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Virology > Virology midterm > Flashcards

Virology midterm Flashcards

1
Q

Morphology of virions

A

size range: 20-300nm

Shape: high variety

Content: nucleic acid, proteint

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2
Q

what is a vegetative virus

A

a virus that has infected a cell

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3
Q

Reproduction of virus

A

no energy and protein synthesis, enzymes

no nucleic acid replication (by the virus itself)

enzyme multiplication 10^3 - 10^6 virion/host cell

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4
Q

Occurence

A

can infect anything

active virus mulitplication in 1-3% of people

5360 accepted species

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5
Q

multitude of viruses

A

200 million tons is the cumulative weight of viruses

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6
Q

origin of viruses

A

suspected to have evolve from bacteriophages

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7
Q

origin of viruses, theories

A

cell degeneration

runway cell components

chromosome fragment

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8
Q

Virion morphology (what does it consit of)

A

core: protected by capsid, contains proteins and nucleic acids

Capsid: proteins +/-

envelope: lipid membrane + proteins

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9
Q

examination methods of virions

A

electron microscopy

negative contrast staining

shadow casting

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10
Q

How does electron microscopy work?

A

ultra thin sections are made

water and uraninan salt

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11
Q

how does contrast staining work?

A

urany acetat is added

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12
Q

how does shadow casting work

A

gold vappour is blown onto the particles and the shadow they form can describe the shape of the virion

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13
Q

what is the capsid composed of?

A

protein units

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14
Q

what are the different shapes of the capsid?

A
  • helical
  • quasihelical
  • isohedral
  • binal
  • complex
  • pleomorphic
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15
Q

what is nucleocapsid?

A

when the nucleic acids and the capsomer are so close that they cannot be separated

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16
Q

give example of a virion with helical structure

A

tobacco mosaid

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17
Q

give an example of a virion with quasihelical structure

A
  • orthomyxo
  • paramyxo
  • thabdovirus
  • ebola
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18
Q

what does it mean that a virion is isohedral

A
  • cubic, spherical
  • 20 equilateral triangle
  • have capsomeres and may have envelope
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19
Q

what does binal structure mean?

A

isohedral head+helical tail

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20
Q

pleomorphic structure?

A
  • no capsid
  • always enveloped
  • shape depends on the environment
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21
Q

What is an important factor to purify nucleic acid?

A

add proteinase K enzyme

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22
Q

what is used to extract nucleic acids?

A

phenol + chloroform + isoamylalchol

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23
Q

is chloroform and ethanol used in the lab for purification?

A

no, it is unhealthy, chromatography is used instead

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24
Q

What is the name of the gel used in electrophoresis for NA purification?

A

Agarose-gel

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25
Q

example of segmented and continous NA thread

A

Continous: picornaviridae

Segmented: reoviridae - 12 segments

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26
Q

Circovirus details

A
  • 1.7kb
  • single stranded nucleic acids
  • short genome
  • no enzymes
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27
Q

pox virus details

A
  • 300 kbp
  • many genes
  • multiplicates without the help of cell (energy + ribosome)
  • double stranded DNA virus
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28
Q
  • What does the core of a virion consist of?
A

Proteins and nucleic acids, protected by a capsid

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29
Q

what does the capsid consist of?

A

proteins

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30
Q

What does the envelope consist of , if present?

A

lipid membrane + proteins

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31
Q

What affects the shape of the virion?

A
  • the size of the capsid
  • symmetry of the capsid
  • the presence or absence of the envelope
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32
Q

What are the different examination methods of the morphology of virions?

A
  • electron microscope
  • Negative contrast staining
  • Shadow casting
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33
Q

How does electron microscopy work in examining virions?

A

Ultra-thin seections 0.1-0.5 um

W and urania salts are used makes the inner structure of virus visible

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34
Q

How does Negative contrast staining work in examining virions?

A

Uranyl acetate

Surface can be seen

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35
Q

How does shadow casting work in examining virions?

A

Au,Pt, Pi vapor

Vapor is blown onto the particles and by the shadow they form their shape can be described 3 dimensional structure

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36
Q

What are the different shapes of a virion based on the capsid?

A
  • Helical
  • Quasihelical
  • Icosahedral
  • Binal
  • Complex
  • Pleomorphic
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37
Q

Where are the nucleic acid of virion found?

A

in the core

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38
Q

What is the function of the viral nucleic acids

A

carries genetic information and determines the viral properties

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39
Q

How is the size of the niral nucleic acids

A

relative small, easy to handle and to investigate

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40
Q

State some general characteristics of viral nucleic acids

(size, structure, chromosomes)

A

Carries genetic information

relatively small - easy to investigate, 3-300 kilobase

dsDNA, ssDNA, dsRNA, ssRNA

continous or segmented

Haploid - usually ( retrovirus are diploid)

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41
Q

on what kind of structure of nucleic acid can we find positive and negative sense

A

Single stranded

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42
Q

Give example of virus with linear and circular nucleic acids

A

Linear: Herpes, parvo

Circular: hepadnaviridae

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43
Q

Give example of virus with continous or segmented nucleic aicds (chains)

A

Continous: Herpes, picorna

Segmented: Influenza viruses, Reoviridae

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44
Q

What is meant by alien nucleic acids in ex: Retrovirus

A

it can contain ONC or SRC genes, which gets integrated into the host cell genome, the integration leads to the containment of these genes in the next generation cells - this can cause sarcomas or tumours in organs and is how HIV operates

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45
Q

NA defiance in virus

A

incomplete or defective particles

complete= everything is present, nucleic acid and capsid

Incomplete: lacks nucleic acids, these cannot multiplicate with infected cells

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46
Q

What are the steps of nuvleiv avid purification?

A
  1. Proteinase K enzyme is introduced to open the virion capsid and release the nucleic acid
  2. the nucleic acids are extracte by either
  • Phenol + chloroform + isomylalchol ( not used anymore)
  • Chromatography
  1. Precipitate the NA with ethanol
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47
Q

How does the chromatography NA extraction work?

A

spesific silicon filters are used to centrifuge a the fluid and the NA will bind to the fluid

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48
Q

Why do we need to investigate the viral nucleic acids?

A

initially for morphology and biochemical studies: later we learned how to manipulate by genetic engineering and we can use them as vectors, marker vaccines and helps differentiate between wild and vaccine

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49
Q

How does the electrophoresis work? ( what is the name of the gels used)

A

The nucleic acids travels through a gel, this happens with different speed depending on the size of the nucleic acid - smaller runs faster

Gels: Agarose-gel, polyacrylamice-gel

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50
Q

What is an restriction endonuclase enzyme?

A

Enxyme that cleaves DNA into fragments at, or near spesific recognition sites within the molecule

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51
Q

Endonuclease within the cells and their function

A

they are bacterial defence enzymes which digest the NA and protect themselfs from virobacteriophage

they can recognize certain sequences - palindrome

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52
Q

What is meant by sticky or blunt end?

A

After restriction endonuclase enzymes has cleaved an NA it will leave an blunt or sticky end

Sticky end: different length, will have a part ready to attach to another nucleic acid

Blunt end: both pieces ends at the same position, cannot stick to other nucleic acids

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53
Q

What are restriction fragment length polymorphism used for?

A
  • Genetic markers in physical mapping
  • Identification and taxonomy
  • Epidemiological investigations
    • Separate between ex difference on chicken or pidgeon virus - newcastle disease
    • see if the farms have the same or different disease
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54
Q

What is the role of the viral protein?

A
  • protects the nucleic acid of the virus
  • defense and targeting of the genome - helical tail
  • shape of the virion
  • enzymes for multiplication, cleaves polypeptides
  • receptors, antigen
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55
Q

Southern blot?

A

Agarose-gel is put on a special filter (nylon) and then the direction of electricity is changed, this will cause the NA to migrate to the filter

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56
Q

In regard to grouping, what are structural proteins?

A

Surface proteins and core proteins

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57
Q

What and where are surface proteins?

A

Capsid or envelope

  • it defines the:
    • shape
    • adsorption
    • HA activity
    • enzymes for penetration
    • release of virion
    • antigenicity
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58
Q

What is Core protein?

A

Proteins which protects the Nucleic acids and stabilizes.

Enzymes for viral multiplication

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59
Q

What two categories do we talk about regarding grouping?

A

Structural and non-structural proteins

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60
Q

What are non-structural proteins (grouping)

A
  • proteins which are coded for in th viral genome but is not carried by the virion
  • present only in vegetative virus - infected
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61
Q

What is the sub-group of non-structural proteins (grouping)?

A

Early or immidiate proteins

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62
Q

What are early or immediate proteins (grouping)?

A

Proteins produced following entry into the host cell, but prior to replication

Proteins of cell invading

Regulating cell

inhibit cell defense

enzymes of replication

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63
Q

What are late proteins (grouping)?

A

Viral protein formed after replication

  • enzymes for structural maturation, cuts polyproteins
  • virion particle assembling
  • the majority of the late proteins are structural
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64
Q

What are some methods to investigate the proteins of the virion?

A

PAGE (Sds-Polyacrylamide-gel electrophoresis)

Immunoblotting - Western blot

Immunoperoxidase staining

Monoclonal antibody production

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65
Q

How does PAGE work?

A

(Sds-polyacrylamide-gel elecrophoresis

  • The size and number of proteins will show different bend’s and different number of them
  • Concentrated virus suspension
  • Linearization (polypeptides) -makes them linear
  • The gel lies on the side, electricity passes thorugh
  • staining: silver, coomassie brilliant blue
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66
Q

Why do we use PAGE?

A

To determine number and size of viral polypeptide

polypeptide map

We can see the characteristic of the virus

PAGE: less sensitive for drying out, long term storage of protein

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67
Q

How does immunoblotting work as a method of protein investigation?

A

Western blot

Nitrocellulose filter, proteins migrate to this filter

Transfer of viral proteins from PAGE into nitrocellulose filte

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68
Q

How does immunoperoxidase staining work?

A

after sds-PAGE and western blot the sample is put into histological sections

We are to detect antigens:

  1. cover with primary AB
  2. incubate, wash
  3. Cover with conjugat
  • peroxidase labeled AB
  • spesific to the primary AB
  1. Incubation, washing
  2. Cover with substarte, gets digested and shows a color change
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69
Q

Why do we use immunoperoxidase staining?

A

it is a diagnostic methode, we identify antigens

check the mechanism and timing of protein production

epitope investigation

  • Investigate the surface one by one
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70
Q

What is monoclonal antibody production?

A
  • mAb are antibodies that are made by identical immune cells that are all clones of a unique parent cell.
  • it is spesific for a particular epitope
    • B-lymphocyte
  1. mouse immunization with viral antigen - lymphocytes learns the antibodies and produces antigens
  2. isolation of lymphocytes from the spleen - Bcells: AB production, but no mitotic division
  3. mixing with myeloma cells: mitosis but no AB, type of cancer
  4. fusion of cells by polyethylen glucon - tetraploid hybridoma cells
  5. cloning - cultivation of the hybridomas
  • Selection of the successful fusions
  • HAT medium
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71
Q

How do we test the clones that we created during Monoclonal antibody production?

A

ELISA, IF, IPS - epitope spesific mAbs

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72
Q

What do we use mAb for?

A

Diagnostic of viruses, cancer treatment, and other medical use

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73
Q

What are and where are viral lipid?

A

Enevelope of the virus consist of 30-35% lipid

Aquired from cellular membrane structures, goligi - budding

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74
Q

How does budding work?

A

The virion gets out of the cell by putting a stress on the inside of the cell wall and makes a bump and takes a part of the cell membrane with them when they leave

phospholipids, cholesterol + virus spesific proteins

pox virus, ASF does this

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75
Q

What are some viral carbohydrates?

A

Ribose, deoxyribose - in NA

Glycoprotein - surface of virus, specific antigen, Pox has int in the core

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76
Q

What are the 6 steps of the multiplication cycle of the viruses

A
  1. Adsorption
  2. Penetration
  3. Decapsulation
  4. Eclipse
  5. Maturation
  6. Release
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77
Q

How does adsorption work in viral reproduction?

A

The virus attaches to the cell membrane of the host cell and injects its DNA/RNA

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78
Q

Explain cell surface receptors (adsorption, replication)

A

They are genetically coded

  • H19 chromosome - poliovirus
  • H3 chromosome - HSV

Often expressed in embryonic life/after birth

it is necessary for cellular functions

  • CD4 - HIV
  • acetylcholine receptor - rabies virus
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79
Q

What are virus surface antireceptors? (adsorption, replication)

A

Variable receptors making it possible for the virus to adapt easily to the cell surface

the viruses will adapt the cellular surface receptors during their evolution

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80
Q

Does related viruses target the seme cell surface receptors?

A

usually yes.

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81
Q

How is the specificity of the virus determined?

A

by the tissue or species of receptor proteins (virus evolution)

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82
Q

how is the releationship between receptors and antireceptors?

A

The negative charge between them will cause repulsion and collision happens only by chance

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83
Q

reversible vs irreversible connection (virus surface antireceptor)

A

reversible: cations neutralize the electrostatic power

Irreversible: chemical bonds between the proteins

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84
Q

What are the three general forms of penetration? (replication)

A

Translocation

Endocytosis

Membrane fusion

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85
Q

How does penetration happen in viral replication?

A

Energy dependent: 4x activation energy than adsorption

only in living cells

only over 4+ degrees

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86
Q

How does translocation work? (replication)

A

Trapdoor mechanism, amorphous RNA-protein complex

When adsorption is happening it will remove its capsid and gets flipped from outside to in (ikea spinning doors) - the transmembrane proteins turns over

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87
Q

How does endocytosis work?

A

this is the most common way (non enveloped viruses + herpes, pox)

cell nutrition endosome –> phagolysosome –> decapsidation

(the endosome gets into the cell, here the cell membrane will be start to suck and digest the capsid)

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88
Q

How does membrane fusion work?

A

only possible for enveloped viruses

special fusion proteins are needed

the viral envelope will mrge into the cytoplasmic membrane of the host cell

only the nucleocapsid will get into the cytosol

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89
Q

What are the steps 1-4 showing?

A
  1. non enveloped - phagocytosis
  2. trapdoor mechanism
  3. enveloped, fusion of cell membrane
  4. phagocytosis of the cell
90
Q

What are the alternative forms of penetration?

A

Injection

sexfimbria

passive

91
Q

How does injection work (penetration)?

A

Tailed bacteriophage uses this method

lysozyme enzyme will help with cell wall digestion and weaken a part of the bacterial cell wall before the contractile proteins will inject the content

92
Q

How does Sexfimbria work? (penetration)

A

ribophages

Lack of cellular wall - weak points

they share nucleic plasmid with eachother

known as the bacterial sexual disease

93
Q

Passive penetration?

A

Plant viruses

the cellular wall gets damaged by arthropod bites

94
Q

What is decapsidation and why do they do it?

A

when the nucleic acid is released from the capsid

they do it for transcription - it is dangerous for the virus

95
Q

Which viruses are the ones that is most easily discovered by the cell during decapsidation?

A

double stranded RNA viruses

96
Q

what are some strategies used by the virus to decapsidate (uncoat)?

A
  • Use the bodys own proteins - in lysosomes
  • using viral uncoating proteins - pox
  • Partial decapsulation
  • simultaneous decpasidation and penetration
97
Q

How does partial decapsulation work?

A

Double stranded RNA - to hide the nucleic acid until early virus protein production

The double capsid will by endocytosis have its outer membrane digested, and let the mRNA out trough little windiws

98
Q

What happens during eclipse? (general)

A

transcription, translation and nucleic acid replication

there are different strategies according to the type of nucleic acid -Baltimore system is based on this

99
Q

What happens during maturation?

A

the polypeptides are cleaved and cut

capsid are formed from the proteins and glycosylation

dimer formation, antigen development

this happens at the ER and golgi apparatus

100
Q

what happens during virus assembly and where?

A

The capsid and nucleic acids find eachother to form the virus protein. usually happens at the site of replication

101
Q

what can be formed during protein transport?

A

inclusion bodies

  • intranuclear or intracytoplasmic
102
Q

What makes the nucleic acids and capsomere find eachother during virus assembly?

A

Nucleic acid signal

103
Q

How fail proof is virus assembly?

A

mistakes happens frequently

incomplete virus at 70%

104
Q

What are the methods of virus assembly?

A

the nucleic acid enters into the capsid - icosahedral

the capsomeres surround the nucleic acid - helical

105
Q

What regulates the virus assembly and what is needed?

A

Scaffolding proteins regulate

envelope and matrix proteins are acquired from cellular membranes

106
Q

What are the two ways the virus can be released?

A

passive: the cell will die
active: energy is needed

107
Q

How is the enveloped viruses released?

A

through Budding - it will push on the cell membrane and exit with a part of it

rapid budding: toagv, paramyxo, rhabdo

slow budding: arena, retro

108
Q

What about the budding sites for virus release?

A

They are spesific

Herpes virus: at nuclear membrane

Flavivirus: ER

Coronoa, bunyavirus: Golgi

Asfar, Toga, orthomyxo, paramyxo, rhabdo: cytoplasmic membrane

109
Q

How are cell-associated viruses released

A

released at cell death or injuries

110
Q

Why does cell fuse and what is another name for it?

A

syncytium formation - membrane tunnels

  • it is a safe way to spread
111
Q

What are some alternative forms of virus release?

A

lysosome disintegration: exocytosis

The t-bacteriophage will digest the cellular wall of the bacteria

112
Q

What are the 6 categories of the baltimore system based on

A

what type of nucleic acid they have and their multiplication strategy

113
Q

What are the 6 categories of the baltimore system?

A
  1. dsDNA
  2. ssDNA
  3. dsRNA
  4. +ssRNA
  5. -ssRNA
  6. viruses using reverse transcriptase
114
Q

What is mutation?

A

independent changes in the genetic material

  • source of evolution
  • opportunity for adaption
  • risk of loosing advantages/properties
115
Q

What is the cause of mutation?

A

Mistakes in NA replication - effective polymerase but no proofreading activity

116
Q

What are the types of mutation?

A
  • Spontaneous
  • Induced:
    • Irridation - UV, X-ray, atomic radiation
    • mutagenic drugs - halogenated uridine
117
Q

What are the forms of mutation?

A

point

sequence

substitution

insertion

deletion

inversion - frame shift

118
Q

what are the different results of mutations

A

silent mutation - when there is no phenotypic change

lethal mutation - nonsense or missense

conditional lethal mutation - changes in the multiplication activity, thermo sensitive mutants

beneficial mutation: rare

119
Q

What are some influences the mutations can have on the viral phenotype?

A
  • antigenic change
    • escape mutants
    • influenxa - antigenic drift
  • changes in host species specificity
    • feline panleucopenia –> canine parvoenteritis
  • changes in organ specificity
  • different tissue tropism
  • virulence variants
  • cytopathic effects, plaque formation
  • temperature optimum
120
Q

What is the story of CPV2?

A
  • originally it only spread in small carnivores, but small changes happened and it could only infect dogs
  • this new virus strain got extinct in 1979
  • CPVa continoued and infected dogs (TfR adaption)
  • CPV2b can infect both dogs and cats
  • CPV2c appeared after some mutations and can spread from continents replacing previous types
121
Q

Examples where mutations changed the virus organ specificity

A

EHV1: abortion <–> EHV4: rhinopneumonitis

IBR: rhinotracheitis <–> IPV: vulvo-vaginitis

122
Q

Name some virulence variants due to mutation

A
  • newcastle disease - differentiate between strains
    • Lento: only in young chickens, slow
    • Meso: young chickens, but spread faster
    • Velogen: both young and old, spreads fast
  • avian influenza: haemagglutinin protease cleavage site
123
Q

some mutant viruses where the cytopathic effect or plaque formation was altered

A

aujeszky disease

BVDV: mild cell rounding + no cytopathich effect

124
Q

some viruses affected by change in temperature optimum

A

rhinoviruses, canine herpes virus - 33 degrees

rabies vaccine strains

125
Q

Evolution by mutation

A
  • selective advantages
  • environmental pressure
    • immune system, pressure for virus
    • adaption, niche
126
Q

stabilization of virus strains

A

protect from mutations - low passages

seed virus, virus banks

freeze drying: 4, -80 and -196 degrees

127
Q

With what may the virus interact with?

A

another virus

host cells

host organism

128
Q

When will viruses interact?

A

when they are inside the same cell and are multiplying

129
Q

Which viruses are most likely to interact?

A

viruses that are related

130
Q

What are the different types of interactions between viruses

A

Advantageous

Disaadvantageous

Neutral

131
Q

what is meant by advantageous interactions?

A

both of the interacting viruses help each other

  • on a nucleic acid level:
    • they will exchange characters, nucleic acid function/parts - helping the next generation - recombination
  • on protein level:
    • complete eachother, share capsid/surface proteins - complementation/ phenotype mixing
132
Q

What is meant by disadvantageous interactions between viruses?

A

interference, one virus will inhibit the other

133
Q

What is meant by neutral interactions?

A

virusexaltation, they will happily multiply besides eachoter but they dont affect each other

134
Q

what happens with the recombination when there is viral interactions?

A

there may be exchange of genetic information

the effect of the nucleic acid will be inherited in the next generation giving it new properties

there must be atleast 20-40 nucleotide homology, relatated

135
Q

What are some different ways virus can recombine when they interact?

A

intramolecular recombination

genetic reassortment

reactivation

phenotype mixing

interference

virusexalteration

136
Q

what happens during intramolecular recombination when there is interaction between viruses?

A

the polymerase will derail during replication and mix the two genetic informations

during aujeszkys disease there is a 70% transfer

it can happen between related, and some times non-related + RNA viruses

137
Q

What happens during genetic reassortment in regards with virus ainteractions?

A

When viruses with segmented genome (such as orthomyxoviridae) exchange their segments during viral assembly, and the different segments enters the wrong capsid

this causes a sudden and major antigenic change

138
Q

How does reactivation work in regards to virus interactions?

A

Cross- reactivation and multiple reactivation

Cross: attenuated vaccine strain + related genes, repair of the defected virulence-genes

multiple: between two attenuated virus-strains, different defected genomic reasons

139
Q

Why shouldnt we give different live vaccines within a short time?

A

because of the multiple reactivation, different parts of the genoome may be altered and when they are put together they can exchange information and correct the missing genes in the next generation

140
Q

How does complementation work in regards to virus interactions?

A

it is between a defective and a competent virus.

they will exchange enzymess - where the competent virus will help the defect with multiplication

ex:

heat-sensitive mutant + wild type virus

avirulent virus + inactivated virulent virus

dependovirus + adenovirus

141
Q

How does phenotype mixing work in regards to virus interactions?

A

they exhange structural proteins

eks: leukosis + sarcoma virus: aquires envelope proteins ( the sarcoma virus cannot replicate but will cause tumors, it cannot spread without the envelope protein of leukosis

Transcapsidation: after multiplication the polio and coxsackie virus genes will enter the wrong capsid - will only affect this generation

142
Q

Interference in regards to virus interaction and two different ways it does interact?

A

one virus inhibits the multiplication of the other

Adsorption interference and heterologous interference

143
Q

How does adsorption interference work?

A

there will be a competition for the same cell-surface receptors

infection by accident

can happen between related viruses or after phenotype mixing or different viruses looking for the same receptors

144
Q

How does auto interference workj?

A

between complete and incomplete forms of the same virus (genome is completely missing of shorter)

  • it can happen at adsorption
  • Incomplete virions have shorter, or is missing genome, this means easier work for the enzymes to replicate and is chosen more often - higher mobility, polymerase affinit
145
Q

What are defective interfering particles?

A

spnatneously generated virus mutants in which a critical portion of the particles genome has been lost due to defective replication of non-homologous recombination

when viruses compete for enzymes, ribosomes

146
Q

what is the efect of autointerference?

A

large amounts of incomplete progeny viruses

147
Q

How does heterologous interference work?

A

when two non-related virus produces proteins which inhibit the other

  • herpes, adenovirus inhibit pox

viral suppressor protein production

148
Q

How does virusexalteration work?

A

the viruses will multiplicate independently, and they will not affect eachother but

  • there can be changes in the viral influence on the host cell or organism such as increased pathogenicity, and cytopathic effects will appear
149
Q

Give some examples of virusexalttion

A

poliovirus + coxsackievirus in mokey: increased pathogenicity

classical swine fever virus, BVDV + newcastle disease: cytopathic affect will appear

150
Q

What can be the extent of virus propagation

A

localized and/or genrealized infection

localized: only an organ or area of body
generalized: viraemia

151
Q

What are the 7 different infectiour routes?

A
  1. transcutaneous
  2. airborne
  3. oral
  4. venreal
  5. transplacental
  6. germinative
  7. iatrogenic
152
Q

Describe the transcutaneous infection and give examples

A
  • via the skin

due to the dead keratinized cells of the skin there needs to be a wound for the virus to enter

arthropod vectors - arbovirus

  • mosquito, tick, fly, louse

Special - herpes

  • conjuctiva
  • latent infection
153
Q

describe the airvorne infections and how the body defends them

A
  • via respiratory tract, respiratory diseases (paramyxo, rhinovirus)

droplet infection - aerosol

defense

  • drying out - UV light
  • mucosal immunity: IgA, lymphoid cells, alv. macrophages
  • temperature: polymerase activitylow at 33 degrees
  • microvillis
154
Q

Describe how the body defends against oral infections

A
  • via the enteric system
  • lysosomes in the saliva can inactivate the virus
  • low pH in the stomach - affects the enveloped virus
  • small intestines have digestive enzymes and bile which is a detergent
155
Q

What viruses can cause oral infections?

A

mainly non enveloped

  • corona cirus

reo, adeno, picorna, calici (food poisoning), astro

proteolytic enzymes sometimes actaivete virus receptors

156
Q

How does the venereal infection happen?

A

urogenital tract

  • sexual intercourse
  • cell-associated transmission (sperm)
  • sensitive viruses can spread

Herpes

pappilloma - human

hepadna: blood transufion, needles, sex

arteritis - horse semen

retrovirus - HIV

157
Q

How does the Transplacental or intrauterine infection start?

(tolerance, abortion, mummification)

A

via the placenta

  • Different placenta structure
  • Placental artery and vein
  • Age and development the outcome can be different, young, few cells, resorption can happen - abortion
  • Tolerance - at the time of embryonic life when the immune system is developing, recognize as part of body
  • Abortion - older, when the last embryo dies
  • Mummification - when not all of them die, and it leads to the death of the other
  • Horse herpes vs arteri: vessels of the mother and placenta, nutrition supply stopped in arteritis, see the different symptoms herpes: spread from mother to embryo through the placenta, kills the embryo, respiratory symptoms a long time ago
158
Q

What is germinatitive infections and the different ways it can infect and whatcan influence the outcome?

A
  • via the egg
  1. Virus on the surface of the egg, will infect the chick at hatching
  2. inside the egg, while the egg is beeing formed it will enter (circo, adeno, picorna, retro)

Yolk immunity may influence the outcome

159
Q

what is latrogenic infections?

A

infections caused to faulty of the veterinarian

  • non-sterile equipment

needle, syringe

160
Q

Mixed form of infection?

A

oronasal - infleunza

161
Q

What are the main factors influencing the result of an infection?

A
  • susceptibility
  • infectivity
  • amount of viruses
  • pathogenicity
  • virulence
162
Q

what does stenoxen mean?

A

narrow host spectrum, specificity

163
Q

What does euryoxen mean?

A

infects many, low specificity

164
Q

What are the parameters of virus infections?

A
  • presence of infectious virions in the host
  • sheding of infective virions
  • clinical signs
  • immune response
165
Q

What are acute infections and their outcomes?

A
  • after infection the virus multiplicates rapidly
  • immediate virus shedding
  • clinical signs are shown after a certain concentration of virus is present
  • antibodies will be produced after a few days

outcome

  • recovery
  • death
  • chronic infection
166
Q

What are the types of chronic infections?

A
  • latent infection
  • tolerated infections
  • persisting infections
  • slow infections
167
Q

what are the phases of a latent infection?

A
  • acute phase
    • initial infection, multiplication, shedding and defense by immune ssytem
  • latent phase
    • low level of immune response, antibodies can be detected after half a year
  • reactivation:
    • ​new immune response
    • immunosuppression, pregnancy, skiing
168
Q

What are tolerated infections?

A

infections at the 2nd trimester of pregnancy: which is during the self-recognition phase

the virus antigen will be regarded as own, menaing no immune response and continous shedding

169
Q

What are persisting infections?

A
  • african swine fever

hidden neutralizing agent, it will hide from the antibodies

constant virus concentration until end of life, different times of shedding

there will be clinical symptoms, high level of antibody and immunocomplex deposition

170
Q

Name some hidden viruses

A

equine arteritis: stallion venereal tract

foot and mouth disease: lymphoid tissue

canine distemper: CNS

171
Q

What are slow infection?

A

retroviruses

when it is integrated into the genome, antigenic changes

the immune system is destructed, shedding is continous

the clinical signs comes at later age

the immune response will in the begining be at a very high level, but it will in the end give up.

prions can also cause slow infections

172
Q

What is resistance? (virus cell-interactions)

A

when the cell has no surface receptor for the viral attachement

173
Q

What is the response of the innate immunity? (cell-virus interaction)

A
  • immediate response on cellular level
  • Detection of viral components:
    • some viral components are easy for the cell to recognize, Double stranded RNA
  • Different cascade mechanismes are initiated
    • apoptosis
    • interferon production
    • inflammatory signalling
174
Q

what is an interferon?

A

a group of signaling proteins made and released by host cells in response to the prescense of several viruses

cell-coded mediator protein

175
Q

What is an interferon inducer?

A

A component which is recognised by the cell as non cell - dsRNA, RI forms

they will cause a cascade which will lead to IFN release

176
Q

How does the interferons affect the neighbouring cells?

A

there will be structural changes on the cytoplasmic membrane to decrease the penetration

L-RNase: it will destroy all RNA within the cell (cellular and viral)

proteinkinase: protein production will be inhibited

177
Q

List 3 IFN types and some properties

178
Q

What is the timeline of interferon production?

A
  • 2-4h after infection
  • maximum after 12h
  • clearance after 24h
179
Q

Are the interferons host or virus specific?

A

interfoerons are not virus spesific, but they have host specificity

180
Q

what are the problems of using interferons in therapy?

A

expensive

parental use, short term efficiacy

the inducers are toxic

toxic side effects

181
Q

What is meant by latency

A

The virus have infected the cell, but it it is not multiplicating as it tries to get into balance with the cell. There is no virus shedding or clinical signs but host is a carrier

182
Q

What is present in the virus during the latency period?

A

only the nucleic acid and early proteins

  • episoma
  • integration -provirus
183
Q

What is meant by persistent infection?

A

There s virus production but there is no severe cell dammage, in this state there will be continous shedding

(flavi, retro, paramyxo)

184
Q

What is the oncogenic effect?

A

When there is uncontrolled cell proliferation - no control

there is less differentiated cell forms which are less effective

tthey are not able to function effectively and can cause tumors

185
Q

What is cellular oncogenesis?

A

Oncogenes are genes that has the potential to cause cancer. They wil keep the cell alive even though they are ready to induce apoptosis

186
Q

What is the proto-oncogenes?

A

genes necessary for cell division and maturation, these can turn into oncogenes if they are mutated or in increased expression.

187
Q

What are some oncogenic viruses?

A

DNA viruses

  • papilloma
  • polyoma
  • adeno
  • herpes
  • pox
  • hepadnaviridae

RNA viruses

  • Retroviridae
188
Q

What are the different types of tumor?

A

Benignant: limited, less invasive, less destructive (c-onc)

Malignant: invasive, destructive (v-onc)

189
Q

How is cellular oncogenesis activated?

A

Virus such as retroviridae enters the cell, and will integrate DNA into the cellular genome, when this virus binds to a LTR region near a c-onc gene having a promotor activity this will:

initiated translation

C-onc gene activated: oncoprotein expression, cell proliferation

slow developing lymphatic tumors

190
Q

Expression of the viral oncogenes

A

Recombination between the cellular and proviral genome - the c-onc gene will be transfered into the virus genome: V-onc

this means when the virus infects there will be quick oncoprotein production which will be the cause for fast developing malignant tumors

191
Q

is the v-onc gene good for the virus?

A

no, becuase it is replacing essential genes such as the envelope protein gene

192
Q

Viral proteins which have consequent oncogenic effect

A
  • oncogenic DNA viruses, Hepatitis C virus
  • viral modulator proteins control the cell machinery
  • inactivation of cellular anti-oncogenic proteins
  • activation of inflammatory proteins
  • inhibition of the apoptosis (Adenoviridae)
  • usually benignant tumors
193
Q

What are cytopathogenic effects?

A

alterations in the morphology of cells due to virus infections

  • they are usually degenerative processes
194
Q

name 6 different direct damages of viruses on the cells?

A
  • toxic effect of adsorption
  • virus proteins inhibit cellular translation
  • early proteins inhibit celullar nucleic acid transcription and replication
  • viral proteins or virions are deposited in the cells
    • they can damage the cytoplasmic membrane permeability, osmotic changes
  • cytoskeleton depolymerisation
  • expression of fusion proteins
195
Q

How can we investigate DPEs in vitro?

A

usually by light microscope with or without staining

196
Q

Will allk virus infections result in CPE?

A

no, the cytopathic character of a virus strain may change due to mutations

197
Q

is the CPEs always connected to the pathogenicity of the virus?

A

no

ex: CSF: no CPE but pathogen
spumaviruses - obvious CPE but is an orphan

198
Q

In what case can the most characteristic CPEs be seen?

A

when the multiplicity of infections are low (MOI)

199
Q

Mention some different ways CPE can occur

A

they can occur independently or jointly

Different viruses may cause different CPE

CPE may vary according to the host cell

200
Q

What are the main types of CPE?

A
  1. Inclusion bodies
    • Intranuclear inclusion bodies
    • Intracytoplasmic inclusion bodies
  2. Cell rounding
  3. Syncytium-formation
  4. lumpy cell nucleus
  5. call vacuolization
  6. hemadsorption
201
Q

Describe the location and investigation if inclusion body formation

A

it happens at the site of the nucleocapsid assembly

it can be seen in homogenous stained cells

they will be surrounded by a halo after staining - and will shirnk after fixation

202
Q

What causes intranuclear inclusion bodies?

A

Nucleus replicating DNA viruses and sometimes by RNA viruses

203
Q

What are cowdry bodies and what do they depend on?

A

eosiniophilic nuclear inclusions composed of nucleic acid and proteins. The two types are dependent on the state of the synthesis of macromolecules

204
Q

What causes intracytoplasmic inclusion bodies?

A

usually caused by RNA viruses and DNA viruses which can replicate in the cytoplasm

mostly eosiniphilic, rarely basophilic

205
Q

What are some pathognomic intracytoplasmic inclusion bodies?

A

negri bodies - rabies

guarnieri bodies - pox

206
Q

What is cell rounding?

A

the most common CPE, cytosceleton depolymerisation.

The cells loses electrolytes

207
Q

How is cell rounding determined?

A

unstained: double refraction, detachemnt, shrinkage

Stained: intensive staining

208
Q

What kind of viruses causes syncytium-formation?

A

exclusively formed by enveloped viruses

  • alphaherpes, paramyxo, pneumo, corona
209
Q

Why is syncytium formed?

A

there are fusion proteins present on the surface of the virus and they are fusogenic directly at the host cell membrane, it happens when the viruses are able to directly fuse at the cellular surface without the need of endocytosis

210
Q

What is syncytium-formation?

A

when there is a fusion of an infected and non-infected cell membrane, they form membrane tunnnels to induce intracellular spread, they create multi-nucleated enlarged cells which is most often seen in lymphatic cells

211
Q

Lumpy cell nucleus

A

Chromatin conglomeration, rearrangement

changed refraction

nucleus lympy disintegration

  • EHV in the liver of foals, ASFV in lymphatic system
213
Q

Cell vacuolisation

A

when small vacuoles (bubbles) are formed in the cell, depending on where they multiplicate (cytoplasm vs nucleus)

214
Q

What is hemadsorption?

A

when a viral hemagglutinin is expressed ion the surface of the infected cell

215
Q

How is hemaglutin viruses proved?

A

RBC are added into the culturing medium and after 30 min incubation the unbound RBC will be washed away - the infected cells will capture the RBS - paramyxo and ASFV are diagnosticed this way

216
Q

How does the CPEs appear?

A

They can appear all over the cell and some of them causes focal plaque

217
Q

Where can plaques be found?

A

are seen more frequently in some viruses, formd more frequently in low MOI.

syncytia are seen as plaques

I

218
Q

How is plaque formation facilitated?

A

we force the viruses to form plaques by supplementing the fluid with agar gel, carboxymethyl cellulose or metrazamide. this will make the cell culture thicker and keep the viruses from swimming, forcing it to spread to neighbouring cells

219
Q

What are the advantages of plaques?

A

They are easier to pick out, separate and transfer

virus purification: subsequent passages of viruses taken from singular plaques - establishments of virus strains

Virus quantification: easy to count - virus concentration

220
Q

What are non-spesific CPEs?

A

morphological changes in cells independently from virus infections

they can be caused by

  • againg of the cell
  • alteration of the pH range of the medium
  • alterations of the incubations temperature
  • toxic component in the inoculum
  • bacterial contamination
221
Q

How to differentiate the non-spesific CPE

A

negative control

compare with the uninfected control

passage the isolate

perform direct demonstrations: PCR, IHC, ISH IF, VN

Virology (2 decks)

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