Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IIH > Cytotoxic T Cells and Antiviral Killing > Flashcards

Cytotoxic T Cells and Antiviral Killing Flashcards

1
Q

Define incubation period.

A

The period between exposure to an infection and the appearance of initial symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define prodromal period.

A
  • The period between the appearance of initial symptoms and the full development of a rash or fever.
  • The period following the incubation period.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

To which Baltimore group do Rhinoviruses belong?

A

Group 4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

To which Baltimore group do Adenoviruses belong?

A

Group 1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List 3 pattern recognition receptors used by immune cells to recognise viral PAMPs.

A

1 - Toll-like receptors.

2 - RIG-I-like receptors.

3 - Nod-like receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are interferons?

List the types of interferons.

A
  • A large family of cytokines which interfere with viral infection.
  • Type 1 (includes IF-alpha and IF-beta).
  • Type 2 (includes IF-gamma).
  • Type 3.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List the cells that produce IFN-alpha.

A

1 - Plasmacytoid dendritic cells.

2 - Monocytes.

*Many cells produce IFN-beta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give an example of a disease that can be treated with IFN-alpha.

A

Hepatitis B / C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Give an example of a treatment that can be treated with IFN-beta.

A

Multiple sclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List the cells that produce IFN-gamma.

A

1 - NK cells.

2 - T cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which molecule activates IF-gamma?

A

IL-12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the function of IF-gamma?

A

It is involved in Th1-driven immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of type 3 interferons?

A

They play a role in antifungal and antiviral immunity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why are interferon-stimulated genes (ISGs) highly expressed during infection?

A
  • Viral infection triggers the type 1 interferon system via immune cells.
  • Interferons stimulate the expression of interferon-stimulated genes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the general function of interferon-stimulated genes?

A

They have numerous antiviral effector functions, interfering with all steps in a virus life cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List the stages of the viral life cycle.

A

1 - Entry.

2 - Uncoating.

3 - Transcription.

4 - Translation.

5 - Assembly.

6 - Exit.

17
Q

List 3 examples of interferon-stimulated genes.

A

1 - MX1.

2 - PKR.

3 - OAS1.

18
Q

List 4 specific functions of interferon-stimulated genes.

A

1 - Degradation of viral RNA through activation of RNAse.

2 - Inhibition of viral gene expression and virion assembly.

3 - Upregulation of MHC-1.

4 - Increases p53 activity, promoting apoptosis.

19
Q

How does protein kinase R (PKR) interfere with the viral life cycle?

A
  • Interferons activate protein kinase R.
  • Protein kinase R activates p68 kinase.
  • p68 kinase phosphorylates eIF2-alpha, inactivating it.
  • eIF2-alpha is required for viral translation.
20
Q

How do thiazolides work as antivirals?

A

By acting like interferons to reduce viral translation by activating protein kinase R.

21
Q

Give an example of a viral mechanism that has evolved to turn off the interferon cascade.

A

Influenza A inhibits the RIG-I-like receptor, preventing viral recognition.

22
Q

List 2 risks of dysregulation of interferon production.

A

1 - Autoinflammatory diseases.

2 - Autoimmune diseases.

23
Q

What is STING?

A
  • Stimulator of interferon genes.

- Has a key role in stimulating interferon production.

24
Q

List 2 molecules that are necessary to activate STING.

A

1 - cGAS.

2 - cGAMP.

25
Q

Give an example of a disease associated with STING.

A

STING-associated vasculopathy with onset in infancy (SAVI), where STING is activated all the time.

26
Q

Which MHC class is important in viral recognition?

Which cells recognise this class?

A
  • MHC class I.

- CD8+ T cells.

27
Q

Define cross-presentation.

What is the consequence of cross-presentation?

A
  • The ability of certain antigen-presenting cells to take up, process and present extracellular antigens with MHC class I molecules to CD8+ T cells.
  • The consequence is that endogenous antigens can prime CD4+ T cells, and exogenous antigens can prime CD8+ T cells.
28
Q

What is the effect of MHC class I activation?

A

Proliferation and activation of the peptide-specific CD8+ T cell.

29
Q

Give an example of a viral mechanism that has evolved to interfere with MHC class I signalling.

How, in this case, are these virally infected cells destroyed?

A
  • Some viruses can downregulate MHC class I expression.
  • In cells without MHC class I, there is no way of cells to present self proteins.
  • This enables NK cells to destroy the cell with downregulated MHC class I expression by recognition of non-self.
30
Q

List two methods by which NK cells cause cell death.

A

1 - By activating apoptotic receptors.

2 - By releasing their cytotoxic granules.

31
Q

List 2 roles of antibodies in the adaptive immune response to viruses.

A

1 - Neutralising antibodies, which directly kill the virus.

2 - Indirect killing by antibody-dependent cell cytotoxicity (ADCC) using non-neutralising antibodies.

32
Q

List 4 mechanisms of action of directly neutralising antibodies.

A

1 - Blocking the virus-receptor interaction that allows entry into the cell.

2 - Blocking the process of endocytosis and phagosome formation.

3 - Blocking release of the virus from the phagosome into the cytoplasm.

4 - Aggregating the virus.

33
Q

List 2 ways by which indirect killing occurs by antibody-dependent cell cytotoxicity (ADCC).

A

Antibodies bound to a virus can:

1 - Induce the classic complement cascade.

2 - Bind to Fc-gamma RIII receptors (CD16 receptors) on NK cells, which activates the NK cells.

34
Q

How might antibody-dependent cell cytotoxicity (ADCC) cause antibody-dependent enhancement of infection (ADEI)?

A
  • Some viruses have no easy route into the cell.
  • On secondary infection, specific antibodies have been produced to the virus.
  • Viruses bound to the antigen binding site of the antibody can gain access to a cell if the antibody binds to the Fc receptor site on the cell.
35
Q

Give an example of a virus which gains access to cells via antibody-dependent enhancement of infection (ADEI).

Which Fc receptor does this virus use as its entry receptor?

A
  • Dengue virus.

- The viruses uses the Fc-gamma RIII (CD16) receptor as its entry receptor.

36
Q

Why are viruses that use antibody-dependent enhancement of infection (ADEI) worse upon reexposure?

A

Because upon reexposure, the body has produced non-neutralising antibodies which can facilitate virus uptake into cells via antibody-dependent enhancement of infection.

37
Q

What is Dengue haemorrhagic fever?

A

The syndrome caused by re-exposure to Dengue virus.

IIH (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions