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RUSVM Virology > Virology Test 1 > Flashcards

Virology Test 1 Flashcards

1
Q

What is virology?

A

Study of viruses and viral diseases

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2
Q

What is a virologist?

A

Someone who studies viruses

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3
Q

Why is the study of veterinary virology important?

A

Viruses cause high mortality and morbidity

Viral diseases cause tremendous financial losses to livestock and poultry industries, hampering the economic development of a country

Some are zoonotic

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4
Q

What are characteristics of viruses?

A

Non-living
Nucleic acid genome surrounded by a protein coat
Do not possess standard cellular organisms
Cannot make own energy or proteins
All are obligate intracellular parasites
Cannot multiply by division - replication resembles an assembly line

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5
Q

What is a virion?

A

A complete virus particle that consists of an RNA or DNA core with a protein coat sometimes with external envelopes and that is the extracellular infective form of a virus

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6
Q

What is a virus?

A

Broad general term used to describe the infectious agent and includes: the infectious virion or inactivated virus particle, or viral nucleic acid and protein in the infected cell

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7
Q

What is a viroid?

A

An infectious particle smaller than any known viruses, an agent of certain plant diseases. The particle consists only of an extremely small circular RNA molecule, lacking the protein coat of a virus

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8
Q

What did Edward Jenner do for the world?

A

Inoculated some cowpox repeatedly into arms of a healthy 8 year old boy who became immune and did not succumb to small pox.

Vaccination - comes from the Latin word “vacca” meaning cow

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9
Q

What did Louis Pasteur do for the world?

A

Injected dried, potassium hydroxide treated, infected rabbit brain material in two boys bitten by rabid dogs and both recovered

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10
Q

What is the Chamberland filter?

A

Filter that had pores smaller than bacteria.

Pioneered the discovery of viruses. Used in the famous tobacco mosaic virus experiment

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11
Q

What was the tobacco mosaic experiment?

A

Diseased tobacco leaves were crushed and passed through the Chamberland filter -> the cell debris was placed on a healthy leaf -> remained healthy

->the cell filtrate was placed on a healthy leaf-> leaf died

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12
Q

What did Friedrick Loeffler and Paul Frosch do for the world?

A

Passed the first animal virus through a Chamberland filter and discovered the cause of foot-and-mouth disease (Foot-and-mouth disease virus)

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13
Q

What did Walter Reed do for the world?

A

Discovered yellow fever is transmitted through mosquitoes

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14
Q

What about Peyton Rous?

A

Isolated the first tumor-causing animal virus (oncogenes viruses). Of course named the Rous sarcoma virus.

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15
Q

And Ernst Ruska and Max Knoll did what?

A

Invented the electron microscope

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16
Q

What was the first virus successfully propagated in embryonated hen’s egg?

A

Fowlpoxvirus

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17
Q

Sanford et all did what in history?

A

Culture of isolated mammalian cells

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18
Q

Enders et all did?

A

Growth of poliovirus in cell culture

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19
Q

Bulbecco and Vogt did what?

A

Plaque assay for the first animal virus - poliovirus

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20
Q

The only animal disease declared globally eradicated

A

Rinderpest

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21
Q

What is the smallest animal virus?

A

Porcine circovirus type 1

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22
Q

Largest animal, human and bird virus?

A

Poxvirus (200 nm diameter and 300 nm in length)

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23
Q

What shape is Ebolavirus?

A

Filament-shaped

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24
Q

What shape is Rabies virus?

A

Bullet shaped

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25
Q

What shape is Tobacco Mosaic virus?

A

Rod-shaped

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26
Q

What shape is Poxvirus?

A

Brick-shaped

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27
Q

What shape is Rotavirus?

A

Spherical

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28
Q

What is pleomorphism?

A

The ability of some viruses to alter their shape or size

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29
Q

What are some common methods used to determine morphology of viruses?

A

Electron Microscopy (EM)
Cryo-electron microscopy (Cryo-EM)
X-ray crystallography
Nuclear Magnetic Resonance (NMR)

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30
Q

What are general components of a virus?

A

DNA or RNA genes
Capsid
Envelope (fat bubble)
Molecules of protein

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31
Q

What is a capsid?

A

Protein shell that encases/envelopes the viral nucleic acid or genome.
Made up of capsomeres.
Most viruses have one capsid except Reoviruses which have a double layered capsid.

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32
Q

What is a capsomere?

A

Basic subunit protein in the capsid

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33
Q

What is a nucleocapsid?

A

Capsid + virus nucleic acid (DNA or RNA)/Genome

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34
Q

What is helical symmetry?

A

In all animal viruses, the Helical nucleocapsid is enclosed within a lipoprotein envelope. Naked helical nucleocapsids are common among plant viruses.

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35
Q

What is cubic/Icosahedral symmetry?

A

Two types of capsomeres are present in icosahedral capsids -> pentagonal (pentons) capsomeres at the vertices and hexagonal capsomeres making up the facets (hexons).

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36
Q

True/False: There are always 12 pentons but the number of hexons changes with the viral size.

A

True

ALWAYS 12

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37
Q

What is the triangulation number and how is it calculated?

A

Describes the relationship between the numbers of pentons and hexons in an icosahedron.

T=h2 + h * k + k2

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38
Q

True/False: Icosahedrals can be naked or enveloped?

A

True

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39
Q

Name that virus: T=1, simplest icosahedron, capsid consists of 60 copies of CP proteins.

A

Parvovirus

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40
Q

Name that virus: Outer capsid has a T=13 icosahedral symmetry and the inner has a capsid T=2.

A

Reoviridae

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41
Q

Which virus has a complex capsid symmetry?

A

Pox virus

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42
Q

What are the functions of the viral capsid?

A

Responsible for the structural symmetry of the virus particle.
Encases and protects the nucleic acid from enzymes, chemicals and physical conditions.
Receptor attachment proteins for attachment to specific receptors on host cells.
Interact with host cell membrane to form the envelope.
Uncoating of genome in host cell.
Transport viral genome to appropriate side.
Facilitates packaging of the nucleic acid genome.
Contains antigenic sites which determines antigenicity of virus.

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43
Q

What is the envelope?

A

Lipid bilayer with embedded proteins.

Acquired by budding of viral nucleocapsid through a cellular membrane (nucleus, golgi, cytoplasmic)

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44
Q

Two kinds of viral proteins in the envelope

A

Glycoproteins

Matrix protein

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45
Q

Two glycoproteins in a virus envelope

A

External glycoproteins

Channel proteins

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46
Q

What are external glycoproteins?

A

Major antigens of the virus

Function as hemagglutination, receptor binding, antigenicity and membrane fusion

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47
Q

What are channel proteins?

A

Mostly hydrophobic proteins, form a protein lined channel through the envelope
Alters permeability
Important in modifying the internal environment

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48
Q

What are the virus envelope matrix proteins?

A

Proteins that link the internal nucleocapsid to the lipid membrane envelope.
Have a crucial role in Virus Assembly.
Stabilization of the lipid envelope.
Serve as recognition site of nucleocapsid at the plasma membrane and mediates the encapidation of the RNA-nucleoprotein cores into the membrane envelope.

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49
Q

What is the envelope, how is it acquired and maintained?

A

Bi-layer
Acquired from cell membrane of host (cytoplasmic, nuclear, ER)
Maintained only in aqueous or moist environments.
Is sensitive to desiccation, heat, and pH changes.
Can be inactive by dissolution of lipid membrane with lipid solvents such as: ether, chloroform, sodium deoxycholate, detergents.
Enveloped viruses are easier to sterilize than non-enveloped viruses and cannot survive for longer periods in the environment.

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50
Q 
Which of the following is not a component of a virus?
A. Nucleic Acid
B. Capsid
C. Envelope
D. Capsule
A

Capsule

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51
Q

True/False: The viral matrix protein is located between the viral nucleic acid (DNA/RNA) and the capsid.

A

False

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52
Q

Are viral nucleic acids DNA or RNA? Are they ss or ds?

A

Can be any

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53
Q

Antigenic drift results in ________

A

Mutations

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54
Q

What is recombination?

A

The exchange of nucleotide sequences between different, but usually closely related, viruses during replication. Occurs in a single gene segment.

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55
Q

What is the most important mechanism for high genetic diversity in viruses with segmented genome?

A

Reassortment

Only in viruses with more than one gene segment, i.e. Only in viruses with segmented genome/RNA/DNA.

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56
Q

What is retroviral integrase?

A

Enzyme produced by a retrovirus (such as HIV) that enables it’s genetic material to be integrated into the DNA of the infected cell

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57
Q

What is reverse transcriptase (RT)?

A

Enzyme used to generate complementary DNA (cDNA) from a RNA template.

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58
Q

What is nucleic acid polymerase?

A

Viral genome replication

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59
Q

What are viral nonstructural proteins?

A

Proteins that may play roles within the infected cell during virus replication or act in regulation of virus replication or virus assembly

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60
Q

True/False: Nonstructural proteins are seen in the extracellular virions?

A

False

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61
Q

What are incomplete virions?

A

Virions without nucleic acid [empty capsid]

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62
Q

What are defective virions?

A

A virus that cannot replicate because it lacks a full complement/copy of viral genes. Defective viral particles result from mutations or errors in the production or assembly of virions.

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63
Q

What are pseudovirions?

A

Contains non-viral genome within the viral capsid, such as host nucleic acid instead of viral nucleic acid

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64
Q

What are pseudotypes?

A

When related viruses infect the same cell, the genome of one virus may be enclosed in the heterologous capsid of the second virus

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65
Q

An incomplete virion is composed of ___ _____

A

Only capsid

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66
Q

What is the Baltimore classification system?

A

Viruses are classified into one of the seven groups depending on a combination of their nucleic acid (DNA or RNA), strandness (ss or ds), sense and method of replication. An old system that isn’t currently used.

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67
Q

What is the International Committee on Taxonomy of Viruses (ICTV) Classification System?

A

ICTV is the only body charged by the International Union of Microbiological Societies with the task of developing, refining, and maintaining a universal virus taxonomy. The currently used to classify viruses

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68
Q

How does the ICTV classify viruses?

A

Nature of the virus genome and virus genetic diversity.
Virus replication strategies.
Virus morphology.

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69
Q

How are the viruses ordered using the ICTV classification system?

A 
Order (-virales)
Family (-viridae)
Subfamily (-virinae)
Genus (-virus)
Species
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70
Q

The family of a virus is denoted by suffix ____

A

Viridae

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71
Q

True/False: viruses have the genetic capability to multiply by division

A

False, they do not have the ability.

Outside of the host, they are inert/dormant particles.

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72
Q

What does the virus need to replicate and generate next progeny of viruses?

A

Living host cell.

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73
Q

What happens inside of the host cell?

A

Virus hijacks and uses the host cell machinery to produce its proteins and nucleic acid for the next generation of virus

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74
Q

What are the possibly ways to grow/cultivate viruses?

A

Cell/tissue culture
Inoculation in embryonated eggs
Lab animals

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75
Q

What are monolayer cultures?

A

When the bottom of the culture vessel is covered with a continuous layer of cells, usually one cell in thickness, they are referred to as monolayer cultures

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76
Q

What is a primary cell culture?

A

Maintenance of growth of cells dissociated directly from the parental tissue.
Best culture system for isolation and propagation of viruses.
Used in producing viral vaccines.

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77
Q

What is a subculture (or passage)?

A

Transfer of cells from one culture vessel to another culture vessel.
This is periodically required to provide fresh nutrients and growing space for continuously growing cell lines.

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78
Q

What are the two types of cell lines?

A

Finite/Dipoid Cell lines

Continuous cell lines

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79
Q

What are finite/diploid cell lines?

A

Cell lines which have a limited life span and go through a limited number of cell generations.
Derived mainly from embryos; or from secondary cultures.

Can be used for vaccine production

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80
Q

What are continuous cell lines?

A

Acquire the ability to divide indefinitely. Derived directly from cancer cells.
FDA prohibits their use in vax productions.

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81
Q

What is culture medium?

A

Provides all necessary nutrients (amino acids, inorganic salts, vitamins and glucose) required for growth of cells

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82
Q

Why is serum in culture media important?

A

Required for growth and maintenance of cells. Helps in cell adhesion, regulate cell membrane and permeability and provide nutrients.

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83
Q

What is phenol red pH indicator?

A

Indicates change in pH by changing color of medium from red to orange or yellow

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84
Q

Why is the carbon dioxide level important in growing viruses?

A

It is necessary to use exogenous CO2 when using media buffered with a CO2-bicarbonate based buffer to maintain pH of the medium.

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85
Q

Why are antimicrobial agents used in culture?

A

To prevent contamination with bacteria, mycoplasma, yeast, molds, etc

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86
Q

What is trypsin used for?

A

Proteolytic enzyme used to detach and dissociate cells while subculture grew

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87
Q

What is the cytopathic or cytopathogenic effect?

A

Damage or morphological changes to host cells during virus invasion

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88
Q

Where are the locations within the egg that can be inoculated?

A

Yolk sac
Allantoic cavity
Amniotic cavity
Chorioallantoic membrane (CAM)

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89
Q

Inside of the egg, what are signs of virus growth?

A

Death of embryo
Paralysis (sluggish movement)
Stunted growth
Pocks on CAM

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90
Q

How else can viruses be grown in a lab?

A

Lab animal inoculation

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91
Q

What is an ultracentrifuge?

A

Used for concentration and purification of viruses. Have played a virtual role in virology, efficiently sediments even the smallest viruses.

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92
Q

What is rate-zonal centrifugation?

A

Ultracentrifugation method for purification and concentration of viruses. Separation of virus particles based on their mass. Under centrifugal force, particles move at different rates depending on their mass.

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93
Q

What is isopycnic centrifugation?

A

AKA buoyant or equilibrium separation, particles are separated solely on the basis of they buoyant density

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94
Q

True/False: you can use virus purification with membrane chromatography to purify viruses.

A

True

I basically gave that one to you

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95
Q

What is virus quantification?

A

Counts the number of viruses in a specific volume to determine the virus concentration

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96
Q

What is a virus titer?

A

Lowest concentration of virus that still infects cells. Also defined as the number of infectious units per mL of sample.

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97
Q

What is the biological quantification test?

A

Depends on a virus particle initiating a successful replication cycle.

Plaque Assays
Pock assays
Various endpoint titration methods

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98
Q

What is the physical quantification test?

A

Does not depend on any biological activity of a virus particle.

Electron microscopic particle counts
Hemagglutination
Immunological assays, ELISA
Quantitative PCR assay
Flow cytometry
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99
Q

What are the two ways of direct counting of viral particles in a solution?

A

Direct by transmission electron microscopy (TEM): the most direct method to determine the [virus particle] in a solution

Virus counter 2100

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100
Q

Is hemagglutination assay a physical or biological test? What is it based on?

A

Physical; [antigen]

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101
Q

Is single radial immunodiffusion (SRID) and physical or biological test? What is it based on?

A

Physical; [antigen]

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102
Q

Is Quantitative PCR (qPCR) a physical or biological test? What is it based on?

A

Physical; gene expression

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103
Q

What are the biological assays?

A

Monolayer plaque assay
Pock Assay
Transformation assay
Quintal assay

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104
Q

Monolayer plaque assay: what is a plaque and what is the unit associated with this assay?

A

A circular zone of necrotic cells surrounded by viable cells in a monolayer.

Unit: plaque-forming units/mL (PFU). Measures the number of virus particles capable of forming plaques per unit of volume. Ex. If a solution has a PFU of 1000 PFU/mL, then every mL of solution contains enough virus to form 1000 plaques

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105
Q

Pock assay: what is a pock and what is the unit of measure associated with this assay?

A

Pock: necrotic area on chorioallantoic membrane (CAM) of embryonated egg

Unit: pock-forming units/mL

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106
Q

What is the transformation assay and what unit is involved in this assay?

A

Quantitative determination of titers of oncogenic viruses

Unit: focus-forming units/mL

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107
Q

What is important about the quantal assay?

A

Endpoint: virus dilution that affects 50% of the test subjects

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108
Q

What is the TCID50?

A

The tissue culture infectious dose which will infect 50% of the cell monolayer challenged with the defined inoculum

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109
Q

A 300 PFU/mL means what?

A

The minimum # of viruses present/mL of the sample to form 300 plaques in a monolayer cell culture

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110
Q

What is a permissive cell?

A

A cell in which a virus is able to replicate, i.e. The cell machinery supports replication of the virus

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111
Q

What is a non-permissive cell?

A

Cells in which a factor necessary for viral reproduction is not present or one detrimental to viral reproduction is not present. E.g. Absence of appropriate receptors

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112
Q

What is MOI (Multiplicity of infection)?

A

The number of virions that are added per cell during infection

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113
Q

What is the latent period?

A

After uncoating and until just before the 1st appearance of extracellular new virus particles.

Or the time before new infectious virus appears in the medium i.e. The time from uncoating to just prior to the release of the first extracellular virions. During this phase no extracellular virions are detected

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114
Q

What is the eclipse period?

A

After uncoating and until just before 1st appearance of intracellular new virus particles

Or the time interval between uncoating (“disappearance” of viruses) and appearance, intracellularly, of first infectious progeny virions

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115
Q

What is adsorption?

A

During this period, the virus attaches to and enters cells and the titer of free virus in the medium may actually decline.

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116
Q

What is burst size?

A

Number of infectious virions release per average cell

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117
Q

True/false: Virus attachment to receptor on host cell is non-specific.

A

False, very specific. Each virus has its own specific receptor(s) on specific host cells

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118
Q

What is the first step to virus replication?

A

Attachment to host cell surface

Mediated by interactions between the virus and complimentary receptor on the hose cell surface. Cell that lack the appropriate receptor escape being infected by viruses. In some cases, binding to a cellular receptor is not sufficient for infection: an additional cell surface molecule, or co-receptor, is required for entry.

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119
Q

Can viruses use more than one host cell receptor?

A

Yes

HIV for example.

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120
Q

What is a co-receptor?

A

Binding to a cellular receptor is not sufficient for infection. An additional cells surface molecule, or co-receptor, is required for entry

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121
Q

True/False: viruses can enter the host cell using any receptor present on surface of host cell.

A

False, need specific receptors

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122
Q

What is the next step in viral replication?

A

Penetration and Uncoating

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123
Q

How do nonenveloped/naked viruses penetrate the host cell?

A

Receptor mediated endocytosis (common)
Pore mediated penetration of viral genome into host cell

In many non-enveloped viruses, Clathrin-mediated endocytosis or any other receptor-mediated endocytosis of virus.

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124
Q

How to enveloped viruses penetrate the host cell?

A

Surface membrane fusion (have pH independent Fusion proteins) - Here fusion of virus envelope with host cell membrane occurs directly on surface of host cell. Facilitated by pH independent fusion protein.

Receptor mediated endocytosis (have pH dependent Fusion proteins) - Fusion of virus membrane with host endosomal membrane release viral genome. The fusion protein requires low pH to get activated, which is achieved in endosome and facilitate virus envelope fusion with endosomal membrane.

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125
Q

How do others penetrate, or other uncommon methods of entry?

A

Antibody-mediated attachment and penetration

Ex FIPV

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126
Q

Is exocytosis a method of penetrating into the host cell?

A

No

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127
Q

What is uncoating?

A

Release of viral genome in host cell

Virion can no longer be detected - loss of infectivity

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128
Q

What are the two functions of parent viruses?

A
  1. Multiple copies for new viruses (children/progeny)

2. Viral proteins for capsid and successful replication

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129
Q

What is reverse transcriptase?

A

Conversion of viral RNA to cDNA during virus replication

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130
Q

What happens during the processing of primary RNA transcript?

A

Viral mRNA must conform to the requirements of host cell translation system (the host cell can recognize the mRNA and translate same).

A series of modifications occur, known as Processing of Primary RNA Transcript/Pre-RNA. 1. Capping. 2. Addition of Poly-A tail. 3. Splicing

After, mRNAs are translated in the cytoplasm

Viral mRNAs produced in the nucleus must also be exported to the cytoplasm

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131
Q

What is the first modification that occurs during RNA transcript?

A

Capping - addition of 7- methylguanosine to the 5’ end of RNA

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132
Q

What is the second modification?

A

Addition of 3’ poly-adenylated tails

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133
Q

What is the third modification to RNA transcript?

A

Splicing - Process that removes introns and joins exon in a primary transcript

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134
Q

What is an exon?

A

Portion of a genera that codes for amino acids

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135
Q

What is an intron?

A

Portion of a gene that does not code for amino acids

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136
Q

True/false: the poly-A tail is added to the 3’-end of viral mRNA.

A

True

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137
Q

What are the two types of viral mRNA?

A

Monocistronic: mRNA that encodes one polypeptide

Polycistronic: mRNA that encodes several polypeptides

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138
Q

What is assembly and maturation part of viral replication?

A

Assembly of virus genome and proteins into new virions follow a specific order.
All components, including nucleic acids and proteins, are packaged to form mature virions.
May take place in nucleus, cytoplasm, plasma/cell membrane

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139
Q

There are two types of progeny virions that can be released. What are they?

A

Naked virions - lysis of host cell, cannot exit host by budding since they lack an envelope
Enveloped virions - budding from host cell

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140
Q

True/false: cell lysis is induced by non-enveloped viruses facilitating virus release

A

True

141
Q

What is exocytosis?

A

Viruses mature by budding through the membrane of the Golgi or ER. Vesicles containing the virus then migrate to the plasma to the plasma membrane and are released by exocytosis.

142
Q

What are the two important enzymes of replication of retroviruses?

A

Reverse transcriptase - synthesis of RNA into DNA

Integrase - integrates viral DNA into host genome

143
Q

How are viruses spread from one cell to the next?

A

Extracellular spread

Intracellular spread - results in rapid virus dissemination, evasion of immune system, and persistent infections

Nuclear spread of virus genome

144
Q

What is pathogenicity?

A

Ability of a virus to cause disease in host.

145
Q

What is a pathogen?

A

Virus that causes disease

146
Q

What is pathogenesis?

A

Manner/mechanism of development of a disease

147
Q

What is virulence?

A

Quantitative or relative measure of the degree of pathogenicity of the infecting virus

148
Q

What is avirulent?

A

Not virulent or not harmful to the host

149
Q

True/false: virulence is an absolute property of a virus

A

False, not absolute, depends on many variables.

150
Q

What is the LD50?

A

The dose of the virus required to cause death in 50% of animals

151
Q

What is infectious dose 50 (ID50)?

A

Dose of virus that will infect 50% of an experimental group of hosts/animals

152
Q

True/false: the lower the ID50 and LD50, the more virulent the organism

A

True

153
Q

Virus A: LD50 is 30
Virus B: LD50 is 50
Which is more virulent?

A

A because the LD50 is lower

154
Q

What are the routes of entry into the host body?

A

Skin
Mucous membrane
GI tract
Respiratory tract

155
Q

What are the defenses of the skin?

A 
Dense outer layer of keratin
Low pH
Presence of fatty acids
Bacterial flora
Dryness
Components of innate and adaptive immunity
156
Q

What are 3 main ways to break the skin defenses?

A

Transcutaneous injection - bite of Arthropods
Bites of infected animals
Contaminated objects

157
Q

What are the GI tract defenses?

A 
Mucous membrane of oral cavity and esophagus 
Acidity of the stomach
Alkalinity of intestine
Layer of mucus covering the gut
Lipolytic activity of bile
Proteolytic activity of pancreatic enzymes
Defensins
IgA
Scavenging macrophages
158
Q

Defenses of the respiratory tract

A 
Mucociliary blanket
Alveolar macrophages
NALT
BALT
Temperature gradient
159
Q

What is a disseminated infection?

A

Infection spreads beyond the primary site of infection

160
Q

What is a systemic infection?

A

Number of organs or tissues are infected

161
Q

How do apical and basolateral release play roles in the spread of viruses?

A

Directional shedding of viruses from the infected epithelium is critical to subepithelial spread. Apical release facilitates virus dispersal, whilst basolateral release provides access to underlying tissues, facilitating system spread

162
Q

What is viremia?

A

The presence of a virus in the blood. Virus may be free in blood or in a cell such as lymphocytes

163
Q

What is primary viremia?

A

Initial entry of virus into the blood after injection

164
Q

Secondary viremia

A

Virus has replicated in major organs and once more entered the circulation

165
Q

Active viremia

A

Following initial virus replication in host. Release of virions from the initial site of replication, such as lymphatics or epithelium of investing to the blood stream

166
Q

Passive viremia

A

Direct inoculation of virus in host, such as contaminated syringe or bite of arthropods. No initial replication elsewhere in host before

167
Q

Neurotrophic virus

A

Virus that can infect neural cells. Infection may occur by neural or hematogenous spread

168
Q

Neuroinvasive virus

A

Viruses that enter the central nervous system (spinal cord and brain) after infection of a peripheral site

169
Q

Neurovirulent virus

A

Virus that cause disease of nervous tissue, manifested by neurological symptoms and often death

170
Q

A virus that exhibits low neuroinvasiveness of the CNS, but high _______. It always enters the PNS, but rarely enters the CNS. When it does, the consequences are almost always severe, if not fatal

A

Neurovirulence

171
Q

Virus exhibits _______, but low neurovirulence. Most infections lead to invasion of the CNS but neurological disease is mild

A

Neuroinvasiveness

172
Q

Virus that exhibits both high ________ and _______. It readily infects the PNS and spreads to the CNS with 100% lethality unless antiviral therapy is administered shortly after infection

A

Neuroinvasiveness; neurovirulence

173
Q

Retrograde spread

A

Travel opposite direction of nerve impulse flow. Invades axon terminals and then spread to dendrite or cell body, and then cross synapse to reach next axon terminal

174
Q

Anterograde spread

A

Travel in direction of nerve impulse flow. Virus invades dendrites or cell bodies and then spreads to axon terminals, and then cross synaptic contacts to invade dendrite of next neuron

175
Q

Neural spread of viruses to CNS through what two routes?

A

Olfactory

BBB

176
Q

Acute infection

A

usually intensive shedding over a short period of time

177
Q

Persistent infections

A

Can be shed at a lower titer for months to years

178
Q

Tropism

A

The specificity/affinity of a virus for a particular host tissue

179
Q

Pantropic viruses

A

Can replicate in more than one host organ/tissue

180
Q

Viral injury to the skin usually appears how?

A

Vesicles - fluid filled sacs/elevations
Ulcers - opening caused by sloughing of necrotic tissue, extending past the epidermis
Nodule/tumor - palpable, solid, elevated mass. Nodules with distinct borders. Tumors extending deep into dermis
Warts - benign skin growths that appear when a virus infects the top layer of the skin
Papule- solid elevations without fluid with sharp borders
Erythema - reddening of skin, consequences of systemic viral infections

181
Q

GI viral injury happens how?

A

Ingestion or hematogenous spread, systemic infection -> Destruction of enterocytes due to viral replication, hypersecretion -> GI disease, malabsorption, diarrhea -> pronounced dehydration, acidosis, hemoconcentration

182
Q

How does injury to the respiratory tract appear?

A 
Loss of ciliary activity
Loss of integrity of the lining mucus layer
Multifocal destruction of epithelium
Inflammation
Exudation
Influx of inflammatory cells
Obstruction of air passages
Hypoxia & respiratory distress
Secondary bacterial infection
183
Q

Injury to the CNS appears how?

A

Encephalitis or encephalomyelitis characterized by neuronal necrosis, phagocytosis of neurons (neuronophagia), and perivascular infiltrations of inflammatory cells (perivascular cuffing)

Progressive demyelination (canine distemper)
Neural vacuolation in prion disease
184
Q

Damage to the endothelium appears how?

A

Hemorrhages - petechiae hemorrhage (pin-point/small spots), ecchymoses hemorrhage (larger areas of hemorrhage, ill-defined margins)

185
Q

What happens with disseminated intravascular coagulation (DIC)?

A

Clots form in small blood vessels throughout the body -> organs do not get blood -> organ failure

Later stages, raw material from clot exhausted due to over use -> no clot formation in later stages -> hemorrhages throughout body

186
Q

Teratogenesis

A

Abnormal development or arrests in development of the embryo or fetus
May result in death or malformations during the antenatal period

187
Q

Virus-induced immunopathology

A

Tissue injury mediated by host immune response to virus infection. It is the price paid by the host to clear a viral infection.

Depends on the delicate balance between the protective and destructive effects of the host immune response to viruses

188
Q

Immunopathology

A

Tissue damage mediated by hypersensitivity reactions.
Autoimmune diseases e.g. Moon blindness in a horse
Inflammation-mediated tissue damage e.g. Fibrosis
Immunodeficiency disorders

189
Q

What is the role of T cells in viral injury to host tissue

A

Cytotoxic cell mediated lysis/killing of infected host cells

Release of cytokines from T cells (CD4+ and CD8+) and other cells that cause inflammation of tissue damage that becomes chronic against persistent virus infections

190
Q

What is the roll of TLRs in viral injury to host tissues?

A

Persistent activation of these receptors of innate host cells by viruses causes production of pro-inflammatory cytokines and interferons, as well as signals that recruit and activate cells involved in inflammation.

Injury can also be mediated by free radicals, such as NO and superoxide

191
Q

Toxicity from antibody responses - response to virus injury to host tissue

A

Antibody responses to viruses may also contribute to tissue damage

192
Q

Virus-induced immunopathology

A

Immunosuppression - infectious burial disease: virus replication causes atrophy of the bursa and a sever deficiency of B lymphocytes, resulting in immuno-suppression. As a result, infected birds become susceptible to other pathogens

193
Q

Inapparent infections

A

Clinical signs and symptoms are not evident.
Too few cells may be infected
Stimulate host immune response
Possible source of virus spread

194
Q

Acute infection (short term infection)

A

Short clinical course

Rapid clearance from host immune response

195
Q

Latent infections

A

Infectious virus is not demonstrable except when deactivation occurs. Reactivation is often stimulated by immunosuppression and/or by the action of a cytokine or hormone

196
Q

Chronic infection

A

Follows acute infection in which the virus is continuously shed from or is present in infected tissue

197
Q

Slow or persistent infection

A

Prolonged incubation period, lasting months or years.

Slow progressive lethal disease

198
Q

True/false: rapid clearance from host immune response is a feature of persistent viral infection

A

False

199
Q

Effects of viruses on host cells

A

Cytocidal -> cell death: lysis or apoptosis

Non-cytocidal -> persistent infection

Cell transformation -> tumor cells

200
Q

Cytopathic effect or cytopathogenic effect

A

Damage or morphological changes to host cells during virus invasion

201
Q

Cell fusion: syncytium or polykaryon formation

A

fusion of the plasma membrane of four or more cells to produce an enlarged cell with four or more nuclei. Prone to premature cell death.

Results from the fusion of an infected cell with neighboring infected or uninflected cells

202
Q

Inclusion bodies in host cell during viral infection

A

Any abnormal structure in a cell nucleus or cytoplasm or both, such as aggregates of proteins, having characteristic staining properties and associated with certain viral infections.

Help to ID certain viral infections

203
Q

Inclusion bodies can be:

A

Accumulation of viral components. Results from degenerative changes in cells. Crystalline aggregates of virions.

Intracytoplasmic or intranuclear (or both)
Single or multiple
Large or small
Round or irregular in shape
Eosinophilic/acidophilic or basophilic
204
Q

Acidophilic staining

A

Recognizes/affinity for acid dyes, such as eosin. Appear pinkish upon staining

205
Q

Basophilic staining

A

Recognizes/affinity for basic dyes, such as hematoxylin.

Appear purplish blue upon staining

206
Q

In tissue culture, visible morphological changes/damages to monolayer cells resulting from virus infection is also known as ______

A

Cytopathic effect

207
Q

General mechanisms of virus-induced cell injury and death

A

Inhibition of host-cell nucleic acid synthesis.
Inhibition of host-cell RNA transcription (mRNA production and processing).
Inhibition of host-cell protein synthesis.
Some viruses cause lysosomes to release their hydrolytic enzymes, which then destroy the host cell
Interference with cellular membrane function.

208
Q

What is apoptosis?

A

Process of programmed cell death, which is essentially a mechanism of cell suicide that the host activates as a last resort to eliminate viral factories before progeny virus production is complete.
Different from lysis where viral replication is complete, host cell is destroyed and new virions released

209
Q

What mediates death of the host cell?

A

Activation of host-cell caspase enzymes mediate death of the cell. Once activated, caspases are responsible for degradation of the cell’s own DNA and proteins

210
Q

What are the two apoptotic pathways?

A

Intrinsic pathway

Extrinsic pathway

211
Q

What is the intrinsic (mitochondrial) pathway?

A

Activated as a result of increased permeability of mitochondrial membranes subsequent to cell injury, such as that associated with a viral infection

212
Q

What is the extrinsic (death receptor) pathway?

A

Activated by engagement of specific cell-membrane receptors, which are members of the TNF receptor family. Thus binding of the cytokine TNF to its cellular receptor can trigger apoptosis

213
Q

What two things can also initiate apoptosis of virus-infected target cells?

A

Cytotoxic T lymphocytes and NK cells. Using preformed mediators such as perforin and granzyme that directly activate caspases in the target cell

214
Q

What results from surface membrane fusion of enveloped viruses?

A

Antibody-dependent mediated cytotoxicity.

Viral glycoproteins are retained on the cell surface, and since these are antigenic, the cell can become a target of the immune system of the host

215
Q

What are the steps in antibody-dependent cell mediated cytotoxicity?

A

Antibody binds antigens on the surface of target cells

Fc receptors on NK cells recognize bound antibody

Cross-linking of Fc receptor signals the NK cell to kill the target cell

Target cell dies by apoptosis

216
Q

What is cell transformation?

A

Changing of a normal cell into a cancer cell

217
Q

Neoplasia

A

Descriptive term that denotes an abnormal tissue overgrowth that may be either localized or disseminated. It is the process that leads to the formation of neoplasms

218
Q

Oncology

A

Study of neoplasia and neoplasms

219
Q

Benign neoplasm

A

Growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue

220
Q

Malignant Neoplasms

A

Locally invasive and may also be spread to other parts of the body

221
Q

Oncogenic viruses

A

Viruses that cause or give rise to tumors

222
Q

Metastasis

A

Spread of cancer cells from the part of the body where it started to other parts of the body

223
Q

Proto-oncogenes

A

Encode proteins that function in normal cellular growth and differentiation

224
Q

Tumor suppressor genes

A

Plays a role in keeping cell division in check. Encodes proteins that regulates and inhibits uncontrolled growth

225
Q

Oncogenes

A

Mutated forms of proto-oncogenes or aberrantly expressed proto-oncogenes

226
Q

What are Retinoblastoma proteins (Rb)?

A

Important tumor suppressor gene/protein that blocks E2F and keeps cell division in check. E2F facilitates cell division

227
Q

What is p53 protein?

A

Tumor suppressor gene/protein that prevents cells with damaged DNA from entering into cell division. Tries to mediate repairing of the damaged host cell DNA. If the damaged DNA cannot be repaired, p53 mediates apoptosis of the cell with damaged DNA

228
Q

Tumor viruses/oncogenic viruses

A

Viruses that cause cancer

Oncogenic viruses generally have a DNA genome, or generate a DNA provirus after infection (retrovirus)

229
Q

Oncogenic DNA viruses

A

Have viral oncogenes in the viral DNA. These oncogenes cause cancer in host cells and also may help in the virus replication process.
A. When oncogenic DNA viruses infect permissive cells, they can replicate successfully. No cancer.
B. When oncogenic DNA viruses infect non-permissive cells, they cannot replicate. The viral DNA integrates into host DNA or in some viruses- the viral DNA remain episcopal. Cancer results

230
Q

What two ways do oncogenic DNA viruses interact with cells?

A
  1. Productive infection in permissive cells: the virus completes its replication cycle, resulting in cell lysis -> no cancer
  2. Non-productive infection in nonpermissive cells: virus transforms the cell without completing its replication cycle -> cancer

During such non-productive infection, the viral genome or a truncated version of it is integrated into the cellular DNA; alternatively, the complete genome persists as an autonomously replicating plasmid (episome)

231
Q

Acutely transforming retroviruses

A

These viruses steal the proto-oncogene from the infected host cell DNA, and then the virus converts the proto-oncogene into the oncogene

232
Q

Slow/chronic transforming retrovirus

A

RNA virus. The virus genome gets inserted into the regulatory gene of the host cell DNA. As a result, the regulatory gene cannot function proper. There is no control on proto-oncogenes of the host DNA. The result is excessive cell division, or cancer

233
Q

Tumor antigens

A

New antigens appear on the surface of tumor cells that may provoke an immune response

234
Q

Expression of tumor antigens

A

FOCMA: Feline oncornavirus membrane associated antigen

235
Q

What are the host immune responses to viral infections?

A

Innate immunity
Adaptive immunity
Passive immunity

236
Q

Innate immune system

A

Defenses exhibit neither antigen specificity nor memory.
First line of defense against viral infections
Constantly present
Immediately operational
Only response available for the first few days after infection
Primary physical and chemical defenses

237
Q

What role does the GI tract have in innate immunity?

A

Mucous membrane of oral cavity and esophagus that is refractory to viruses.
Acidity of the stomach
Alkalinity of intestine
Layer of mucus covering gut.
Lipolytic activity of Bile
Proteolytic activity of pancreatic enzymes.
Defensins

238
Q

What role does the respiratory tract play in innate immunity

A

Mucociliary blanket

Temp gradient - the temp difference of the nasal passages (33C) and the alveoli (37C) that plays an important role in the localization of infection. Thus, rhinovirusus, which infect the nasopharynx and cause the common cold, replicate well at 33C but poorly at 37, which flu is the reverse preference

239
Q

NK cells

A

NK cells mediate death of virus infected cells via apoptosis

240
Q

Cellular Pattern Recognition Receptors

A

Cells at portals of virus entry possess surface receptors (PRRs) that recognize specific pathogen-associated molecular patterns (PAMPs). One class of PRRs are TLRs

241
Q

What do TLRs initiate?

A

Phagocytosis
Chemotaxis
Inflammatory mediators
Interferons

242
Q

Interferons

A

A group of cytokines that are secreted by somatic cells in response to viral and to other stimuli.
Possess potent antiviral, immunomodulating and anti-cancer properties.
Show no virus specificity
RNA viruses are stronger inducers than DNA.
Interferons are orally inactive and should be administered to the patient by parenteral route (injection)

243
Q

How many major classes of interferons are there?

A

3

244
Q

Type 1 interferons

A

Many
IFN-alpha : leukocyte interferon, produced in large quantities by plasmacytoid dendritic cells
IFN-beta : fibroblast interferon. Secreted by virus-infected fibroblast

245
Q

Role of type 1 IFNs

A

Inhibit virus replication in host
Activate NK cells to kill
Increase expression of MHC-1 molecules and antigen presentation
Type-1 IFNs also stimulate differentiation of monocytes into dendritic cells
Maturation of dendritic cells
Stimulates memory T cell proliferation

246
Q

Type-II interferons

A

Only one type, IFN-gamma. Mostly immunoregulatory. Produced by antigen-stimulated T cells and NK cells

247
Q

Type-III INF

A

At least 3 identified: IFN-delta1, 2, and 3.
Recently discovered
Expressed in response to viral infections and activation of TLR
Primarily functions as immunoregulator

248
Q

Adaptive immunity

A

Humoral and cellular
Humor is mediated by antibodies from B lymphocytes
Cellular mediated by T lymphocytes
Antigen specific so responses take time
Stimulates long-term memory
Internal viral antigens usually elicit protective cell mediated immune response
Surface antigens elicit protective humoral and CMI responses

249
Q

True/False: interferons are virus specific i.e. For each virus there will be a specific interferon

A

False

250
Q

Humoral immunity

A

Antibodies may be directed against viral proteins on free virions (capsid or envelope), or against viral proteins expressed on surface of infected cells

251
Q

Virus neutralization

A

Neutralizing antibodies prevent virus attachment and entry into host cells. They bind to the viral capsid or host envelope

252
Q

Opsonization

A

Coating of virions with antibodies. Antibody coated virion is recognized and phagocytosed by macrophages and sometimes by neutrophils

253
Q

Some other antiviral effects of antibodies

A

Clumping of viruses (immunocomplex formation)

Activation of complement system

Antibody-dependent cell-mediated cytotoxicity

254
Q

Cell mediated immunity

A

CD4+ or CD8+ T lymphocytes with microbial antigen in phagocyte or infected cell containing microbial antigen (respectively)

-> activation of macrophages, inflammation, stimulation of B lymphocytes, killing of infected cells

255
Q

True/False: Adaptive immunity is virus specific

A

True

256
Q

Evading the immune system: antigenic plasticity is what?

A

Rapid changes in the structure of the viral antigen. May by the result of mutation, reassortment or recombination. Due to change in antigen structure, the virus may become resistant to immunity generated by previous infection

257
Q

Evading the immune system: antigenic multiplicity is?

A

Antigenic variants with little or no cross-reactivity

258
Q

Negative cytokine regulation

A

Virokines: some viruses synthesize proteins which are homologs of cytokines/IFN

Viroreceptors: some viruses encode proteins that are homologous to the receptors for cytokines

259
Q

Other means of evading the immune system

A 
Down-regulation of MHC I pathway
Inhibition of complement activation
Evasion of neutralizing antibodies
Latency
Cell-to-cell spread of viruses
Inhibition of apoptosis
260
Q

Virus epidemiology

A

Study of determinants, frequency, dynamics and distribution of viral diseases in populations

261
Q

Why study epidemiology of viral diseases?

A

The risk of infection and/or disease in an animal or animal population is determined by: characteristics of viruses, host and host population, behavioral, environmental, and ecological factors that affect virus transmission from one host to another

262
Q

The role of epidemiology is viral diseases

A

To ID and/or clarify the role of viruses in the etiology of diseases.
Understand the interaction of viruses with environmental determinants of disease.
Determining factors affecting host susceptibility.
Unraveling modes of viral disease transmission.
Studying impacts of viral disease on health, economy and society.
Studying role of infectious pathogens isn’t he pathogenesis of chronic non-communicable diseases, such as oncogenic viruses.
Large-scale testing of vaccines and drugs

263
Q

How does studying epidemiology help?

A

Advancing our understanding of the nature of diseases.
In alerting and directing disease treatment, control and prevention activities.
Providing early warning systems and tracking diseases.
Assessment of economic and social impacts.
Assessment of the efficacy and cost of diseases control and prevention

264
Q

Case fatality rate

A

The percentage of deaths among the clinically ill animals.

Animal pop: 100
Number of sick: 25
Number of dead: 10
Case-fatality rate: 10/25 * 100 = 40%

265
Q

Mortality rate

A

Number (%) of animals in a population that die from a particular disease over a specified period of time

Animal pop: 100
# of sick: 25
# of dead: 10
Mortality rate= 10/100 * 100 = 10%
266
Q

Morbidity rate

A

The percentage of animals in a population that develop clinical signs attributable to a particular virus over a defined period of time (commonly the duration of an outbreak)

267
Q

Incidence

A

Number of new cases that occur in a population over a specified period of time.

Incidence rate= (# of cases * 10^n)/population in a specified period of time

AKA attack rate is a measure of the occurrence of infection or disease in a population over time- for example, a month or a year, and is especially useful for describing acute diseases of short duration

268
Q

Prevalence

A

Number of occurrences of disease (old and new), infection or related attributes (antibodies) in a population, at a particular point of time

Prevalence = (# of cases * 10^n)/population at risk at a particular time

269
Q

Sporadic viral disease

A

Occurring occasionally, singly, or in scattered instances, and in an irregular and haphazard manner

270
Q

Enzootic viral disease (endemic in humans)

A

The constant presence of a viral disease within a given geographic area or population group

271
Q

Epizootic viral disease (epidemic in humans)

A

Occurrence of more cases of viral diseases than expected in a given area or among a specific group of people/animals over a particular period of time. Refers to peaks in disease incidence that exceed the endemic/enzootic baseline or expected incidence of disease

272
Q

Panzootic viral diseases (pandemic in humans)

A

A virus epidemic occurring over a very wide area (several countries or continents) and usually affecting a large proportion of the population

273
Q

Asymptomatic carrier

A

Animals that have contracted an infectious viral disease, but display no clinical symptoms. Shed virus, transmitting disease to others. Shedding of virus may be continuous or intermittent

274
Q

Contagious disease

A

A disease that is spread from one person or organism to another by direct or indirect contact

275
Q

Period of contagiousness

A

Time during which an infected animals sheds virus

276
Q

Exotic disease

A

Disease not known to occur in a particular country or geographical area

277
Q

Rabies has never been reported before in St. Kitts. Suddenly, a few cases of canine rabies are reported from St. Kitts, especially among dogs that accompanied incoming RUSVM students from the USA. In this context, rabies would be ____ disease in St. Kitts

A

Exotic

278
Q

Seroepidemiology

A

Denotes the use of serological data as the basis of epidemiological investigation, as determined by diagnostic serological techniques

279
Q

Molecular epidemiology of viruses

A

The use of molecular biological data as the basis of epidemiological investigation of viral diseases

280
Q

Horizontal transmission of disease

A

Contact: direct (bites, sex, licking, droplets), indirect (air-borne, fomites)
Vector transmission: mechanical or biological
Vehicle-borne
Iatrogenic
Nosocomial

281
Q

Vertical transmission of virus

A

From mom to baby

282
Q

Define horizontal (Lateral) transmission

A

Spread of an infectious agent from one person/animal or group to another person/animal or group.

Most viruses are transmitted by horizontal route

283
Q

Contact transmission

A

Spread of infectious agent by direct or indirect contact

Infected Host -> susceptible host by direct transmission

Infected host -> intermediate object by indirect transmission

Intermediate object -> susceptible host by indirect transmission

284
Q

Direct-contact transmission

A

Involves actually physical contact between an infected animal and a susceptible animal. This includes sexual contact

285
Q

Direct-contact transmission: droplet transmission

A

Transmission of virus in droplet nuclei that travel less than 1 meter from the source to the susceptible host

286
Q

Indirect-contact transmission

A

Indirect-contact transmission occurs via fomites, such as eating containers, bedding, dander, restraint devices, vehicles, clothing, improperly sterilized surgical equipment or improperly sterilized syringes or needles

287
Q

Fomite

A

Inanimate object or substance that is contaminated with the infectious agent and is capable of transmitting infectious organisms from one individual to another.

288
Q

Airborne transmission

A

Spread of infectious agents by droplets nuclei in dust that travel more than one meter, sometimes for miles, from the infected to the susceptible host.

289
Q

Vector transmission

A

AKA arthropod-borne transmission. Arthropod vectors carry the viruses from the infected host to susceptible host.

Mechanical transmission: passive transport of the infectious agent on the feet or other body parts of the arthropod vector

Biological transmission: Infectious agent undergoes either a necessary part of it’s life cycle, or multiplication, in the vector before transmission to susceptible host

290
Q

Arboviruses

A

A class of viruses transmitted to humans by arthropods such as mosquitoes and ticks

291
Q

Enzootic cycle (Sylvatic or Jungle Cycle)

A

The natural transmission of virus between wild animals/ birds (vertebrate hosts) and primary insect vectors.

292
Q

Epizootic cycle (rural cycle)

A

The virus is transmitted between non-wild or domestic animals and the primary or accessory insect vectors.

293
Q

Urban cycle

A

The virus cycles between humans and insect vectors

294
Q

Types of transmission cycles?

A

Enzootic cycle
Epizootic cycle
Urban cycle

295
Q

Amplifying host

A

The level of virus can become high enough that an insect vector such as a mosquito that feeds on it will probably become infectious

296
Q

Dead-end host or incidental host

A

A host from which infectious agents are not transmitted to other susceptible hosts. They do not develop sufficient viremia to be picked up by the insect vectors.

297
Q

Common-vehicle transmission

A

Includes fecal contamination of food and water supplies and virus-contaminated mea or bone products

Fecal contamination of water or food and virus contamination of meat or meat products

298
Q

Iatrogenic transmission

A

Infection that is transferred during medical or surgical practice

299
Q

2 ways of iatrogenic transmission

A

Introduction of pathogens by contaminated instruments, or contaminated body surface. Ex. Spread of equine infectious anemia virus via multiple-use syringes and needles

Introduction of pathogen through contaminated prophylactic or therapeutic preparations

300
Q

Nosocomial transmission

A

Occurs while an animal is in a veterinary hospital or clinic. AKA hospital acquired infection

301
Q

Vertical transmission

A

Infection that is transferred from dam to embryo or fetus or newborn before, during, or shortly after parturition

302
Q

Zoonosis

A

Infections that are transmissible from animals to humans

303
Q

Herd immunity

A

Immunity that occurs when the vaccination of a significant large portion of a population (or herd) provides a measure of protection for individuals who have not developed immunity

304
Q

Incubation period

A

Interval between infection and the onset of clinical signs. In many diseases there is a period during which animals are infectious before they become sick

305
Q

Prodromal period

A

The first signs and feelings of illness after incubation period. The period of early symptoms of a disease occurring after the incubation period and just before the appearance of the characteristic symptoms of the disease

306
Q

Acute period

A

When the disease is at its height. Severe clinical signs

307
Q

Decline period

A

Period when clinical signs begin to subside

308
Q

Convalescent period

A

The body gradually returns to it’s pre-diseased state, and health is restored

309
Q

True/false: hospital acquired viral infection is also known as nosocomial transmission

A

True

310
Q

True/false: Enteric viruses have been shown to be more stable in environment than respiratory viruses

A

True

311
Q

Classification of infective micro organisms by risk group: what are those risk groups?

A

Group 1: no or low individual and community risk
Group 2: moderate individual risk, low community risk
Group 3: high individuals risk, low community risk - A pathogen that usually causes serious human or animal disease but does not ordinarily spread from one infected individual to another. Effective treatment and preventive measures are available
Group 4: High individual and community risk - A pathogen that usually causes serious human or animal disease and that can be readily transmitted from one individual to another, directly or indirectly. Effective treatment and preventive measures are not usually available.

312
Q

What does it mean to be at BSL4?

A

Maximum containment lab. BSL4 labs handle dangerous and exotic pathogens belonging to the highest risk group (i.e. Risk group 4 or Ebola virus)

313
Q

Biohazard

A

Biological substances that pose a threat to the health of living organisms, primarily that of humans

314
Q

Biosafety

A

Laboratory biosafety describes the containment principles, technologies and practices that are implemented to prevent the unintentional exposure to pathogens and toxins, or their accidental release

315
Q

Aerosol

A

Very small droplets of fluid that can spread via air. Viruses can spread in lab through aerosol route

316
Q

Biosecurity

A

Laboratory biosecurity describes the protection, control and accountability for valuable biological materials within labs, in order to prevent their unauthorized access, loss, theft, misuse, diversion or intentional release

317
Q

What should be done for virus isolation?

A

Specimens should be collected as soon after onset of symptoms as possible, because maximal amounts of virus are usually present at the onset of signs. The chance of viral recovery is best during the first three days after onset and is greatly reduced beyond 5 delays with many viruses

318
Q

What should be done for serological tests?

A

Two blood specimens are generally collected - one during the acute phase of the illness and the second sample during the convalescence period

319
Q

When should specimens be collected for molecular diagnostics?

A

Should be obtained during the early part of the illness

320
Q

How do you transport virus to the medium (VTM):

A

Swabs

321
Q

How should virus samples be transported to prevent spillage?

A

Basic triple packaging system

322
Q

At what exams do you diagnose viral infections by gross evaluation?

A

Clinical signs
Necropsy
Histopathology

323
Q

Methods of detection of viruses by cultivation/isolation

A

In cells/tissue culture

Inoculation in eggs

324
Q

How is electron microscopy used in virology?

A

Can be used to demonsttate viruses in samples and detect viruses that cannot be grown in-vitro

325
Q

What are the two types of electron microscopes used?

A

Scanning

Transmission

326
Q

Transmission electron microscopy (TEM)

A

Method used in TEM is based on transmitted electrons

TEM seeks to see what is inside of beyond the surface

327
Q

Advantages of TEM

A

Might be used in preference to an SEM because:

TEM can produce images that have higher magnification and greater resolution than images produced by SEM

328
Q

Scanning electron microscopy (SEM)

A

Based on scattered electrons

Focuses on the samples surface and it’s composition

329
Q

Advantages of SEM

A

Might be used in preference to TEM because:

SEM produce 3D images while TEM only produce flat images

330
Q

True/false: A TEM yields 3D images

A

False

331
Q

Gold standard test

A

A diagnostic test that is considered to be the most accurate and best available under a particular condition or set of conditions

332
Q

Sensitivity

A

The probability that cases with the infection (determined by the result of the reference or ‘gold standard’ test) will have a positive result using the test under evaluation

333
Q

Specificity

A

The probability that cases without the infection (determined by the results of the reference or ‘gold standard’ test) will have a negative result using the test under evaluation

334
Q

Collection of serum should be in what?

A

Red-top vacutainer tube

335
Q

Collection of plasma should be in what?

A

Lavender-top EDTA vacutainer tube

336
Q

Vacutainer tubes used to collect blood sample to obtain serum for diagnostic purposes usually have ___ caps?

A

Red

337
Q

Typical ELISA (Enzyme-linked immunosorbent assay)

A 
Antigen coated in a well
Add antibody tagged with an enzyme
Antigen binds to enzyme-tagged antibody
Wash the excess unbound antibodies
Add substrate
Enzyme tagged to antibody which is bound to antigen will change color of substrate. Intensity of color indicates more positive reaction
338
Q

Direct ELISA

A

Antigens are immobilized and enzyme-conjugated primary antibodies are used to detect or quantify antigen concentration. The specificity of the primary antibody is very important

339
Q

Indirect ELISA

A

Primary antibodies are not labeled, but detected instead with enzyme-conjugated secondary antibodies that recognize the primary antibodies.

340
Q

Sandwich ELISA

A

The antigen to be measure is bound between a layer of capture antibodies and a layer of detection antibodies. The two antibodies must be very critically chosen to prevent cross-reactivity or competition of binding sites

341
Q

Competitive ELISA

A

A decrease in signal when compared to assay wells with purified antigen alone indicated the presence of antigens in the sample.

Weaker signal indicates presence of antigens in sample.

342
Q

Fluorescence antibody test (FAT)

A

Direct FAT: labeled antibodies are added onto the sample (antigen). Visible fluorescence appears at the binding sites of the specific antibodies (antigen-antibody binding).

Indirect FAT: IFAT employs a secondary antibody labeled with a fluorescent marker that recognizes the primary antibody bound to antigen

343
Q

Immunohistochemistry

A

The antibody is tagged with an enzyme, generally horseradish peroxidase. The enzyme reacts with a substrate to produce a colored product that can be visualized in the infected cells with a standard light microscope

344
Q

Immunochromatography (lateral flow devices)

A

A form of POC (point-of-care) test that is simple to perform, easy to carry, and does not require specialized equipment

345
Q

Agglutination

A

Method using the property of specific antibodies to bind many antigens (antigens on pathogen, or antigen coated particles, latex beads) into single clumps thereby forming large complexes, which are easily precipitated. The precipitation can be macroscopically or microscopically visible

346
Q

Hemagglutination and Hemagglutination inhibition test

A

Relies on the property of some pathogens (mainly viruses) to nonspecifically agglutinate erythrocytes

347
Q

Agar gel immunodiffusion test

A

Antigen and antibody placed in separate wells of an agar gel.
Antigen and antibody diffuse toward each other.
A thin white line is formed due to precipitation of antigen/antibody complex.

348
Q

Complement fixation test

A

Let us say that the serum from patient has antibody against virus A. -> Intact sheep RBCs settle at bottom (positive reaction).
Let us say that the serum from patient is negative to virus A. It will have no antibodies -> you find hemolysis of sheep RBCs, destruction/hemolysis of sheep RBC indicated negative reaction

349
Q

Neutralization assay

A

Neutralization of a virus is defined as the loss of infectivity through reaction of the virus with specific antibody

RUSVM Virology (10 decks)

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