

viremia leads to direct fetal infection or infection of uterus/placental

165
Q

do fetal infections result in death of the fetus?

A

not necessarily- if fetal death occurs, the consequence could be SMEDI (stillbirth, mummification, embryonic death, infertility)

166
Q

if the fetus survives infection, what is the result?

A

either born malformed or born normal and immune to the virus

typically, fetal infection during the 1st trimester is more apt to result in congenital defects
infection later in pregnancy results in fetal death or survivability

167
Q

What are the physical barriers to infection?

A

skin
respiratory tract
digestive tract
reproductive tract

168
Q

physical barriers to infection: skin

A

most difficult barrier to penetrate

cells on surface are dead, so no virus replication

169
Q

physical barriers to infection: respiratory tract

A

epithelial cells have cilia and are covered by mucus

viruses get trapped in mucus and cilia move the mucus towards respiratory opening (swallowed or spat out)

170
Q

Physical barriers to infection: digestive tract

A

saliva inactivates many viruses

pH and trypsin in stomach and digestive enzymes in duodenum destroy most viruses by breaking down the lipid envelope and capsid

171
Q

Physical barriers to infection: Reproductive tract

A

stratified epithelium covered by mucus

172
Q

Innate immune response

A

non-specific response (recognizes all viruses)

does not develop memory cells

activated within minutes of infection

173
Q

what are the 3 most important components of the innate immune system

A

interferons (alpha and beta)
macrophages and dendritic cells
natural killer cells

174
Q

what role neutrophils have in innate immunity to viruses?

A

none

neutrophils only work on bacteria

175
Q

What is CPRR?

A

cellular pattern recognition receptors

present on macrophages, dendritic cells, nk cells, fibroblasts, etc

recognize pathogen-associated molecular patterns (PAMP)

176
Q

What are examples of CPRRs?

A

toll like receptors

177
Q

what is the most important CPRR and where is it located?

A

TLR-3, located inside endosomes (NOT on cell surface)

178
Q

what does TLR-3 recognize, and what cascade does it initiate?

A

TLR-3 recognizes viral dsRNA and ssRNA

TLR-3 activates cytoplasmic kinases that phosphorylate NFkB, which then translocates to the nucleus where it initiates the transcription of cytokine mRNA.

the cytokine mRNA are translated into cytokines and are exported by the cell to initiate inflammation and antiviral response

179
Q

what cytokines plaly a role in controlling viral infections?

A
TNF-alpha
IL-12
IFN-alpha
IFN-beta
IFN-gamma
180
Q

what is the most important arm of the innate resistance to viruses?

A

the interferon system

181
Q

what type of cells produce IFN-alpha, IFN-beta, and IFN-gamma

A

IFN alpha and beta are made by any viral infected cell

IFN-gamma is produced onlly by activated NK cells and Th cells

182
Q

How are Interferons produced?

A

When a virus infects a cell, the viral RNA binds to TLR3 within an endosome. This activates cellular kinases that phosphorylate NFkB that activates the cellular IFN genes that encode for IFN-alpha and beta mRNAs. The mRNA is then translated into IFN-alpha and IFN-beta that are exported out of the viral infected cell

183
Q

are IFN-alpha and IFN-beta active in the induced cell (i.e. the cell that produces them)?

A

NO, they are exported out of the cell and interact with specific receptors on adjacent, non-infected cells

184
Q

what happens to the cell that produces the interferons?

A

the infected cell will usually die from viral infection

185
Q

What happens when IFN-alpha and IFN-beta bind to surface receptors of non-infected host cells?

A

the non-infected cells induce the production of antiviral proteins–> these antiviral proteins cause the cells to resist a viral infection

186
Q

are IFN-alha and beta antiviral?

A

NO

the interferons are not directly antiviral, but they induce antiviral proteins which causes the cells to destroy viruses

187
Q

what are the jobs of IFN alpha and beta?

A

induce antiviral proteins

activate NK cells in the vicinity of the infection

188
Q

what do NK cells do?

A

secrete IFN-gamma that then activates macrophages and dendritic cells to secrete TNF-alpha and IL-12

189
Q

What do activated macrophages and dendritic cells do?

A

they produce TNF-alpha and IL-12
dendritic cells move to the LN to present viral Ag to T-cells

the macs initiate an inflammatory response in the vicinity of the viral infected cells

190
Q

What are the three antiviral proteins?

A

2-5(A) Synthetase
protein kinase (PK-1)
RNase L enzyme

191
Q

where are the antiviral proteins present?

A

all are present in the cytoplasm in an inactive form

192
Q

when are antiviral proteins activated?

A

when the cells are infected by a virus

193
Q

How is 2-5(A) Synthetase activated, and what does it do?

A

it is activated by dsRNA

it synthesizes 2-5(A), which activates RNase L which chews up viral mRNAs

194
Q

What activates PK-1, and what does it do?

A

PK-1 is actvated by dsRNA
it phosphorylates the translation of initiationg factor (eIF-2) which binds to viral mRNA to prevent viral protein translation and formation

195
Q

are IFNs broad or narrow spectrum? potent or not potent?

A

IFNs are very broad spectrum (not virus specific) and extremely potent

196
Q

What are natural killer cells?

A

large granular lymphocytes that exhibit spontaneous cytotoxicity against viral infected cells

197
Q

what percent of the circulating leukocytes does natural killer cells make up?>

A

10%

198
Q

do NK cells need to be sensitized to a virus before they attack?

A

NO
NK cells are broad spectrum- they can kill all virally infected cells without needing to be sensitized to the specific virus

199
Q

how are NK cells activated?

A

they are activated by IFN-alpha and beta or by the inflammatory cytokines TNF-alpha and IL-12 produced by macrophages

200
Q

What are the 3 receptors on NK cells?

A

Natural cytotoxic receptors- recognize and bind structural viral protiens (peplomers) on viral infected cells

Inhibitory MHC-1 receptors-recognize MHC-1 molecules naturally present on all host cells

Fc receptors that bind to Fc portion of Ab that have attached to peplomers on viral infected cells

201
Q

what is the dominant receptor on NK cells?

A

the inhibitory MHC-1 receptor

if it is activated by the present on normal MHC-1, it will prevent the natural cytotoxic receptor from activating the NK cell

202
Q

what happens when the NCR is activated by viral infected cells that do not display normal MHC-1

A

NK cell kills the cell by secreting PERFORIN and then injecting GRANZYME in the cell (Granzyme activates the death proteins which induces apoptosis)

203
Q

what does the NK cell use to kill virus infected cells

A

first, inserts perforin, then injects granzyme to induce apoptosis

204
Q

What is ADCC?

A

Antibody dependent cell cytotoxicity

when the NK cell binds to an Ab that is attached to a virus infected cell

NK kills these cells using perforin/granzyme pathway

205
Q

When does NK cell activity peak?

A

3 days post infection, then it declines

CTLs appear later, around 7 days

206
Q

What is the function of NK cells

A

to build up rapidly following virus infection and bind non-specifically to limit viral infection while CTLs are being built (takes about a week). CTLs are more efficient at recognizing and killing viral infected cells

207
Q

what is more efficient at killing viral infected cells: NK cells or CTL?

A

CTLs

208
Q

when does the level of IFN produced peak? When do NK cells peak? When do CTLs appear? When do Ab appear?

A

IFN peaks 3-5 days post infection
NK cells peak 3 days post infection
CTLs appear 7 days post infection
Ab appear 10 days post infection

209
Q

Where are macrophages seen?

A

they are seen in circulation as monocytes and found fixed in tissues/mucosal surfaces (kupffer cells, dendritic cells, lung magrophages)

210
Q

What is the function of macrophages and DC?

A

take up viruses by phagocytosis (macs) or micropinocytosis (DC) and bring them to LN

Both also recruit NK cells and Th cells by producing IL-12 and TNF-alpha

211
Q

How can macrophages destroy viruses that are inside them?

A

only when macrophages are activated by IFN-gamma (produced by NK cells and T-lymphocytes)

212
Q

What is humoral immunity?

A

adaptive immunity that includes antibodies

213
Q

What is the significance of IgM?

A

it is important in primary response to viral infection, but level of IgM quickly drops off

IgM activates complement and is important in opsonization, neutralization, and agglutination

IgM is only present in high levels during active infection, so can determine active infection vs prior exposures

214
Q

significance of IgG

A

enters tissue spaces during inflammation and can escape onto damaged mucosal surfaces

able to opsonize, agglutinate, and neutralize

IgG persista for a very long time, so can’t be used to determine active infection

215
Q

significance of IgA

A

secretory Antibody

protects mucosal surface

dimer with J-chain and secretory piece

the major Ig in body secretions (tears, respiratory mucosa, gut, milk)

agglutinates and neutralizes the virus… PREVENTS VIRAL ADHERENCE

important in lactogenic immunity

trypsin-resistant (since it can be found in gut)

216
Q

Define Seronegative, Seropositive, and seroconversion

A

Seronegative: animal has NO circulating antibodies to a particular virus

seropositive: animal has circulating Ab to a particular virus
seroconversion: when an animal changes from seronegative to seropositive (4 fold)

217
Q

What are the ways antibodies prevent viral infection?

A

neutralization- Ab binds epitopes on the virion surface and prevents viral attachment to cells (can also cause conformation changes so it can’t bind)

lysis- Ab bound to virus particles activates complement cascade, resulting in viral lysis

aid in phagocytosis- Ab arms macrophages or opsonize viral particles. Fc receptors on macs bind Abs and initiate phagocytosis… or complement system may be activated

cause lysis of host cell- Ab bind to virus infected cells, activate complement system or ADCC (NK cells/CTLs). Phospholipases are released and cause cell lysis, and cells are lysed before virus particles released, preventing virus spread

218
Q

What regulates cell mediated immunity

A

T cells regulate cell mediated immunity via secretion of cytokines

219
Q

What kind of antigens do CTLs respond to?

A

endogenous antigens

220
Q

how do CTLs work?

A

during virus replication, small viral peptides are formed which bind to the groove on MHC-1 molecules and are transported to the cell surface and exposed to CTLs.

CTLs that recognize their peptide:MHC molecule are activated and become cytotoxic- they recognize and lyse any viral infected cells that present these specific viral peptides to their MHC-molecules

221
Q

what do Th cells do?

A

produce various cytokines that activate B cells and T cells

Th1 is primarily responsible for stimulating cell mediated immune responses

Th2 is primarily responsible for stimulating humoral response

222
Q

what are the 2 types of vaccines?

A

inactivated/killed vaccine- whole virus or part of the virus is inactivated

attenuated/live vaccines- live virus that has been rendered less pathogenic/virulent

223
Q

how are inactivated vaccines presented?

A

presented as exogenous antivens

224
Q

what response does inactivated vaccines give?

A

humoral Ab response dominated by Th2 cells

very little or no cell mediated immune response

225
Q

how are attenuated vaccines presented?

A

presented as both exogenous and endogenous antigens

226
Q

what response does attenuated vaccines give?

A

both humoral Ab and cell mediated immune response via Th1 and Th2 cells

227
Q

do viruses in attenuated vaccine replicate within body?

A

yes, they replicate within the animal, so they present as both endogenous and exogenous antigens

228
Q

What are the 4 types of live vaccines?

A

Live virulent virus (rarely used)
Attenuated- modified live vaccine
Genetically altered viruses
Recombinant vector vaccines

229
Q

How are live virulent virus vaccines given?

A

given by an abnormal route or given to another host to induce immunity (i.e. given at the wrong site, chicken getting turkey virus)

230
Q

what is the main disadvantage of live virulent virus vaccines?

A

the virus can spread to other animals

231
Q

What is the basis behind modified live vaccines?>

A

the virulence of the virus or bacteria reduced by growing and passaging the virus through tissue culture cells, eggs, or animals.

232
Q

what are ways to produce modified live vaccines?

A

1) passing it through a wrong animal (ex: passing virus thru rabbit–> inoculating rabit>allowing rabbit to develop disease>re-isolating virus from rabbit>re-inoculation of virus into another rabbit… basically virus adapts to causing disease only in rabbit and not original host–> when virus is re-inovulated into the original host, a mild infection follows, which causes strong humoral and CMI responses
2) UV light mutagenization
3) Temperature sensitive mutants (viruses are selected that cannot grow at normal body temperature

233
Q

What are most virus vaccines used in vet med?

A

Modified live vaccines that have been stabilized by lyophilization

confers good immunity after only one inoculation (since the virus replicates in the animal)

234
Q

What is the basis behind genetically altered viruses?

A

gene deletion or site-directed mutagenesis causes attenuation

the GENE DELETED VIRUS can infect animals but cannot cause disease

235
Q

What are some examples of genetically altered viruses?

A

Thymidine kinase deficient vaccines or glycoprotein E deleted vaccines

236
Q

How does genetically altered virus vaccines work with test and slaughter programs?

A

Differentiation/discrimination of infected from vaccinated animals (DIVA) strategy

pigs are inoculated with TK-deficient pseudorabies vaccine. the pigs do not make Ab to TK protein since it is not in the vaccine. Therefore, if a vaccinated pig becomes infected with wild-type pseudorabies, it will make antibodies to TK protein expressed by the wild virus.

By testing annually for TK protein, we can do serology do determine which have been infected with PRV and slaughter

serology we use is indirect ELISA

237
Q

What is the basis of recombinant vector vaccines?>

A

a gene that encodes for an important protective immunogenic protein of one virus is inserted into (recombined) with the genome of another virus, usually pox virus. The recombinant vaccinia virus vaccine now carries an extra gene. When foxes/raccoonns eat bait laced with this vaccinia virus, the virus replicates and the rabies virus protein is translated with the rest of the virus. The body now mounts an immune response and a CMI and humoral immune response now recognizes rabies.

238
Q

What are the types of non-replicating, killeld virus vaccines?

A

Inactivated whole virus

Purified native viral proteins

subunit vaccines (expression of viral proteins in cells)

vaccines produced by expression of viral proteins that self-assemble into virus-like particles

Naked DNA vaccines

239
Q

inactivated whole virus

A

virus inactivated by agents render them non-infectious or non-toxic while retaining antigenic sites

240
Q

what are commonly used agents to inactivate whole viruses?

A

formaldehyde

alkylating agents (B-propiolactone)- cross links the nucleic acid but leaves the proteins intact

241
Q

Purified native viral protiens

A

lipid solvents solubilize enveloped viruses and release the glycoproteins which are then separated and harvested for injection in animals

basically inject glycoproteins to allow immune response

242
Q

Subunit vaccines

A

produced by expression of viral proteins in cells

yeast, mammalian cells, insects, and bacteria can produce viral proteins in large quantities (the viral gene of interest is translated into viral proteins in those eukaryotic cells)

Ex: hepatitis B, Hemagglutinin of influenza A, subunits of e.coli and FeLV

243
Q

vaccines produced by expression of viral proteins that self-assemble into virus like particles

A

by mixing capsomeres and different proteins together, they self-assemble into virus-like particle

do not produce a genome, just a capsid

244
Q

what do inactivated vaccines need to be injected with?

A

inactivated vaccines must be injected with adjuvants to maximize immunogenicity

245
Q

what are adjuvants?

A

materials that are added to vaccines to potentiate the humoral and CMI responses (increase the duration of immunostimulation)

adjuvants act as vehicles that slow down the degradation of the Ag so that it is released over a longer period of time

adjuvants also act as immunomodulators that localize tha antigen creating non-specific prolonged cell-mediated inflammatory response

246
Q

what are examples of adjuvants

A

aluminum salts

bacterial cell wall fractions such ass LPS

Surface active agents

Freund’s complete adjuvant (inactivated mycobacterium oil)

247
Q

what is the problem with Freund’s complete adjuvant?

A

causes sterile granulomas/abscesses

248
Q

What is the basis of naked DNA vaccines?

A

inoculation of a naked gene instead of protein

when the gene is inoculated IM, the myocytes take up the naked DNA–> DNA is transcribed into mRNA and mRNA is translated into immunogenic protein that stimulates immune response

the protein is treated as endogenous and exogenous protein, stimulating both CMI and humoral immunity

249
Q

what is the disadvantage of naked DNA vaccines?

A

they can integrate in the DNA and activate ancogenes

250
Q

What type of protection do vaccines provide?

A

Partial or incomplete protection

a vaccinated animal may get a subclinical infection or superficial mucosal infection

251
Q

what do vaccines protect against

A

vaccines protect against disease, but do not prevent sub-clinical infection (they can still be infected and shed virus)

252
Q

are vaccination and immunization synonymous?

A

no, you can vaccinate without immunizing

253
Q

what are precautions you should take when handling vaccines?

A

read label
protect vaccs against excessive heat and light
don’t mix vaccines into one vial and give as cocktail
be careful with disinfectants (MLV can be destroyed)
one vaccine may block immune response of another… ex: distemper is immunosuppressive

254
Q

adverse consequences of vaccination

A
residual virulence
toxicity
allergic reactions
harmful effects on fetus
post-vaccinal sarcoma
255
Q

what are the toxicity concerns with vaccination?

A

local reaction at sites of vaccination for a few days

vaccines containing killed gram-negative organisms may be extrinsically toxic due to presence of endotoxins

256
Q

What harmful effects on the fetus can vaccines have?

A

modified live vaccines can cross placenta and affect fetal development (blue tongue virus)

257
Q

where have we seen post-vaccinal sarcomas?

A

mostly cats at the site of vaccination

cats receiving FeLV are 5.5 times more likely to develop sarcoma

number of vaccs cats receive is important in increasing incidence of sarcomas: 50% with 1 vaccine
127% with 2 doses
175 with 3-4 doses of vaccine

258
Q

What are the major causes of vaccine failure?

A

1) vaccination with a different virus or serotype than the one causing disease
2) presence of maternal Abs
3) Vaccine may be inactive (improper storage, expired)
4) Incorrect manufacturing (too little Ag, contamination)
5) not enough protection was elicited from vaccine
6) short time between vaccination and infection with virulent virus
7) IgA was not produced
8) vaccine given incorrectly (SQ instead of IM)

259
Q

How do maternal antibodies cause vaccine failure?

A

maternal antibodies prevent MLV from replicating if levels of Ab is high. Attenuated viruses get neutralized by maternal Ab

260
Q

Why is IgA important for enteric and respiratory viruses, and when is IgA not produced when vaccinated?

A

IgA is important because most enteric and respiratory viruses cause local disease and not systemic–> IgA protects the mucosa better than IgG (better for systemic viral infections)

IgA is not produced well during parenteral vaccines

261
Q

What is passive immunization?>

A

antibodies (in the form of antiserum) are injected into animals to protect them against infection

262
Q

When is passive immunization important?

A

important in protection against toxins and against life threatening infections

263
Q

what is the problem with passive immunization?

A

antiserum administration may interfere with active immunization

264
Q

Advantages of passive immunity

A

provides immediate protection

works well against pathogens that are poor immunogens

265
Q

Disadvantages of passive immunity

A

protection is short lived

interferes/delays the ability to vaccinate animals

because it is Ab produced by other animals, can cause hypersensitivity reaction (type I or III)

antisera can transfer blood borne diseases (FeLV, FIV, etc)

266
Q

What is heterologous antisera?

A

basically like the mouse monoclonal antibody (MAb) given to dogs

type of passive immunization- quickly catabolized by recipient animal via trypsin into Fc and Fab fragments

Fab fragments are catabolized more slowly then the whole Ab, and they are as efficacious as the entire Ab molecule to neutralize pathogens

for enteric pathogens (E. coli), heterologous antisera can be given orally