Antiviral Immunity Flashcards

1
Q

What are the 2 divisions of the immune response to viral infection? Give some examples of each.

A
  1. INNATE IMMUNE RESPONSE: natural barriers; early and non-specific responses using IFNs, NK cells, and macrophages
  2. ADAPTIVE IMMUNE RESPONSE: antiviral antibodies, cytotoxic T cells, helper T cells
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2
Q

What are the most important organs of the immune system?

A

thymus - t cells
bone marrow - b cells
Bursa of Fabricius in birds - b cells
lymph nodes
spleen

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3
Q

Diversity of innate surface protein protection mechanisms:

A
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4
Q

Structure of Igs:

A
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5
Q

What are the 4 stages of phagocytosis?

A
  1. chemotaxis
  2. adherence
  3. ingestion
  4. destruction
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6
Q

What are IFNs? What induces the production of them? Why are they considered cell specific?

A

antiviral substances produced by viral infected cells of many vertebrates in response to viral infection

foreign nucleic acids from viruses

specific cells make specific types of IFNs that are able to work on other cells of the same family - NOT virus specific

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7
Q

How do IFNs affect viruses? How can they be deactivated? What has no effect on them?

A

non-toxic to the cell, but are able to inhibit the multiplication of the virus in cells of the homologous species

proteolytic enzymes, like trypsin, pepsin, and chymotrypsin

not affected by DNAse, RNAse, or lipase

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8
Q

How does temperature affect IFNs? What significance does this have in infection symptoms?

A

increase in temperature up to 40 degrees C causes an increase in production

fever increases IFN production to stimulate immune responses and get rid of the source of infection

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9
Q

What are the 2 types of IFNs? What IFNs are divided into these categories and what cells create them?

A

TYPE I
- IFN-α: leukocytes (+monocytes), B-lymphocytes
- IFN-β: fibroblasts, epithelial cells

TYPE II
- IFN-γ: immune cells, like NK cells and activated T-cells

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10
Q

How much longer after exposure to an infectious or inactivated virus will cells start producing IFNs? What kind of viruses and nucleic acids make for good IFN inducers?

A

20-50 hours

viruses that multiply slowly and do not damage the cell or protein synthesis pathway
polynucleotides, like Poly-IC

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11
Q

How do Type I interferons induce a response in immune cells? What 2 pathways are activated? What proteins are produced as a result?

A

binds to receptors on the immune cell and triggers JAK/STAT

  1. antiviral pathway —> 2’5’ OAS, Mx proteins, ISG15, protein kinase R
  2. immunoregulatory pathway —> MHC class I, cytokines
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12
Q

What are the main 2 antiviral mechanisms of action induced by IFNs?

A
  1. block viral mRNA synthesis
  2. block the translation of viral mRNA
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13
Q

How does MHC-I present viral proteins?

A
  • viral peptides are produced from proteins in the cytosol and transported to the ER to bind to Class I MHC complex
  • MHC-I/peptide complex is then transported to the cell surface and displayed for recognition by the CD8+ cytotoxic T cells
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14
Q

How does MHC-II present viral proteins?

A
  • viral proteins are ingested into vesicles and degraded into peptides
  • peptides bind to Class II MHC that is transported to the same vesicle
  • MHC-II/peptide complex are expressed on the cell surface and recognized by CD4+ T helper cells
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15
Q

What are the 3 major players in antiviral adaptive immunity? What do they do?

A
  1. B lymphocyte - secrete antibodies
  2. CD4+ T helper lymphocyte - activates macrophages, causes inflammation, stimulated B lymphocytes
  3. CD8+ cytotoxic T lymphocyte - kills infected cells
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16
Q

What is the general order of immune response to viral infection?

A
  1. Type-I IFNs
  2. NK cells
  3. cytotoxic T cells
  4. antibodies

(innate —> adaptive)

17
Q

What are the 2 receptors on T cells that help them recognize virus-infected cells? What are the general responses after binding to these receptors?

A
  1. CD4+ on T helper cells: attract other cells and stimulate B cells to produce antibodies
  2. CD8+ on cytotoxic T cells: slow down viral infection, kills the virus-infected cells
18
Q

How do cytotoxic T cells recognize viral antigens? How do they kill virus-infected cells?

A

T cell receptors (TCRs) on the cytotoxic T cell surface recognize and bind to antigenic peptide bound to MHC-! on the infected cell

kills virus-infected cells through the release of toxic chemical mediators

19
Q

How are NK cells able to recognize virus-infected cells? How are they able to kill these cells?

A

virus-infected cells express multiple stress indicators and virus infection inhibits the expression of cell proteins; when the activating stress indicators out-bind the inhibiting signals, cell death is initiated

  • cytotoxic granules orient to the cell junction and are released
  • perforin creates access to the target cytosol allowing for the delivery of the granzymes (serine protease)
20
Q

What are the main 2 ways that antibodies inactivate viruses?

A
  1. agglutination of virus particles
  2. antibody-mediated triggering of phagocytosis
21
Q

What are the main 4 ways that the immune system protects against viruses?

A
  1. ANTIBODY/COMPLEMENT: virolysis, blockage of viral adherence, cytolysis
  2. NK CELLS: apoptosis
  3. CYTOTOXIC T CELLS: apoptosis
  4. ACTIVATED MACROPHAGES: phagocytosis, apoptosis
22
Q

What organs of the immune system are developed first? Antibodies?

A

thymus —> bone marrow
IgM —> IgG

23
Q

What are the 3 types of placenta? How much Ig transfer do they allow?

A
  1. EPITHELIOCHORIAL: no transfer
  2. ENDOTHELIOCHORIAL: 10% transfer
  3. HEMOCHORIAL: 100% transfer
24
Q

Why is it so important for neonates to ingest colostrum quickly?

A

colostrum is rich in proteins and Ig’s - within 24 hours it becomes milk and the GI tract closes, no longer allowing for contribution to systemic immunity

25
Q

What is the relationship between a mother’s antibody titer and the age at which to vaccinate her offspring?

A

higher titer = wait longer to vaccinate offspring
- if mother antibodies are high = no real need to vaccinate yet, since she can pass antiobies through her milk

26
Q

What is Blue Eye Disease? When does the blue-eyed symptom occur? What kind of hypersensitivity is this?

A

immune response in animals infected or vaccinated with ICHV-1 live vaccines, where dogs develop anterior uveitis leading to corneal edema and opacity due to the infiltration of neutrophils attracted by the virus/antibody complexes and release enzymes that damage the corneal epithelial cells

1-3 weeks after onset of infection and tends to resolve spontaneously when the virus is eliminated

Type III

27
Q

What is Aleutian disease in mink? How is it diagnosed?

A

persistent Parvovirus infection causes mink to develop complex immune lesions, causing glomerulonephritis and arteritis

serum protein electrophoretic patterns show polyclonal gammopathy (62.4% of serum proteins are gamma globulins, which is very high)

28
Q

What are 7 ways that viruses are able to evade the host immune system?

A
  1. antigenic variation
  2. prevention of apoptosis
  3. cytokine targeting
  4. infection/destruction of immune cells
  5. latency
  6. modulation of MHC I expression
  7. inhibition of antigen presentation
29
Q

How do amantadine and acyclovir have antiviral effects? What viruses do they work on?

A

AMANTADINE: causes the virus to be unable to penetrate host cells and uncoating; Influenza

ACYCLOVIR: blocks DNA replication; Herpes (ointment)