Lecture 5: Antiviral immunity and Prophylaxis Flashcards

1
Q

What are the parts of the innate immune system? Adaptive immune system?

A
  • Innate immunity: Natural barriers, IFN, NK, Macrophages.
  • Adaptive immunity: Cytotoxic T cells, antiviral antibodies, helper T cells
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2
Q

Where are B cells made in the bird?

A

Bursa of fabricius

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3
Q

What antibody is present mainly in the mucus membranes? What about near the alveoli?

A

MM: IGA is present here mostly.
IgG is alveoli areas

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4
Q

What size of foreign antibodies can pass through the nose, bronchi, bronchioles, alveoli?

A
  • Foreign antigen through nose 15 mcL
  • Bronchi : 10 mcL
  • Bronchioles: 5 mcL
  • Alveoli: 1 mcL
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5
Q

What are the stages of phagocytosis?

A
  • Stages of phagocytosis
  • CAID -> Chemotaxis -> adherence -> Ingestion -> Destruction
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6
Q

What is the purpose of IFN’s? Are IFN’s specific to viruses? What about cell specific? Species specidic?

A
  • IFN -> Chemical produced by viral infected cells to alert for response to viral infections.
  • IFNs not virus specific but cell specific in production and effects and is Species specific.
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7
Q

What are IFN’s? What can inactivate them?

A
  • Glycoprotein’s, stable at ph2 and resistant at 56 degrees c for 1 hour
  • Can be inactivated by treatment with proteolytic enzymes.
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8
Q

What is the purpose of developing a fever when sick? What does the fever mean?

A
  • Fever helps induce immune response.
  • Fever is important. It is synthesizing the immune response. The more fever the larger the immune response. The fever will trigger IFN when it gets above 40 degrees c
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9
Q

Which IFN has the most genes that encode it?

A
  • IFN-a : 20 genes incode this
  • 1 gene encodes Beta and gamma
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10
Q

What is the definition of an IFN?

A

IFNs: sets of proteins released by the virus infected cells which react with the surrounding non infected cells rendering them resistant to this type of viral infection

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11
Q

What are type 1 IFNs?

A

IFN alpha (leukocyte IFN (monocytes) B lymphocytes)

IFN beta (fibroblast IFN, Epithelial cells)

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12
Q

What are type 2 IFNs?

A

IFN gamma

(Immune IFN ( some activated t cells, NK cells)

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13
Q

What are IFN inducers?

A
  • Infectious or inactivated virus induce the production of IFNs for 20-50 hrs after exposure
  • Viruses that might multiply slowly and not damage the cell or the synthesis of protein early are good IFN inducers
  • Cells of bone marrow, spleen, and macrophages are highly IFN producers
  • Polynucleotides (Poly-IC) are good IFN inducers
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14
Q

What is the antiviral mechanisms induced by IFNs?

A
  • 1.Block viral mRNA synthesis
  • 2.Block the translation of viral mRNA
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15
Q

How does antigen processing/ display occur with MHC - I Molecules?

A

Viral peptides are produced from proteins in the cytosol and transported to the ER to bind to Class I MHC complex

The peptide/Class I MHC complex transported to the cell surface and displayed for recognition by the CD8+

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16
Q

How does antigen processing/ display occur with MHC - II Molecules?

A
Viral proteins are ingested into vesicles and degraded into peptides -\> 
They bind to the class II-MHC that transported to the same vesicles -\>
The class II-peptide complex are expressed on the cell surface and recognized by CD4 T cells
17
Q

What immune cells are important for stimulating NK cells?

A

decrease in MHC I, increase in stimulatory ligand, IFN alpha and Beta , and IL- 12, IL 18

18
Q

How do B lymphocytes react to a virus?

A

B lymphocytes trigger plasma cells and antibody secretion.

19
Q

How do monoclonal cells prevent virus infectiow

A

They act as a barrier, so it competes for the receptors on the cell and the virus cant transmit active infection.

20
Q

How do CD4+ T lymphocytes and macrophages prevent virus infection?

A
  • releases cytokines which:
  • activates macrophages
  • Inflammation
  • Stimulates B lymphocytes
21
Q

How do CD8+ T lymphocytes and macrophages prevent virus infection?

A

This cell is a cytotoxic t cell. It will kill the infected cell and cut its losses.

22
Q

What cells are involved in the immune response to viral infection? When does each cell peak? How long does the innate immune system last? When does the adaptive immune system kick in?

A
  1. ) Type - 1 IFN’s ( peak about day 2 and then declines)
  2. ) NK cells ( peaks about day 3 and then declines)
  3. ) CTL (Starts around day 2 but plateus around day 7 then declines around day 10)
  4. ) Antibodies (Starts around day 5 sometimes, but mostly at day 7)

Innate immunity begins at day 1-5, at day 5 adaptive immune system takes over.

23
Q

What does CD4+ T cells do when they recognize a virus? CD8+

A

CD 4+: Attract other immune cells and stimulate B- cells to produce

CD8+ : -Slow down the viral infection

-Kill the virus infected cells

Cytotoxic-T cells: Kills the virus-infected cells through
the release of some toxic chemical mediators

24
Q

What are TCRs?

A

T cell receptors (TCRs): specifically recognize and bind to some antigenic peptide bound to MHC molecules

25
Q

What is the mechanism of the NK cell destruction of a virus?

A
  • Virus infected cells express multiple stress indicators and virus infection inhibits expression of cell proteins
  • NK cell’s multiple activating and inhibiting receptors are bound
  • When activation stimuli overcome inhibition, cell death is initiated
  • Cytotoxic granules orient to the cell junction and are released
  • Perforin creates access to the target cytosol delivering Granzymes (serine proteases that mediates cell death)
26
Q

What happens when activation stimul overcome inhibition? What are perforins?

A
  • Cell death is initiated.

Perforins: allows access to target cytosol to send in granzymes

27
Q

What is the mechanism of cytotoxic t cell killing virus infected cells?

A

Viral proteins degraded into peptides and subsequently bound by recently synthesised class I MHC proteins which transported to cell surface

CTL with the T cell receptors specific for that peptide/MHC complex determine or see the cell infected by this binding interaction

Once multiple receptors including CD8 also bind and tight cellular junction established . Cytotoxic granules directed into cell junction

NK cells and perforins (serine like proteases) get access to the cytosol of the target cells

Cell death

28
Q

What are the antiviral effects of antibodies?

A
  • agglutination of viral particles by antibodies.
  • Antibody mediated triggering of phagocytosis.
29
Q

How does complement try to prevent virus infection of cells?

A

Complement competes for receptors to block entry. Multiple things are occuring at once and working synergistically to protect the host.

30
Q

In what kind of placenta is their 100% transfer of blood between mother and offspring? How can this affect vaccines?

A

Hemochoral placentas have 100% placental transfer. Must be careful with vaccines because maternal antibodies can neutralize vaccines.

31
Q

How does colostrum protect young animals? When should they receive it? What happens after 2 days? Where does the immunity go after that?

A

Colostrum intake is required to protect young animals against septicemic disease
Needs to be given in first few hours before the intestinal pore closes and the newborn cannot benefit the same way.

After a few hours the pores of the intestines become to narrow to accept the immunoglobulins from the colostrum.

32
Q

What is some of the disadvantages of immune response? What is one clinical example?

A

Immune response to viruses could be on some occasions, a disadvantage

  • Animals infected or vaccinated with the ICHV-1 live vaccine
  • Dogs develop anterior uveitis leading to corneal edema and opacity
  • The cornea is infiltrated by neutrophils, attracted by virus antibody complexes deposited in tissue

• Accumulation of neutrophils which release enzymes damage corneal epithelial cells resulting in
inflammation and edema, then corneal opacity in dogs

• Blue-eye develops about 1 to 3 weeks after the onset of infection and usually resolves spontaneously once the virus is eliminated.

Example: BLUE EYE DISEASE

33
Q

What is aleution disease? What animals is it affect in? What can you see with their kidneys? What is seen in the serum of infected animals ?

A
  • Aleutian disease: persistent Parvovirus infection first recognized in Aleutian coat color
  • Animals develop complex immune lesions including glomerulonephritis and arteritis
  • Serum protein electrophoretic patterns

• The serum of infected animals shows a polyclonal gammopathy: the gamma globulin accounts for
62.4% of serum proteins

• The normal level is 14.3%
You will see enlarged kidneys with edema in the kidneys. They also will have increased kidney values that indicate renal failure.

34
Q

What are some strategies of viral evasion to host immune destruction?

A
  1. ) inhibition of antigen presentation
  2. ) Modulation of MHC class I expression
  3. ) Antigenic variation
  4. ) Prevention of apoptosis
  5. ) cytokine targeting
  6. ) latency
  7. ) destruction of immune cells
35
Q

How does amantidine kill influenza?

A

penetration and uncoating

36
Q

How does acyclovir affect herpes conjunctivitis?

A

Attacks DNA replication.