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Flashcards in Virology Deck (71)
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1

"Where do pox viruses replicate?

Pox viruses replicate in epithelial-cell cytoplasm, unlike most other dsDNA viruses, which require the host cell's proteins in the nucleus to carry out transcription. 

Pox viruses are large enough to carry their own replication proteins into a host cell & thus don't need to hijack the host cell's nucleus. 

2

What is the site of infection of rotaviruses?

Gastrointestinal Tract:

Replicates in enterocytes at villi tips in small-intestine lining, especially of piglets

3

What is the site of infection of influenza viruses, such as Equine Influenza Virus (family Orthomyxoviridae)?

Respiratory Tract:

Ciliated epithelial cells in nasal lining, bronchi, bronchioles

4

What are the site of infection by members of Parvoviridae, such as FPV?

Immune system:

Haematopoetic & Lymphoreticular Systems

5

Name some viruses that target animals' skin epithelial cells.

Poxviruses:

Parapoxvirus: Orf (sheep, goats, humans)

Squirrelpox (squirrels)

Leporipoxvirus: Myxomatosis (rabbits)

6

What is the target site of the rabies virus (family Rhabdoviridae)?

Central Nervous System:

 

7

Name two types of virus that replicate in neurons.

Rabies & Herpes.

Rabies is shed in saliva & herpes is shed from skin 

8

What is the target site of infection for Equine Herpesvirus (EHV-1)?

Vascular endothelium:

Infection & destruction of endothelial cells & endothelial-cell layer

9

What is the target site of infection for Canine Distemper Virus (CDV)?

Multiple tissues (systemic):

Infects lymphocytes then all tissues

Entry via URT via droplets & aerosols ➔ spread to lymphoid organs via blood ➔ spread to all epithelia (respiratory tract, gut, bladder, skin) & CNS

10

Describe Rotavirus's

structure

genome

target tissue

transmission 

pathogenesis

Structure: Non-enveloped ∴ stable in environment

Genome: segmented, dsRNA genome

Target tissue: GIT, enterocytes, villi tips in small-intestine lining; not systemic

Transmission: Ingestion (orofaecal) & Oropharynx (tonsils)

Pathogenesis

 

11

Describe Equine Influenza Virus's

structure

genome

target tissue

transmission

pathogenesis

Structure: Enveloped ∴ not stable in environment

Genome: Segmented ssRNA genome

Target tissue: Ciliated epithelial cells of respiratory tract ie., nasal lining, bronchi, bronchioles

Transmission: Direct contact & aerosol via URT

Pathogenesis: 

 

12

Describe Feline Panleukopenia Virus

aka

Feline Parvovirus's:

structure

genome

target tissue

transmission

pathogenesis

Structure: Small, non-enveloped, v stable in environment

Genome: ssDNA

Target tissue: Haematopoetic & Lymphoreticular system (macrophages & lymphocytes); lymphoid tissue esp tonsils; rapidly dividing cells in very young animals, so intestinal crypt cells of puppies 

Transmission: Mutual grooming, aerosol

Pathogenesis: Virus ingested or inhaled via oropharynx ➔ arrive at tonsils ➔ replicate in lymphoid tissue/tonsils ➔ viraemia & spread to other sites  ➔ destruction of lymphoid cells leads to immune suppression, leaving animal vulnerable to secondary bacterial infection ➔ virus hides from immune system in carrier

13

Describe Poxviruses':

structure

genome

target tissue

transmission

pathogenesis

Structure: Very large (200-400 nm) ∴ encode all enzymes needed for replication themselves; generally enveloped

Genome: dsDNA

Target tissue: Skin epithelial cells 

Transmission: Entry via skin wounds, insect bites or injections; also via blood in circulation 

Pathogenesis: Direct intro of virus thru epithelium via cuts, abrasions, needles, insect bites OR via blood in circulation, escaping blood vessel, possible invasion of neighbouring dermal cells ➔ formation of macule (flat red) ➔ papule (raised, red), more inflammation, vasodilation, ↑ permeability ➔ intraepidermal vesicle (small blister), virus invades epithelium ➔ ULCER: epithelium ruptures, virus discharges & infects other areas

 

14

Describe the Rhabdovirus's:

stucture

genome

target tissue

transmission

pathogenesis

Structure: Enveloped bullet-shaped virions

Genome: Negatove-sense ssRNA

Target tissue: Neurons, CNS

Transmission: Bite wound (shed in saliva)

Pathogenesis: Virus intro via bite wound ➔ travels to salivary glands via neurons ➔ spread to CNS via neurons ➔ lytic infection of neurons leading to necrosis ➔ invasion of inflammatory cells around blood vessels  ➔ can be furious form or dumb/paralytic form, which can result in paralysis or spasms of pharyngeal muscles, inhibiting swallowing and leading to ↑ salivation/foaming  ➔ virus shed in saliva 

 

15

Describe Equine herpesvirus (EHV-1)'s:

stucture

genome

target tissue

transmission

pathogenesis

Structure: Large, enveloped, icosahedral capsid

Genome: dsDNA

Target tissue: Vascular endothelial cells

Transmission: Aerosol, contact

Pathogenesis: Enters via respiratory tract ➔ respiratory disease ➔ infects lymphocytes & establishes viraemia in blood

abortion: vasculitis in placental blood vessels ➔ thrombi ➔ haemmorhages 

OR

neurological disease: blood vessels of spine & brain infected ➔ ataxia & paralysis ➔ virus becomes latent in lymphocytes & CNS

 

16

Describe Canine Distemper Virus (CDV)'s:

structure

genome

target tissue

transmission

pathogenesis

Structure: Enveloped so not stable in environment

Genome: ssRNA

Target tissue: First lymphocytes then multiple tissues; systemic

Transmission: Aerosols or droplets 

Pathogenesis: Inhaled via URT  ➔ spread to lymphoid organs via blood ➔ spread to all epithelia (respiratory tract, gut, bladder, skin) & CNS

17

Describe clinical signs of rotavirus & how it disease is prevented.

- Group A cause diarrhoea (milk scours) in calves, piglets, foals & young birds
- 1-4-day incubation period
- shortens villi (not crypt cells)
- shed in high numbers in faeces; max shedding on days 3-4 post-infection
- survives in faeces for several months & in water so contamination can build up a lot in unhygienic environment
- no systemic spread
- prevented by antibodies (esp IgA) in colostrum & vaccination

18

Describe clinical signs of Equine Influenza Virus.

Dry cough, nasal discharge, pyrexia, depression

19

Describe the clinical signs of Feline panleukopenia virus (FPV) aka Feline Parvovirus & how the disease can be prevented. 

- After viraemia, virus spreads to all lymphoid organs: thymus, bone marrow, lymph nodes, spleen, Peyer’s patches

- In cats, it destroys all WBCs regardless of type, ∴ panleukopenia ➔ immune suppression
V&D (bloody), dehydration ➔ death possible

- In dogs, targets rapidly dividing intestinal crypt cells, causing diarrhoea

- Can be prevented by vaccine

20

Describe clinical signs of Poxviruses & how they can be treated or prevented.

- Formation of macule (flat red) ➔ papule (raised, red) ➔ intraepidermal vesicle (small blister), virus invades epithelium ➔ ULCER: epithelium ruptures, virus discharges & infects other areas

- Uncomplicated lesions resolve in 3-4 weeks

21

What are the clinical signs of rabies and how can it be prevented?

- Can be furious form or dumb/paralytic form, which can result in paralysis or spasms of pharyngeal muscles, inhibiting swallowing and leading to ↑ salivation/foaming

- Prevented by vaccine

22

What are the clinical signs of Equine Herpesvirus (EHV-1) and how can infection be prevented?

Abortion: vasculitis in placental blood vessels ➔ thrombi ➔ haemmorhages)

OR

Neurological disease: blood vessels of spine & brain infected ➔ ataxia & paralysis ➔ virus becomes latent in lymphocytes & CNS


- Prevented by isolation of mares in late-stage pregnancy

- Vaccination only reduces respiratory disease but incomplete for abortion or CNS disease

23

What are the clinical signs of Canine Distemper Virus in dogs and how is infection prevented?

- Cough, nasal discharge, conjunctivitis

- V&D

- Convulsions, seizures due to CNS infection

- Hard-pad disease in dogs

- Up to 50% of cases are subclinical or mild

- Prevented by vaccine

24

Give an example of a viral diagnostic techniques based on identifying a virus's morphology, and describe its advantages & disadvantages.

 

Electron microscope:  direct visualisation of virus, applying negative staining with heavy metals, ie., stain appears dark and the virus appears light

Advantages: can be used for viruses that can’t be cultured; allows identification of new agents

Disadvantages: requires specialised equipment & experienced personnel; low-sensitivity may require concentration of sample & often purification of sample

25

Give examples of viral diagnostic techniques based on identifying a virus's antigenicity, and describe their advantages & disadvantages.

Detecting virus using antibodies in immunoassays; can use monoclonal antibody specific for one antigenic epitope or polyclonal antibodies, ie., a mix of antibodies to detect several epitopes 

Advantages: fast, don't require live or infectious virus, specific

Disadvantages: no amplification, relatively low sensitivity

Types:

Antigen ELISA - plate covered with antibody in sandwich in capture assay to detect antigen

Immunohisto/cytochemistry (tissue or cells) - viral antigen in cells is detected by specific antibody, which carries fluorescent label (immunofluorescence assay) or enzyme label that reacts with colour substrate (immunoperoxidase assay)

Immunochromatography (fluids) - eg. Rapid ImmunoMigration Witness FeLV test for finding p27 antigen in blood sample, uses antigen-specific antibody labeled with colloidal gold

26

Give examples of viral diagnostic techniques based on detection of antibodies.

Neutralisation assay: serum sample mixed with virus ➔ antibodies in sample bind to virus ➔ mixture added to cells ➔ if antibodies present, virus won’t infect cells ➔ if no antibodies, viruses affect cells, which show cytopathic effects such as Negri inclusion bodies

Haemagglutination inhibition assay: based on some viruses' ability to agglutinate RBCs, esp influenza virus. Either a big blob of blood in the well or a “button” or “dot” of blood in the case of no reaction ie., presence of antibody (positive result for antibody response to virus)

Antibody ELISA - opposite of antigen ELISA; plate is coated with antigen ie. whole virus or purified virus protein ➔ antibody in serum sample binds to antigen ➔ second antibody that recognises IgG is added ➔ second antibody carries enzyme label that changes colour substrate when bound

27

Give examples of viral diagnostic techniques based on  genome composition, and describe advantages & disadvantages.

This involves identifying a virus based on detection of viral nucleic acid. There are two techniques:

1. PCR - polymerase chain reaction:

- amplification of viral sample
- if not a DNA virus but RNA, then RNA needs to be converted to cDNA for PCR analysis
- PCR is based on ability of Taq heat-stable polymerase to amplify DNA, by replicating from short primers specific for virus sequence; Taq can survive repeated cycles of heating to 94 C
- generation of amplicon (viral sequence) of predicted size indicates presence of virus nucleic acid in sample; ie., produces large number of copies that are easy to detect
- separated on agarose gel using electrophoresis
- with electrophoresis must have right positive control

2. Real-time quantitative PCR - fluorescence-tagged:

- labelled DNA provides quantitative measure of amt of viral DNA in sample, eg measure of viral load; no need for electrophoresis

Advantages of both: very sensitive, can use v small amt of starting material; doesn’t require live virus; specific as primers designed for target DNA

Disadvantages: very sensitive, danger of contamination & false positives

28

What are the 10 mechanisms viruses use to avoid detection and/or destruction by the host immune system?

 

1. Interference with Interferon (IFN) of the innate immune system

2. Hiding out in immune-privileged sites such as CNS, eye & gonads

3. Syncytium formation

4. Transformation

5. Viral production of antigen decoys

6. Antigenic DRIFT

7. Antigenic SHIFT

8. Interfering with MHC Class I Pathway of antigen presentation

9. Avoiding detection by NK cells

10. Superantigens

29

How do viruses interfere with Interferon (IFN) to avoid detection by the innate immune system? 

 

(Type 1 IFNs are produced by virus-infected cells to make neighbouring cells more resistant to infection by:
↑ degradation of virus mRNA to block viral transcription
↓ synthesis of virus protein by blocking ribosomes
↑ MHC Class I presentation to cytotoxic CD8+ Killer T-cells, degranulation/caspase cascade/Fas/TNF-alph & apoptosis) 

Some viruses have evolved to circumvent Type I IFNs (α, β, Ω):


- virus produces early proteins that interfere with the signalling cascade produced by the infected cell’s toll-like receptors. This viral interference means the cell can’t produce IFN & its viral-resistance genes are NOT switched on


- virus’s early proteins could BLOCK IFN-receptors, so the cell can’t respond to IFN & its viral-resistance genes are NOT switched on

30

Give an example of a virus that interferes with Interferon (IFN) of  the innate immune system as an immune-evasion mechanism.

Pestiviruses

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