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NMSK (Lectures) > Host-Virus Interactions > Flashcards

Host-Virus Interactions Flashcards

1
Q

Outline the interplay between the host and the virus during infection

A
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2
Q

Outline the pathogenesis of the interaction between host and virus

A

Interaction between virus & host determines:
Whether infection will occur

The type of infection that will be established
	(such as persistence and clearance)

The outcome of the encounter

So these interaction are based on pathogenicity of the infecting virus and also the susceptibility or resistance/tolerance of the host

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3
Q

What effect does the virus have on the host?

A

Morphological
Lysis, rounding & detachment form surface

Functional
	Inhibits or stimulates cell division

Biochemical
	Activation of cell signalling pathways & induction of the immune response

Metabolic reprogramming
	This is done so the host can support viral replication & rapid cell growth
	
Immunological 
            Immune system enacts strategies that could lead to resistance
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4
Q

What is the life cycle of the virus?

A

Invade the host
Via skin/ mucous mebranes

Enact viral tropism to infect susceptible cells

Overcome local innate immunity defences

Viral assembly after replication, to then spread form the site of infection to other organs through the blood system

From here they can undergo further replication

They shed from host in high numbers to infect other hosts ensuring spread and 
    maintenance 

    Viral infection can be spread through urine, faeces, respiritory tract, coughing, 
    sneezing, semen, milk, blood
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5
Q

Describe the host cell immune responses to infection

A
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6
Q

Describe the host cell innate immune responses to infection

A

PAMP’s on the virus interact with hosts PRR

This interaction triggers the adaptor proteins which amplify & send the signal to kinases

Activating Type 1 interferons & cytokines inducing an antiviral state within the host cell

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7
Q

Outline the role of Type I Interferons

A

Modulate innate immune responses to impair virus replication processes
Act to inhibit viral nucleocapsids mRNA of influenza

Degrade viral RNA

   Block viral protein synthesis
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8
Q

Describe the host cell adaptive immune responses to infection

A

Relies on the recognition & binding of viral molecules or by antigens by specific receptors on T & B lymphocytes

Systemic Block to Infection

–Naïve B cell interacts with the virus, internalises it and present the antigen

–CD4+ Th cells activate the B cells leading to B cell proliferation & differentiation into Plasma cells and memory cells

Elimination of Infected Cells

–CD4+ Th cells interact with the APC presenting the viral proteins

–Cytokines released by Th Cell activate CD8+ T cells (cytotoxic) which then release
enzymes to kill the infected cell

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9
Q

How can antibodies act to prevent viruses binding with a host?

A

Antibody mediated Inhibition of Viral Attachment & Entry

Antibodies aggregate viral particle impairing their function and inhibiting steps in the viral life such as fusion

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10
Q

What terminology is used when viruses overwhelm a host?

A

Outbreaks

Epidemics

Pandemics

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11
Q

List the factors which influence viral emergence

A

Virus adaptation & change

Host susceptibility

Climate change

Public health measures & deficiencies in repsonse to & infrastructure

International travel

Economic status

Human demographics & behaviour
- Population growth
- Urbanisation
- Increased interaction between reservoir species & host

Changing ecosystems

Agriculture or economic development

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12
Q

Explain how viruses exploit host cell machinery

A
  • counteract host antiviral defences
  • Hijack host cell resources
  • Shutdown host cell function
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13
Q

How do non-enveloped viruses attach and enter the host cell?

A

Attachment & Entry

–Dependent on presence of appropriate cell surface receptors

–Bind to cell receptor using capsid proteins

–Clatherin- or caveolin mediated endocytosis

–Leads to formation of (clatherin / caveolin) coated vesicles

–Conformational change of capsid allows for insertion onto endosomal membrane

–Release of viral genomes into cytoplasm through pore formation or disassembly id core complex

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14
Q

How do enveloped viruses attach and enter the host cell?

A

–Dependent on presence of appropriate cell surface receptors

E.g. Equine Influenza
–HA bind to sialic acid containing surface receptor on cell leading to endocytosis

–Low pH endocytic compartment acidifies virus particles triggering mebrane fusion

–Viral RNA is released into cytosol

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15
Q

Explain how viruses supress host gene expression and how this benefits them

A
  1. Viral polymerase of RNA virus captures host RNA polymerase II to initiate transcription
  2. Target host gene expression by destroying/suppressing newly synthesised mRNA which makes the host ribosomes available for viral transcription and synthesis
  3. NS1 (a non structural protein of the influenza virus) Enhances translation by binding to mRNAs & ribosomes. This binding promotes an increase recruitment of ribosomes to the mRNA
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16
Q

What are virial replication factories?

A

Specialised membranous compartments which enhance viral propagation

Increase local concentration of host and viral factors required

Protected environment which shields viral RNA and proteins from degradative environment

Coordinates different processes of the viral lifecycle

i.e. RNA translation, replication & assembly

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17
Q

Explain transport of viruses within a host cell

A

Host mebranes can assist in trafficking viruses across cellular compartments

Influenza A virus replicates in the nucleus where RNPs then recruit host factors and use host mebranes for transport across cellular compartments during the infection course

In the case of influenza they dissociate at the plasma mebrane where viral assembly occurs

18
Q

Outline how enveloped viruses assemble and egress from the host cell

A

The envelope of many enveloped viruses, including HIV and Influenza, originates from host membranes acquired during virion assembly and egress

At the plasma mebrane, enveloped viruses bud leading to a mebrane curvature and eventual incision in order to release

Influenza A viruses uses viral protein neuraminidase which cleaves interaction with the receptor between virion and cell surface (there are also neuraminidase inhibitors that can block this interaction)

19
Q

Outline how non enveloped viruses assemble and egress from the host cell

A

Viral progeny is released through cell lysis as apposed to budding

Cytopathic viral infection kill the cell in which they replicate

Lysis is seldom triggered by host cell 
Often actively triggered by late expressed viral proteins in the viral lifecycle

May involve inhibition of host protein, RNA & DNA synthesis, production of degradative enzymes and induction of apoptosis

20
Q

Explain Viroporins and outline their function

A

Viral proteins produced late in viral life cycle

Make hydrophilic holes or aqueous pores within cells

Non enveloped viruses encode these to increase permeability of the plasma membrane to allow for the release of virions

21
Q

How does the host try to prevent egress of the virus

A

Tetherin inhibits influenzas viral release by trapping newly formed virions at the plasma membrane
Virus can have methods to block Tetherin

22
Q

Discuss the main ways that viruses can be identified

A
23
Q

Outline the method of diagnosing a viral infection

A

Reviewing disease history and clinical signs

Clinical exam
	Some infections cannot be diagnosed by this alone
	
Confirmation by laboratory testing

	Detection and measure of infectious virus – Virus isolation in cultured cells
	Detection of viral antigens – Antibody detection of viral protein/antigen 
	Detection of viral nucleic acids  – Amplification of nucleic acid, sequencing
	Detection of virus protein-specific antibody response
	Use of serological tests to detect IgG, IgM or total antibody
24
Q

Describe the detection and measure of infectious virus – Virus isolation in cultured cells

A

Viral growth and isolation can be achieved using:

Cell culture
	Cell line specific
	
Influenza A & Avian viruses typically cultured in embryonated hen eggs
25
Q

Describe the detection of viral antigens – Antibody detection of viral protein/antigen

A

Immunofluorescence/ immunohistochemistry
Viral antigen is identified in cells or tissue specimens by reaction with specific antibody

Antibodies either:

– Posses fluorescent label
– Are enzyme linked and change colour upon reaction with substrates

26
Q

Describe the detection of viral nucleic acids – Amplification of nucleic acid, sequencing

A

Common use of polymerase chain reaction (PCR) is to amplify virus specific nucleic acids

Uses short lengths of DNA (primers) which are complimentary to the virus sequence- amplify a region spanned by the primers
Thermostable DNA polymerase (Taq)

Recognise the presence of the amplification product using a gel-based method and 
    stain for the DNA molecules

For DNA viruses, PCR is a direct method

RNA viruses require conversion of RNA to single stranded complementary DNA (cDNA) by reverse transcription followed by PCR, i.e. (RT-PCR)

RT-PCR has been used as a reliable diagnostic test for SARS-CoV-2 infection

27
Q

Describe the detection of virus protein-specific antibody response

A

Presence of virus protein-specific antibody response
Samples are tested for presence of specific antigens

ELISA
Enzyme-linked immunosorbent assay

Antibody immobilised on solid surface or mebrane

Magnitude of colour change increases with increasing amount of antigen

IDEXX Snap ELISA test
ELISA format can be adapted for practice use

 -  IDEXX Snap ELISA test- detects antigen in serum, plasma or whole blood
28
Q

Describe the use of serological tests to detect IgG, IgM or total antibody

A

Positive Serology - Detect serum levels of antibodies to the virus.

29
Q

What are the limitations to serological tests

A

Indicates previous exposure but not sufficient to indicate when infection occurred

False-negatives and positives can confuse diagnosis

Patient antibody can block test antibody binding

Cross reactions can occur – different virus members within virus family

A good knowledge of clinical symptoms, pathology and limitations of tests need to be applied

Direct detection of virus is more definitive.

30
Q

Understand basic methods of treatment and control

A

Supportive therapy
Antivirals
Vaccination

31
Q

Describe what supportive therapy entails

A

Nursing
TLC
Eyedrops depending on clinical signs
Fluid administration for dehydration
Nutritional considerations
Appetite stimulation

32
Q

Evaluate antivirals as a method of treatment

A

-Target viral proteins that are essential for the virus

-Must be specific to avoid damaging or interfering with host cell function

-Very few licenced drugs for animals available

-High potential for resistance

-Expensive (more suitable for companion animals than livestock)

33
Q

Evaluate vaccination as a method of prevention

A

-More cost effective particularly for livestock

-Economic constraints, safety & efficacy concerns, and virus evolution (influenza viruses) affect effectiveness of vaccines

34
Q

List the viral infections that there are vaccines for

A

-Equine influenza
-Feline leukaemia virus
-Rabies (Cats and wildlife)
-Canine distemper
-Myxomatosis (Rabbit)
-Newcastle disease and influenza (Poultry)
-Classical swine fever
-Feline Calicivirus

35
Q

Outline the mechanism of vaccinations

A

Mechanism:

  1. Host exposure to vaccine antigen/s
  2. Naïve T and/or B cells that recognise this (not many) begin clonal expansion and differentiation
  3. Develop population of memory cells
  4. Next encounter with same antigen(s) induces protective secondary response (more rapid and effective than primary response)
36
Q

Describe live vaccines (natural or attenuated)

A

Natural – e.g. cowpox virus to protect against smallpox virus because they look similar (Only vaccine of this type widely used)

Attenuated – e.g. Equine influenza, myxomatosis, polio, MMR

Highly successful strategy
Change (attenuate) the virus so it is unable to cause disease but still immunogenic
The virus ‘looks’ the same to the immune system but is weaker!

37
Q

Describe inactivated vaccines (killed)

A

E.g. Feline leukaemia virus, Influenza, foot and mouth disease, some rabies vaccines

Made from virulent virus but agents such as formaldehyde are used to destroy infectivity but maintain immunogenicity
Important to ensure aggregates of virus are dispersed before inactivation otherwise can lead to vaccine-associated outbreaks

38
Q

Describe viral-vector based vaccines

A

E.g. Rabies, Equine influenza, Canine distemper, SARS-CoV-2-ChAdOx1

Non-pathogenic live viruses can be used as vaccine vectors
Have insertions of foreign genes coding for the antigen of interest (using recombinant DNA techniques)
Can infect APCs directly and are genetically and physically stable

39
Q

Describe subunit vaccines

A

E.g. Newcastle disease, classical swine fever

Purified antigens of a pathogen or inactivated toxins
Toxins can be rendered harmless without loss of immunogenicity (e.g. Tetanus)

40
Q

Describe DNA vaccines

A

E.g. Infectious hematopoietic necrosis virus (Salmon)

Viral DNA can confer protective immunity-enhances humoral and immune responses
Construct plasmids that contain key viral antigens
Not widely approved in animals or humans
Stable and can be prepared and harvested in large quantities

41
Q

Describe RNA vaccines

A

E.g. SARS CoV-2

Contains a synthetic version (SARS-CoV-2 spike protein) of part of the virus’ genetic code (mRNA)
Prompts the immune system to respond and protect against future SARS-CoV-2 infection
Can be rapidly developed and have potential for low-cost manufacture
Not widely approved in animals or humans
Not as stable as other vaccines– requires -70C and 2-8C for up to 5 days

NMSK (Lectures) (63 decks)

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