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Immuno Exam 3 > Immune Defense Failure > Flashcards

Immune Defense Failure Flashcards

1
Q

What is antigenic drift?

A

the way that point mutations in influenza virus genes cause changes in the protein structure of viral surface antigens

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2
Q

T/F: Antigenic drift can cause antigenic variation

A

True

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3
Q

Which RNA viruses are more error prone?

A

HIV and influenza

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4
Q

What is antigenic shift ?

A

the process by which influenza viruses reassert their segmented genomes and change surface antigens radically

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5
Q

What mechanisms cause an epidemic?

A

Mutations and antigenic drift

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6
Q

What mechanisms cause a pandemic?

A

Recombination and antigenic shift

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7
Q

In what 3 ways can antigenic shift occur?

A
  1. Without undergoing genetic change: a bird strain of influenza A can jump from duck to another bird or human
  2. Without undergoing genetic change: a bird strain of influenza A can jump from duck or bird to an intermediate animal host then to humans
  3. A person passes a strain of influenza A to an intermediate host (i.e chicken), a bird passes bird strain to same host. Virus genes from both viruses mix forming new strain that can go back to humans
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8
Q

What occurs during gene conversion?

A

a gene in the expression site is excised and replaced by a different gene to cause a different expression of protein

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9
Q

Describe trypanosome brucei gene conversion and host defense

A

The protozoan undergoes gene conversion changing the the variable surface glycoprotein (VSG). The host will make antibodies against the VSG but the protozoan makes new ones that the body does not recognize

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10
Q

What is the effect of parasite cycling?

A

The body gets into a state of constant inflammation and accrues neurological damage. The host is not able to clear the infection

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11
Q

Viruses are cleared by _______ cells

A

CD8 T

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12
Q

A virus is hard to clear when it is in what state?

A

Quiescent / latent

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13
Q

Why are neurons a good site for a latent virus?

A

Because neurons express low levels of MHC I molecules

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14
Q

This bacteria evades the immune system by preventing the fusion of phagosome with lysosome within macrophages.

A

Mycobacterium tuberculosis

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15
Q

What is the host for trypanosome brucei

A

insect and human

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16
Q

Where are the HSV reservoirs?

A

neurons

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17
Q

What are the HIV reservoirs?

A

macrophages and CD4 T cells

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18
Q

How does mycobacterium tuberculosis evade the immune system?

A. Encloses itself into a impenetratable membrane enclosed vesicle that does not fuse with other vesicles

B. coats itself in human protein

C. Takes over host cell replication machinery

D. Prevents fusion of phagosome with lysosome within macrophage

A

D. Prevents the function of phagosome and lysosome within macrophages, flourishing inside the vesicle

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19
Q

How does Treponema palladium evade the immune system?

A. Encloses itself into a impenetratable membrane enclosed vesicle that does not fuse with other vesicles

B. coats itself in human protein

C. Takes over host cell replication machinery

D. Prevents fusion of phagosome with lysosome within macrophage

A

B. coats itself with human protein to prevent antibody binding

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20
Q

How does toxoplasma gondii evade the immune system?

A. Encloses itself into a impenetratable membrane enclosed vesicle that does not fuse with other vesicles

B. coats itself in human protein

C. Takes over host cell replication machinery

D. Prevents fusion of phagosome with lysosome within macrophage

A

A.

it prevents fusion with other vesicles thus causing issues with antigen presentation

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21
Q

What bacterium causes syphilis?

A

Treponema pallidum

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22
Q

What are primary immunodeficiency diseases?

A

Immunological Defects that were inherited that causes an enhanced susceptibility to infection or autoimmunity

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23
Q

What are secondary immunodeficiency diseases?

A

immunological defects due to environmental factors such as immunosuppressive drugs

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24
Q

Only one allele is required for a ______ immunodeficiency diseases to be presented.

A

Dominant

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25
Q

______ immunodeficiency diseases are seen in children

A

dominant

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26
Q

A ________ primary immunodeficiency disease requires two alleles for disease to be presented. Person can be a carrier

A

recessive

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27
Q

What is antibody deficiency?

A

poor clearing of extracellular bacteria

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28
Q

People with antibody deficiency are susceptible to _______ bacteria

A

encapsulated

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29
Q

What is important about Bruton’s Tyrosine Kinase

A
  • it is required for B cell activation

- required for pre-B cell activation and differentiation

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30
Q

What is the main defect in X linked agammaglobulinemia

A

Bruton’s Tyrosine Kinase defect

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31
Q

XLA is treatable with

A

antibiotics and injections of immunoglobulin against common pathogens

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32
Q

Is XLA recessive or dominant

A

Recessive

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33
Q

What is the main characteristic of X Linked agammaglobulinemia

A

The absence of mature B cells

*Defect in BTK prevents B cell maturation

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34
Q

When does XLA begin to present?

A

After 6 months of age when maternal IgG is no longer present

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35
Q

Non Bruton Type agammaglobulinemia is

a. Sex Linked Dominant
b. Sex Linked Recessive
C. Autosomal Recessive
D. Autosomal Dominant

A

C.

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36
Q

Defects in phagocyte function leads to enhanced susceptibility to ______ infection.

A. Viral
B. Protozoan
C. Bacterial

A

C: bacterial

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37
Q

Leukocyte adhesion deficiency is

a. Sex Linked Dominant
b. Sex Linked Recessive
C. Autosomal Recessive
D. Autosomal Dominant

A

C: autosomal recessive

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38
Q

Leukocyte adhesion deficiency causes

A. Complement Dysfunction

B. T cell Dysfunction

C. T cell development dysfunction

D. Phagocyte Dysfunction

A

Phagocyte Dysfunction

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39
Q

A defect in LFA-1 protein is characteristic of which immunodeficiency?

A

Leukocyte Adhesion Deficiency

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40
Q

Leukocyte Adhesion Deficiency is characterized by a defect in

A

LFA-1

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41
Q

A defect in _____ prevents the adherence and migration of phagocytes out of blood vessels

A. LYST gene
B. LFA-1
B. NADPH Oxidase

42
Q

List the presentations of LAD-1 (4)

A
  • recurrent bacterial infections
  • absent pus formation
  • poor wound healing
  • delayed separation of umbilical cord
43
Q

Why is neutrophilia seen in peripheral blood smear in those with Leukocyte adhesion deficiency 1?

A

Because of the inability of phagocytes to exit circulation

44
Q

Chediak-Higashi Syndrome (CHS) is caused by a defect in

A. LYST gene
B. LFA-1
B. NADPH Oxidase

A

A: LYST gene

45
Q

CHS is

A. an autosomal dominant immunodeficiency

B. An autosomal recessive immunodeficiency

C. A X linked recessive immune deficiency

D. a Secondary immunodeficiency

A

B: autosomal recessive

46
Q

What is the LYST gene?

A

Lysosomal trafficking regulator gene

47
Q

CHS causes

A. Complement Dysfunction

B. T cell Dysfunction

C. T cell development dysfunction

D. Phagocyte Dysfunction

A

D: Phagocyte dysfunction

48
Q

LYST gene defect

A. prevents phagocyte adherence to the epithelium of blood vessels

B. Leads to microtubule disfunction in phagocytes

C. Causes dysfunctional. neutrophils

D. Causes a deficiency in C1 esterase inhibitor

49
Q

All of the following are presentations found in CHS except:

A. Pyogenic Infections

B. Partial Albinism

C. Peripheral Neuropathy

D. Edema

50
Q

Chronic Granulomatous Disease is characterized by

A

a deficiency of neutrophil NADPH oxidase

51
Q

Which of the following diseases have dysfunctional neutrophils

A. LAD-1

B. Chronic Granulomatous Disease

C. Chediak-Higashi Syndrome

52
Q

Those suffering from CGD have

A. increased susceptibility to infection by catalase producing organisms

B. increased susceptibility to infection by encapsulated bacteria

C. Neutropilia in peripheral blood

53
Q

Chronic granulomatous disease is characterized by a deficiency of

A

Neutrophil NADPH oxidase

54
Q

A deficiency of neutrophil NADHP oxidase is a characteristic of

A

Chronic granulomatous disease

55
Q

Patients with CGD have increased susceptibility to infection by

A

infection by catalase producing organisms

56
Q

What does NADPH oxidase do

A

generates reactive oxygen species in a neutrophil which is converted into hydrogen peroxide which is an antibacterial

57
Q

List 4 catalase positive organisms

A
  • S. aureus.
  • E. coli
  • Pseudomonas
  • Aspergillus
58
Q

What are catalase positive organisms?

A

Bacteria that break down hydrogen peroxide

59
Q

What are the treatments for CGD (3)

A
  1. Lifelong antibiotics and antifungals
  2. IFN-gamma treatment
  3. Hematopoietic Stem Cell Transplant
60
Q

The classical pathway of complement is required for the elimination of

A

Immune complexes

61
Q

What is the effect of C3 deficiency?

A

Susceptibility to encapsulated bacteria

62
Q

What role does C3 play in complement?

A

An opsonin that promotes elimination of bacteria by phagocytosis

63
Q

Deficiency of C1, C2 and C4 results in

A. Susceptibility to encapsulated bacteria

B. Hereditary Angiodema

C. Accumulation of immune complexes in blood

D. Susceptibility to Neisseria

A

C: accumulation of immune complexes in blood and deposition of immune complexes in tissue

64
Q

A patient who presents to the clinic with S. aureus, normal antibody titer levels, and normal neutrophil function is likely to have

A. Antibody Deficiency
B. Dysfunction in phagocytes
C. Chronic Granulomatous Disease
D. C3 Deficiency

A

D: C3 deficiency

* S. aureus is an encapsulated bacteria , C3 Deficiency leads to susceptibility to encapsulated bacteria

65
Q

C4-C9 Deficiency leads to susceptibility to infection by what microbe

A

Increased susceptibility to Neisseria infections

66
Q

Hereditary angiodema is due to deficiency in

A

C1 Esterase Inhibitor

67
Q

How does a deficiency in C1 Esterase inhibitor affect complement?

A

Unchecked activation of complement components leading to a decreased C2 and C4 protein

68
Q

Hereditary Angiodema is

A. an autosomal dominant immunodeficiency

B. An autosomal recessive immunodeficiency

C. A X linked recessive immune deficiency

D. a Secondary immunodeficiency

69
Q

what does SCID stand for

A

Severe combined immunodeficiency

70
Q

What is the most common cause of SCID

A

an X linked defect leading to impaired common gamma chain on cytokine receptors

71
Q

What are the 2 causes of SCID

A
  1. X linked defect causing impaired common gamma chain on cytokine receptors
  2. Cellular absence of adenosine deaminase (ADA) or pure nucleoside phosphorylase (PNP)
72
Q

What is the result of a deficiency in T cells?

A

A decrease in cell mediated immunity and humoral immunity

73
Q

In SCID that is X linked there will be an absence of

A. T cells
B. B Cells
C. NK cells
D. All of the above

A

A.

*X linked SCID–absence of T cells

74
Q

In SCID that is Autosomal recessive there will be an absence of of

A. T cells
B. B Cells
C. NK cells
D. All of the above

A

D

* all of the above

75
Q

What is the defective protein in SCID?

A

gamma chain on cytokine receptors

76
Q

What are the functional effects of a defect in the common gamma chain on cytokine receptors

A

Defects in cytokine signaling resulting in the non development of T cells B cells and NK cells

77
Q

A genetic abnormality caused by a spontaneous deletion of part of chromosome 22 causes

A. SCID
B. Hereditary Angiodema
C. DiGeorge Syndrome
D. Chronic Granulomatous Disease

A

C. DiGeorge Syndrome

78
Q

DiGeorge Syndrome is caused by

A

a spontaneous deletion of a part of chromosome 22

79
Q

Improper formation of the thymus presents in

A. HIV
B. DiGeorge Syndrome
C. Wiskott-Aldridch Syndrome
D. Hyper IgM Syndrome

A

B: DiGeorge Syndrome

* also causes defects in other organ structures

80
Q

List 4 Treatment options for DiGeorge Syndrome

A
  • Occupational and physical therapy
  • Replacement of PTH, GH, and TH
  • Antibiotics to treat infections
  • Calcium supplements
81
Q

Wiskott-Aldrich syndrome is

A. an autosomal dominant immunodeficiency

B. An autosomal recessive immunodeficiency

C. A X linked recessive immune deficiency

D. a Secondary immunodeficiency

82
Q

All of the following are presentations of Wiskott-Aldrich syndrome EXCEPT

A.  Recurrent Bacterial Infections
B. Eczema
C. Elevated IgM
D. Purpura
E. Epistaxis
F. Splenogegaly
A

C: elevated IgM

  • IgM levels are LOW
  • IgE and IgA levels are HIGH
83
Q

T/F: the WASp gene is on the short arm of the X chromosome

84
Q

True/ False: the WASp gene is expressed in all cells

A

False

*only in hematopoietic cells

85
Q

Which antibodies are elevated in Wiskott-Aldrich syndrome?

A

IgA and IgE

86
Q

What is the role of the WASp protein

A

relayes extracellular signals to the actin cytoskeleton of a cell

87
Q

What is the main treatment for Wiskott-Aldrich syndrome?

A

hematopoetic stem cell treatment

88
Q

When does Wiskott-Aldrich syndrome usually present with symptoms

A

Early childhood in males

89
Q

Hyper IgM Syndrome is an immunoglobulin deficiency characterized by

A
  • normal or elevated serum IgM levels

- decreased levels or absence of other serum Immunoglobulins

90
Q

Hyper IgM results in susceptibility to

A

bacterial infections

91
Q

What is the consequence of a deficiency of CD40L in Hyper IgM Syndrome?

A

-T lymphocytes are unable to tell B cells to switch immunoglobulin class from IgM to IgG , IgA and IgE

92
Q

The most common form of HIGM syndrome results from a deficiency or defect of

A

CD40 ligand on activated T cells

93
Q

CD40L deficiency: Hyper IgM Syndrome:: _______: Wiskott-Aldrich Syndrome

94
Q

True or False: IgM levels are high in Wiskott Aldrich Syndrome

95
Q

What is the treatment for HIGM syndrome?

A

immunoglobulin replacement therapy

96
Q

Patients with Hyper IgM have severe_____ deficiency

*an antibody

97
Q

What genetic material does HIV have

98
Q

HIV is a

A

Retrovirus

99
Q

What is the role of intergrase

A

to integrate viral cDNA into host genome

100
Q

What cells doe HIV infect

A

Macrophages
CD4 T cells
Dendritic Cells

101
Q

Tat protein

A. Amplifies transcription of viral RNA
B. Integrates viral DNA into host genome
C. Forms the viral spike envelope

A

A: amplifies viral RNA

102
Q

What receptors are required for HIV to infect cells

A

CCR5 and CD4

Immuno Exam 3 (5 decks)

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