Brainscape's Knowledge GenomeTM

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


See full index

IMMUNOLOGY > Lecture 15: immune Response to Viruses and Parasites > Flashcards

Lecture 15: immune Response to Viruses and Parasites Flashcards

1
Q

what is the primary mechanism in the defense against viruses

A

the killing of virus infected cells by cytotoxic T cells

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

explain virus pathogenesis

A

virus binds receptor
- enters cell via endocytosis or fusion
- nucleic acid released from capsid
- replication occurs (host machinery hijacked, only viral components produced)
- new nucleic acids are packaged into new capsids
- new virions exit cell or cell disintegrates, releasing virions

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

What TLRs detect foreign nucleic acids

A

TLR 3, 7, 8, 9

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

what are intracellular nucelic acid sensors, present in all nucleated cells

A

RIG 1, MDA5

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

innate response to viruses includes…

A
  • interferons
  • lysozyme
  • bile / intestinal enzymes
  • conglutinin
  • mannose binding lectin
  • surfactant proteins A + D
  • defensins
  • apoptosis of host cells to prevent viral replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

immunity response to parasites is characterized by what?

A

Th2 response and IgE production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how do obligate intracellular pathogens work

A

they use cellular machinery of the host
limits the # of identifiable pathogen-specific antigens

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

what is the result of the downregulating of MHC-1 expression

A

reduced effectiveness of NK cells and cytotoxic T cells

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

what type of parasites are helminths (worms)

A

obligate parasites, host-adaptation is important

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

what are the 5 ways parasites are able to evade the immune system

A
  • immunosuppressants
  • prostaglandins
  • antioxidants
  • protease inhibitors
  • immunoglobulin splitting proteases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the ‘additional’ mechanisms by which parasites are able to evade the immune system

A
  • shedding of glycocalyx upon antibody exposure
  • absorption of host antigens onto worm
  • interference w/ antigen presentation
  • antigenic variation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is Taeniastatin, what are its functions

A

a protease inhibitor produced by taenia taeniaformis
1. inhibits neutrophil chemotaxis
2. inhibits complement activation
3. inhibits Tcell proliferation
4. inhibits IL-2 production

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

what is the the IgE mediated self-cure reaction to helminths

A
  1. worm secretes antigens in saliva
  2. triggers mast cell degranulation
  3. vasoactive, other molecules released
  4. stimulates smooth muscle contractions, vascular permeability (dislodges and flushes worm)
  5. IL-13 stimulates epithelial proliferation, sloughs worm

*results in detachment of worms, expulsion in feces

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

what type of reaction is the IgE mediated ‘self cure’ reaction

A

Allergic (type I, immediate hypersensitivity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does it mean that viruses are obligate intracellular pathogens

A

they require the use of the cell’s own machinery to replicate

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

what does it mean for viruses to be host-adapted

A

they have evolved mechanisms to evade the host’s immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do DNA viruses (like canine parvovirus) replicate inside a cell

A

undergo replication of the viral DNA, followed by transcription to viral RNA and then translation into viral proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do RNA viruses (such as influenza) replicate inside a cell

A

they undergo replication and translation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do “lentiviruses” or “retroviruses” replicate inside a cell

ex: equine infectious anemia virus, feline immunodeficiency virus, and human immunodeficiency virus

A

RNA is reverse transcribed into DNA, then transcribed into RNA and then protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

recognition of viruses occurs via….

A

TLRs 3, 7, 8, 9
intracellular nucleic acid receptors RIG-1 and MDA5 NOD-like receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is a major effector mechanism of the innate immune system to viruses

A

The production of interferons

22
Q

what are interferons

A

glycoproteins secreted by virus infected cells

23
Q

Interferon- _____ is secreted by plasmacytic dendritic cells (via TLR7/9), lymphocytes, monocytes, macrophages

A

Interferon-α

24
Q

what interferon is secreted by virus-infected fibroblasts

A

Interferon-β

25
Q

what interferon is produced by lymphocytes, monocytes, and trophoblast of many species.

A

Interferon-ω/αII

26
Q

what interferon is produced by ruminant trophoblast and is involved in maternal recognition of pregnancy

A

Interferon-τ

27
Q

what interferon is produced by pig trophoblast

A

Interferon-δ

28
Q

what interferon is produced by keratinocytes

A

Interferon-κ

29
Q

what is the one type II interferon?

A

interferon-γ (produced by antigen-stimulated T-cells and pig trophoblast)

30
Q

what interferons are produced very rapidly by virus-infected cells

A

Interferons α, β

31
Q

what is the importance of Natural killer cells in viral infections?

A
  • they have a more rapid response than cytotoxic T cells
  • they kill virus-infected cells
  • they are stimulated by interferon
  • produce interferon-γ
32
Q

do neutrophils produce interferons?

A

no

33
Q

what are the 6 important viral defense pathways

A

1) 2’5’ OAS: degrades viral RNA
2) protein kinase R: prevents viral translation
3) Mx GTPase: blocks the assembly of viral components
4) ISG15: destroys viral proteins
5) viperin: inhibits lipid rafts formation
6) tetherin prevents the release of virions

34
Q

antibody-mediated mechanisms response to viruses

A
  • respond to capsid and envelope proteins as antigenic targets
  • can target viral antigens produced by infected cells
  • can block adsorption of virus into cells
  • can stimulate phagocytosis
  • can initiate complement-mediated lysis of virus.
35
Q

Antibody-mediated destruction of host cells is important in what cases of disease

A
  • Newcastle disease
  • rabies
  • BVD (bovine virus diarrhea virus)
  • FLV (feline leukemia virus)
  • avian infectious bronchitis
36
Q

Cell-mediated mechanisms in response to viruses

A

Viral antigens may be expressed on infected cells before new virus is reassembled, resulting in the destruction of the cell

  • antigens are presented on the cell surface by
    MHC-I
  • Cytotoxic T-cells recognize the viral peptide as foreign and kill the infected cells, thus preventing the
    release of more virus
37
Q

How does antigenic variation allow viruses to evade the host’s immune defense

A

Antigenic drift- creates influenza viruses with slightly modified antigens
antigenic shift - generates viruses with entirely new antigens

**These mechanisms result in the reduced effectiveness of antibodies.

38
Q

What are other ways besides antigenic variation that viruses can evade the immune system

A
  • blocking of interferon
  • downregulate expression of MHC-I, which reduces the effectiveness of NK-cells and cytotoxic T-cells
39
Q

How does Equine herpesvirus type 1 (EHV-1) evade the host’s defense

A

downregulation MHC-I
- reduces the effectiveness of antigen presentation and limits the ability of additional virus to enter the cell.

40
Q

What makes EHV-1 a notable virus

A
  • it can enter cells of many species and can enter multiple cell types in the horse (epithelial cells, endothelial cells, and mononuclear cells)
  • It uses MHC-I as an entry molecule
  • Cell associated viremia allows rapid spread throughout the body, resulting in neurologic disease and abortion.
  • It has several strategies for immune evasion including hiding envelope proteins, downregulating MHC-I and inhibiting cytokines via its gG protein
41
Q

what allows helminth parasites present their own unique challenges to the immune system

A
  • they have many life stages and each stage can have different antigens
  • they are obligate parasites so host-adaptation is key = many mechanisms to evade immune system
  • they have a thick cuticle that protects them from damage (can’t be destroyed easily by complement/MAC or cytotoxic T cells)
  • Eosinophils are important effectors in the destruction of parasites.
42
Q

What cell type is an important effector in the destruction of parasites?

A

eosinophils

43
Q

factors of host that play a role in immunity to helminths

A

-** genetics:** some MHC-1 haplotypes are more resistant to infections
- age and gender
- Chitinases (substances that act upon chitin in helminth cuticle) produced by mast cells, macrophages and neutrophils
**- L-arginases: drive granuloma formation, reduce local availability of arginine and have an anti-inflammatory effect via reduced T cell function
- population dynamics of parasite: if high burden exists, it may prevent additional infection**

44
Q

aquired immunity to helminths

A

A Th2 response is the primary response,
involving interleukin 4 (also 10, 13), IgE, mast cells and eosinophils

45
Q

the role of eosinophils in parasite immunity

A
  • degranulating mast cells produce substances chemotactic for eosinophils
  • Th2 cells produce IL5, mobilizing eosinophils from bone marrow
  • macrophages produce molecules that influence eosinophils
  • Fc receptors on eosinophils bind antibody covered parasites and degranulate, applying granule contents directly to the cuticle.
46
Q

what are the granule contents of eosinophils

A
  • Major basic protein
  • eosinophil cationic protein
  • eosinophil neurotoxin
  • eosinophil peroxidase
47
Q

ways that eosinophils can degranulate

A
  • classic degranulation : the
    granule membrane fuses with the cell membrane to release contents
  • piecemeal degranulation :certain substances are released via a vesicle transport system. Intact granules may also be released
48
Q

immune and homeostatic functions of eosinophils

A
  • T-cell activation
  • dendritic cell, and T-cell recruitment
  • maintenance of plasma cells
  • tissue repair and regeneration
  • angiogenesis
  • fibrosis
  • metabolic homeostasis and adipose cell function
  • mammary gland and intestinal development.
49
Q

when might T-cells attack worms

-

A
  • if worms are deeply embedded such as during migration
  • if parasite is dying and can’t moodulate an immune respnse, so Th1 response occurs
50
Q

what 2 mechanisms are used by T-cells to attack worms

A
  • delayed type hypersensitivity (Type IV) involving T-cells and NK cells
  • or a direct attack.
51
Q

explain how defense against parasites can depend on life stage

A

**Larvae **- can be walled off, immobilized or destroyed. Their development can also be delayed
Adults - can be subjected to cuticular destruction, other morphologic changes, reduced fertility and granulomatous reactions
**Eggs ** - can be subject to granulomatous reactions and decreased fertility

IMMUNOLOGY (26 decks)

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