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Virology > Exam II: Lecture 5 > Flashcards

Exam II: Lecture 5 Flashcards

1
Q

What are the two main components of the adaptive immune response?

A
  1. Cytotoxic T lymphocytes (CTLs)

2. Humoral antibodies

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2
Q

Is the innate response specific or non-specific? Does it render the host immune to future infection?

A

It is non-specific

Does not render the host immune to future infection

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3
Q

What does the innate response produce?

A

Cytokines such as interferon and interleukins

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4
Q

Not all genomes are the same, what does this imply for your immune system?

A

We all make antibodies differently

Think colonizers and smallpox

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5
Q

What are the 6 main components of the innate immunity?

A
  1. Apoptosis
  2. Natural killer cells
  3. Complement activation
  4. Complement production
  5. Interferons
  6. The antiviral state
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6
Q

How is apoptosis used as a defense mechanism?

A

Denies the virus the opportunity to replicate and spread

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7
Q

What is the mechanism for apoptosis in innate immunity?

A

Irreversible damage > Mdm2 degraded (p53 is always made and degraded via ubiquitination by Mdm2) > p53 stabilized > activates caspases = cystiene proteases > cleave target proteins after aspartic acid&raquo_space;> DNA degredation, cytoskeleton eaten > apoptosis

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8
Q

What genes regulated apoptosis? (2)

A
  1. Antiapoptotic: BCL2

2. Pro-apoptotic: BH123 (Bax, Bak)

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9
Q

Cytochrome C in mitochondria can activate what?

A

Caspases

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10
Q

Are NK cells antigen-independent or antigen-dependent?

A

Antigen independent

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11
Q

NK activation occurs within how many days after viral infection?

A

2-3 days

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12
Q

NK cells are believed to kill what kind of cells?

A

Cells that do not express MHC I

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13
Q

If the virus decreases the production of MHC I to escape detection, what cells are responsible for killing the virus-infected cells?

A

NK cells

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14
Q

Complement Cascade Mechanism

A

Antibody finds antigen > C1 complex forms > C2a and C4b fragments > C3 convertase > C3 hydrolysis > C3b and C3a fragments > C3b cleaves C5 > C5a and C5b > C5b, C6, C7, C8, C9 form the pore > cell swells and bursts

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15
Q

The complement cascade is a part of which system?

A

It can be a part of both the adaptive and innate immune system

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16
Q

Define Opsonization

A

Marking a pathogen for phagocytosis

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17
Q

What complement protein binds to the surface of pathogens?

A

C3b

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18
Q

What are the final results of complement activation? (4)

A
  1. Phagocytosis
  2. Virus neutralization
  3. Induction of inflammatory response
  4. Activation of B cells
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19
Q

What are cytokines?

A

A family of over 30 proteins that are induced by different stimuli

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20
Q

Why is cytokine production low or absent?

A

Because they lead to inflammation, cell proliferation, and differentiation state which can be bad for a healthy body

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21
Q

Upon induction, they are produced for a short or long period of time?

A

Short

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22
Q

They bind to receptors on the surface of target cells with low or high affinity?

A

High

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23
Q

What can cytokines cause? (3)

A
  1. Changes in gene expression
  2. Cell proliferation
  3. Differentiation state
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24
Q

What are some common cytokines? 3 categories and examples

A
  1. Antivirial; IFN I and IFN II
  2. Inflammatory; TNF, IL-1, IL-6
  3. Lympokines; Interlukins
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25
Q

What is a PAMP?

A

Pathogen Associated Molecular Pathway

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26
Q

What is a PRR?

A

Pattern Recognition Receptor

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27
Q

What is an example of a PAMP? (2)

A

Triphosphorylated RNA, LPS

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28
Q

What are the two categories of PRRs?

A
  1. Cytoplasmic

2. Membrane Bound

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29
Q

What is an example of a cytoplasmic PRR? What do they contain? What kind of activity do they possess?

A

RIG-I, Mda5
Contain CARD domains
RNA helicase activity

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30
Q

What is an example of a membrane-bound PRR? What kind of PAMP do they detect?

A

Toll-like receptors (TLRs)

Detect extracellular PAMPS

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31
Q

What is a DAMP?

A

Damage Associated Molecular Pathway

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32
Q

What is a general example of a DAMP?

A

Stick yourself with a needle > Split cells > DNA escapes nucleus > triggers the immune response

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33
Q

Define Edema

A

Swelling due to liquid accumulation from blood vessels

34
Q

Talk me through the RIG-I pathway

A

DNA/RNA virus enters cell > releases genome = PAMP = triphosphorylated ds RNA > activate RIG-I / MOAS > Uq chains come over > Uq chains act as a scaffold > RIG-I binds to MAVS on surface of mitochondrial membrane = assembly point > TRAPs assemble > TRAP activate TDK > TDK phosphorylate and activate IKK > IKK phosphylates IR3 and IkB&raquo_space;> production of interferons

35
Q

When RIG-I is inactive what does it look like? How does this change when its active?

A

RIG-I has a CARD domain and its folded up when in active
When it is active it is unfolded which exposes its CARD domain
MAVS CARD domain finds RIG-I CARD domain

36
Q

What are the 2 uses for ubiquinization in the cell?

A
  1. Degredation

2. Localization

37
Q

What are interferons?

A

Members of the cytokine family

Induce the antiviral state

38
Q

What are the two groups of the interferons?

A
  1. IFN I

2. IFN II

39
Q

What is IFN I involved in?

A

Defense against viruses and bacteria

40
Q

What is IFN II involved in?

A

Defense against bacteria only

41
Q

What are the two IFN I family members?

A

IFNalpha

IFNbeta

42
Q

What members of the IFN II family?

A

IFNgamma

43
Q

Which interferon is the main activator of the antiviral state?

A

IFNbeta

44
Q

What is the general signaling pathway from PRR to antiviral response?

A

PAMP > recognized by PRR&raquo_space;> IFN I > autocrine I paracrine signaling > secondary set of genes > more proteins > produce antiviral state

45
Q

Type I IFNs are induced by what type of viral genome OR what type of cytokine?

A

ds RNA

TNF-alpha

46
Q

IFNalpha and IFNbeta are produced by what cell types? What is the inducing agent? What are their functions (3)?

A

All cell types
Viral infection, dsRNA
Antiviral, increases MHC I, antitumor

47
Q

IFNgamma is produced by what cell types? What is the inducing agent? What is its function (3)?

A

T-cells
Antigen or mitogen
Increase MHC I and II, decrease MHC II in B cells, NK cell activation

48
Q

What is unique about the interferon promoter? Why?

A

It requires a complex enhanceosome because it needs to be highly regulated

49
Q

What are the 4 main components of the interferon enhanceosome?

A
  1. ATF2
  2. C-JUN
  3. IRF-3
  4. NFKB
50
Q

How do interferons effect their response?

A

By binding to receptors on the surface of cells

51
Q

Do type I and type II interferons bind to the same receptors?

A

No, they bind to different receptors

52
Q

Binding of an IFN leads to the activation of what?

A

A tyrosine kinase domain within the receptor

53
Q

What is the ISRE?

A

Interferon stimulated responsive element

54
Q

Talk me through the generalized mechanism after an interferon binds to a cell

A

IFN bind to receptor > activate tyrosine kinase domain > phosphrylation cascade > activation of TF > bind to ISRE sequence in DNA > expression of IFN responsive genes

55
Q

What makes RNA unstable?

A

RNA has a built in AU rich element at the 3’ end which causes its destruction

56
Q

What does the AU rich region on the RNA signal for?

A

Signals for an RNAase to come degrade it

57
Q

Induction by the type I interferons is short or long lived? How does this differ compared to type II (IFN gamma)?

A

IFN I induction is transient = short lived

IFN gamma = long lived, slower

58
Q

What are the 3 ways IFN I signal transduction is regulated?

A
  1. Complex enhanceosome
  2. AU rich region > mRNA degradation
  3. Makes its own inhibitor (NFKB makes IKK)
59
Q

Talk me through the Jak/Stat pathway

A

IFNalpha/beta > IFNR > JAKI > STAT I + STAT II localize and dimerize > enter nucleus > bind to ISRE > turn on genes

IFNgamma > IFNR > JAK I > STAT I > Dimerize > enter nucleus > bind GAS > turn on genes

60
Q

IFN I turn on which gene sequence? What about IFN II?

A

IFN I : ISRE

IFN II : GAS

61
Q

What are the 5 specific genes stimulated by IFN disucess in class? Which IFN are they stimulated by?

A
  1. 2’-5’ Oligo A synthetase ; IFN I
  2. MxA ; IFN I
  3. IRF-2 ; IFN I and II
  4. MHC I ; IFN I and II
  5. MHC II ; IFN II
62
Q

What is the function of 2’-5’OligoA synthetase?

A

Induction of antiviral state

63
Q

What is the function of MxA?

A

Inhibits replication of Influenza and BZV by binding to polymerase

64
Q

What is the function of IRF-2?

A

Transcription factor that turns on antiviral state gens

65
Q

Waht is the function of MHC I?

A

Increases antigen presentation

66
Q

What is the function of MHC II?

A

Increase antigen presentation

67
Q

What is one detectable biological effect of interferons? What does this do?

A

IFNs induce a fever

The high temperature inhibits replication of many viruses

68
Q

What does TAP do?

A

Presents peptides on the surface of cells

69
Q

What is APC?

A

Antigen-presenting Cell

70
Q

Both IFN types lead to the activation of what 5 immune cells?

A
  1. Monocytes
  2. Macrophages
  3. NK cells
  4. CTLs
  5. Synthesis of Ig by B cells
71
Q

What is an evolutionary reason why inflammation cannot go on forever?

A

Anhedonia?

72
Q

IFN can inhibit cell growth and was found to be effective against some forms of cancer

A

True

73
Q

What does 2’-5’OligoA synthetase do once made in response to IFN stimulation?

A

IFN I/II > promoter > OAS (OligoAsynthetase) > polymerizes ATP > 2’-5’OligoA > activates RNAaseL > RNAase L cleaves ss mRNA > decreases production of viral proteins&raquo_space;> apoptosis

74
Q

What does PKR do once made in response to IFN stimulation?

A

dsRNA > PKR > phosphorylates eIF-2alpha ( eIF-2alpha recognizes eIF-4 which is on the mRNA cap > switches out GTP for GDP > ribosomal translation) > eIF-2 cannot switch out GTP for GDP > ribosome freezes > translation shuts down&raquo_space;> apoptosis

75
Q

IFN turns on the transcription of what 3 proteins which help ready the cell before it is infected with virus?

A
  1. Inactive OAS
  2. Latent PKR
  3. Inactive RNAase L
76
Q

Talk to me through the process by which an infected cell will protect other cells around it

A

Cell becomes infected > PAMP > PRR > IFN I > autocrine/paracrine signaling > JAK/STAT > promoter > OAS, PKR, RNAase L > ds RNA enters second cell > activation of PKR, OAS > active RNAaseL&raquo_space;> apoptosis

77
Q

Apoptosis

A

cells sacrifice themselves to save the organism

78
Q

Natural Killer Cells

A

Attack cells that harbor virus (but do not display antigen)

79
Q

Complement activation

A

Activate immune cells and act as chemokines

80
Q

Interferons

A

first line of defense against infection

81
Q

Antiviral state

A

prepares the cell to destroy viral RNA and prevent translation of viral proteins

Virology (22 decks)

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