Host Defense Flashcards

1
Q

What must happen for a microbe to cause disease?

A

Must evade the host immune system

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2
Q

How long does it take for the adaptive immune system to respond to an antigen? What about if it is a memory response?

A

7 days ish

3 days if memory

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3
Q

What is the cytopathic effect of viruses?

A

Lysing of cells once virus replicates within the cell

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4
Q

What indicates a successful virus infection?

A

Entry, replication, spread, transmission

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5
Q

Why can’t microbes enter through the skin?

A

Keratinization

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6
Q

What is the role of bile in immunity?

A

Destroys lipids of enveloped viruses

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7
Q

What is the role of the nasal turbinates in immunity?

A

Impeded virus entry (narrow and complicated path)

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8
Q

True or false: there are no major physical barriers to microbe entry through the eyes and GU tract

A

True

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9
Q

What are the two hepatitis viruses that are transmitted via the fecal-oral route?

A

A and E

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10
Q

What is the major cause of the common cold?

A

Rhinoviruses and adenoviruses

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11
Q

What is the viral family of RSV?

A

Paramyxoviridae

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12
Q

What are the two major viral causes of conjunctivitis?

A

Adenoviruses

Enteroviruses

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13
Q

What is the route of transmission for the MMR viruses?

A

Respiratory

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14
Q

What are the three major components of the innate immune system?

A
  • IFN-alpha/beta
  • Natural killer cells
  • Macrophages
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15
Q

What is another name for type 2 IFN? What does this do?

A

IFN-gamma

Activates macrophages

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16
Q

What are the antiviral IFNs?

A

IFN alpha and beta

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17
Q

What are the roles of IFN alpha and beta? (4)

A
  • Prevent infection of uninfected neighboring cells
  • Increase MHC class I expression and antigen presentation
  • Activate dendritic cells and macrophages
  • Activate NK cells
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18
Q

What are the cells that produce IFN-alpha? IFN-beta?

A

IFN alpha = Leukocyte

IFN beta = Fibroblasts and other non-leukocytes

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19
Q

True or false: IFN alpha and beta have the same receptor on cells

A

True

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20
Q

What are the two pathways that IFN receptor binding can activate to inhibit protein synthesis and interrupt viral replication?

A
  • induce 2’-5’ oligoadenylate synthetase to activate RNase L to degrade mRNA
  • induce dsRNA depended protein kinase to phosphorylate eIF2 alpha and inactivate it
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21
Q

If IFN-alpha/beta activates 2’5’-oligoadenylate synthetase, what are the next two steps that lead to the inhibition of viral protein synthesis and replication?

A

Activation of RNase L, which degrades mRNA

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22
Q

If IFN-alpha/beta activates dsRNA-dependent protein kinase, what are the next two steps that lead to the inhibition of viral protein synthesis and replication?

A

eIF2-alpha is phosphorylated, inactivating it, and preventing viral protein synthesis/virus replication

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23
Q

What is the role of NK cells?

A

Lyse virus-infected cells early in viral infection

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24
Q

What activates NK cells?

A

The downregulation of MHC-class I

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25
Q

If a virus downregulates MHC class I proteins to avoid CTLs, how can the immune system counter this?

A

Upregulate NK cells

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26
Q

What is the role of IFNs in NK cell activity?

A

Enhanced activity

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27
Q

What is the first line of defense against virus infected cells?

A

NK cells

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28
Q

How is it that a lack of MHC class I activates NK cells?

A

MHC-class I has an inhibitory effect on NK cells. Lack of inhibition will thus activate it

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29
Q

What are the cells in the body that express class I MHC?

A

All nucleated cells except corneal epithelial cells

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30
Q

What is ADCC? What cells perform this?

A

Antibody dependent cell-mediated cytotoxicity–cross linking of IgG Fc receptors triggers it, and induces apoptosis/perforin mediated cel death

NK cells

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31
Q

Crosslinking of what type of antibody activates ADCC and NK cell killing of cells?

A

IgG

32
Q

What are the two killing mechanisms that can be activated with ADCC?

A

Apoptosis or perforin mediated osmotic death

33
Q

What are the antiviral effects of macrophages?

A

Production of TNF-alpha and NO to interfere with viral replication

34
Q

What are the viruses that can infect macrophages? (5)

A
CMV
Ebola
AIDS
Rubeola
Rubella

(RACER)

35
Q

What is the benefit to viruses if they can infect macrophages?

A

Facilitates viral spread

36
Q

When in an infection is humoral immunity most important?

A

Early

37
Q

What is the duration of the immunological memory at mucosal sites?

A

Short lived (months)

38
Q

Where are most plasma cells locateD?

A

Bone marrow

39
Q

Where do memory B cells reside? What happens when these cells encouter antigen?

A

Lymph nodes and the spleen

Differentiate into plasma cells

40
Q

What are the three main funtions of antibody?

A

Opsonization
Neutralization
Complement activation

41
Q

What is the role of antibodies in the expression of viral genes?

A

Downregulates the expression of viral genes inside infected cells following binding of cell surface viral glycoproteins (unknown MOA)

42
Q

How do antibodies neutralize microbes?

A

Prevent the microbe from binding to the host target cell

43
Q

What is the role of CD8+ T cells?

A

Cell mediated destruction during an established viral infection

44
Q

How do CD8+ T cells kill?

A

Perforin mediated mechanisms or apoptosis

45
Q

What chemical do CD8+ T cells produce to enhance immunity? How does it do this?

A

Increase TNF-alpha

Interferes with viral replication

46
Q

How long does it take CD8 memory cells to become activated to prevent infection?

A

as little as 1 day

47
Q

What MHC protein expresses endogenous proteins?

A

MHC class I

48
Q

What happens to the CD8 cells once the infection is resolved? What happens to the rest?

A

95% die off

Remainder become memory cells

49
Q

What is the major difference between memory B cells, and memory T cells?

A

T cells are dormant

B cells continually produce low levels of Ab to ward off recurrent infection

50
Q

What is the half-life of serum Abs?

A

3 weeks or less

51
Q

How long do most plasma cells live before dying?

A

several days

52
Q

What are the mechanisms for long term antibody levels?

A

Periodic re-exposure to a virus leading to an asymptomatic chronic infection

53
Q

What are the viral strategies for evasion of the immune system?

A

Antigen alteration through point mutations or reassortment of segmented RNA genomes

54
Q

EBV viruses can remain latent in what cells?

A

B cells

55
Q

Why is the CNS an ideal location for infections?

A

Immunologically privileged site

56
Q

What percent of all neonates become chronic carriers of Hep B?

A

90%

57
Q

What is the role of CTLs in hepatitis B infection?

A

CTLs will destroy hepatocytes, leading to cirrhosis

58
Q

What is the molecular mimicry the some viruses can undergo?

A

Express proteins that are similar to endogenous ones to hide themselves

59
Q

What are the bacteria that can survive in monocytes? (3) What is the advantage of this?

A

Listeria, mycobacteria, Chlamydia

Abs cannot get to them

60
Q

How do macrophages attempt to rid themselves of intracellular bacteria?

A

Express IL-12, which activates NK cells to release IFN-gamma

61
Q

What is the effect of IFN-gamma on macrophages?

A

Makes macrophages more efficient at killing intracellular bacteria, and produce NO

62
Q

What is the effect of IL-12 on NK cells?

A

Encourages the release of IFN-gamma

63
Q

True or false: some intracellular bacteria may be killed via the IFN-gamma released by NK cells, but adaptive immunity is generally required for eradication

A

True

64
Q

What are the two cell types that can release IFN-gamma to macrophages to encourage the clearance in intracellular bacteria?

A

NK cells

Th1 cells

65
Q

What is the result of the inability to kill mycobacteria?

A

Granuloma formation

66
Q

What are the cells that mediate a granuloma formation? What are the roles of each of these?

A

Th1 cells and macrophages

Th1 cells secrete IFN-gamma,

Macrophages secrete IL-12 and wall off infection

67
Q

What is the IL that stimulates the immune system to Th2 immunity?

A

IL-4

68
Q

What is the IL that stimulates the immune system to Th1 immunity?

A

IL-12

69
Q

How do granulomas impair bacterial replication? (3)

A
  • Macrophages release NO
  • Fibrosis and calcification of bacteria
  • Decrease nutrient and oxygen supply
70
Q

How can CTLs kill off intracellular bacteria?

A

If bacterial peptides are presented via MHC I, then CTLs will kill off cell

71
Q

How do mycobacteria survive in macrophages?

A

Inhibit the fusion of phagosomes and lysosomes, and may scavenge ROS

72
Q

How does listeria survive in macrophages?

A

Disrupts phagosome, and escapes into cytosol

73
Q

What is tuberculoid leprosy?

A

TB Th1 mediated = granuloma formation + few bacteria present

74
Q

What is lepromatous leprosy?

A

Th2 mediated response

75
Q

What are the immunoglobin levels in tuberculoid leprosy? Lepromatous?

A
Tuberculoid = normal
Lepromatous = hypergammaglobulinemia
76
Q

What are the T cell levels in tuberculoid leprosy? Lepromatous?

A
Tuberculoid = Normal
Lepromatous = low or absent