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Microbiology Y2 > Interferon > Flashcards

Interferon Flashcards

1
Q

Which gene is key to the interferon induction pathway? What does deficiency in this lead to?

A

IRF-7

lack of IFN-alpha

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2
Q

IRF-3 gene does what?

A

Influences IFN resposne

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3
Q

IRF-7 gene does what?

A

key to the interferon induction pathway

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4
Q

3 levels of virus immunity and examples?

A
  • Intrinsic – skin, mucous, all barriers that keep viruses out of the body
  • Innate – fast acting and non-specific which is switched on when viruses are detected. Is what makes you feel ill because it switches on inflammatory chemokines and cytokines
  • Acquired – takes a longer time to respond and remembers the virus for the future.
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5
Q

What inside host cells decides if a nucleic acid is self or pathogenic

A

ZAP

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6
Q

What does ZAP do and where is it

A

Inside host cells decides if a nucleic acid is self or pathogenic

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7
Q

What indicates to ZAP that a nucleic acid is foreign

A

If it has a lot of CpG (CG dinucleotides)

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8
Q

3 functions of IFN?

A
  1. Induce antimicrobial state in infected and neighbouring cells
  2. Modulate innate response to promote antigen presentation and natural killers but inhibit pro-inflammation
  3. Activate the adaptive immune response (by enhancing B and T cells)
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9
Q

What are type 1 IFNs?

A

alpha and beta

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10
Q

What cells secrete IFN beta

A

All

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11
Q

What cells have IFN-alpha receptors

A

All

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12
Q

What triggers IFN-beta induction

A

IRF3

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13
Q

What cells secrete IFN-alpha

A

plasmacytoid Dendritic cells

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14
Q

How many types of INF alpha and beta are there

A
  • One gene for IFN- so only one type, 13/14 isotypes of IFN-
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15
Q

What triggers IFN-alpha induction

A

IRF-7

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16
Q

What is T2 IFN?

A

IFN-gamma

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17
Q

What produces IFN-g

A
  • Produced by activated T cells and NK cells
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18
Q

What type of cells do IFN-lambda signal through

A

Epithelial

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19
Q

Where is IFN-lambda important (2)

A

Epithelial surfaces and liver

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20
Q

Epithelial cells make what interferons

A

IFN-lambda, and IFN-alpha or IFN-beta

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21
Q

How do we differentiate self from non-self (mention 2 key things - what differentiates us, and how do we notice this different thing)

A
  • Pathogen Associated Molecular Patterns (PAMPs) are things that all viruses have that our own cells do not have
  • Pattern Recognition Receptors (PRRs) see these viral PAMPs
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22
Q

3 PRR examples?

A

RLR, TLR, NLR
cytoplasmic RIG-I like receptors RLRs (sitting in the cytoplasm to bind to viruses in the cytoplasm) , endosomal Toll like receptors TLRs (membrane proteins), cytoplasmic nucleotide oligomerization domain receptors NLRs

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23
Q

Examples of a DNA sensor?

A

cGAS

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24
Q

What is cGAS an example of?

A

DNA sensor

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25
Q

What downstream molecule do PRRs interact with which causes phosphorylation of IRF3 or IRF7

A

MAVS

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26
Q

What activates MAVS

A

PRRs

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27
Q

What does MAVS cause

A

phosphorylation of IRF3 (or IRF7 in the plasmacytoid dendritic cells)

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28
Q

What causes phosphorylation of IRF3

A

MAVS

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29
Q

What causes phosphorylation of IRF7

A

MAVS

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30
Q

Where is IRF7 found

A

in plasmacytoid dendritic cells

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31
Q

Describe the pathway taken for IFN to be produced starting from virus entering cell

A

enters a cell and produces RNA (for the purpose of this example it is an RNA virus)

  • The RNA is recognised by a PRR in the cytoplasm, e.g. RIG-I
  • Upon binding viral RNA, PRRs change shape, unfold and interact with a downstream molecule called Mavs
  • Mavs sends a signal through other pathways which ends up phosphorylating IRF3 (or IRF7 in the plasmacytoid dendritic cells)
  • IRF3 then moves into the nucleus and sits on the promotor of the IFN- gene
  • This causes production of IFN- and the desired response
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32
Q

What does MAVS stand for

A

mitochondrial associated viral signaller

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33
Q

where do TLRs sit (2)

A

mitochondrial associated viral signaller

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34
Q

What do TLRs recognise

A
  • TLRs will see single stranded RNA inside the endosome/cell surface
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35
Q

what does activation of a TLR do (does X by Y Z)

y is a verb

A
  • TLRs will see single stranded RNA inside the endosome/cell surface, activate and send a signal into the nucleus of a cell
  • This will switch on the expression of the IFN-  gene by phosphorylating IRF3
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36
Q

What does cGAS signal through

37
Q

Where is cGAS found

A

In the cytoplasm of a cell

38
Q

What does cGAS bind to

39
Q

What does cGAS synthesise once bound to a DNA PAMP

40
Q

what does cGAMP bind to

41
Q

What binds to STING

42
Q

What synthesises cGAMP

43
Q

Where is STING found

A

On the rER in the cytoplasm

44
Q

Describe the cGAS detection of DNA

A
  • Sensors (cGAS) in the cytoplasm which sense and bind the DNA PAMPS, and synthesise a small molecule dinucleotide called cGAMP
  • cGAMP binds to STING (which sits on the membrane of the rER), and STING is phosphorylated and uses the IRF3 dimerisation pathway
45
Q

What happens to STING when cGAMP binds to it

A

STING is phosphorylated and uses the IRF3 dimerisation pathway

46
Q

What type of signalling does IFN do

A

Autocrine and paracrin

47
Q

What does IFN bind to and what does this cause

A
  • It can act on IFN- receptors on other cells, causing their dimerization
  • This will cause phosphorylations which make a new dimer, and a subsequent trimer which moves to the nucleus of the cell to bring about transcription/translation of interferon stimulated (IS) genes
48
Q

Describe type 1 IFN signalling

A
  • IFN- gene cause translation of the IFN- protein
  • This protein will be secreted from the cell to do autocrine and paracrine signalling
  • It can act on IFN- receptors on other cells, causing their dimerization
  • This will cause phosphorylations which make a new dimer, and a subsequent trimer which moves to the nucleus of the cell to bring about transcription/translation of interferon stimulated (IS) genes
  • These genes code for antiviral signal proteins and mean that viruses from the original cell can’t spread to neighbouring cells
49
Q

Examples of IFN stimulated genes? (7)

A
  • (PKR) Protein Kinase R inhibits translation, this stops new viral products being made, but also means that the host cell is likely to die
  • 2’5’OAS activates RNAse L that destroys ss RNA (including mRNA, not just viral RNA)
  • Mx inhibits incoming viral genomes
  • ADAR induces errors during viral replication
  • Serpine activates proteases
  • Viperin inhibits viral budding
  • IFITM3 Restricts virus entry through endosome, they stop the virus being able to leave the endosome
50
Q

What does PKR do

A

inhibits translation, this stops new viral products being made, but also means that the host cell is likely to die

51
Q

What does 2’5’OAS do

A

activates RNAse L that destroys ss RNA (including mRNA, not just viral RNA)

52
Q

What does Mx do

A

inhibits incoming viral genomes

53
Q

What does ADAR do

A

induces errors during viral replication

54
Q

What does Serpine do

A

activates proteases

55
Q

What does viperin do

A

inhibits viral budding

56
Q

What does IFITM3 do

A

Restricts virus entry through endosome, they stop the virus being able to leave the endosome

57
Q

what gene mutation causes more severe influenza

58
Q

What gene product inhibits viral budding

59
Q

What gene product inhibits incoming viral genomes

60
Q

What gene product activates RNAse L that destroys ss RNA (including mRNA, not just viral RNA)

A
  • 2’5’OAS
61
Q

What gene product activates proteases to kill viruses

62
Q

What gene product induces errors during viral replication

63
Q

What gene product activates Restricts virus entry through endosome, they stop the virus being able to leave the endosome

64
Q

What gene product inhibits translation, this stops new viral products being made, but also means that the host cell is likely to die

A
  • (PKR) Protein Kinase R
65
Q

What virus does Mx1 inhibit

66
Q

What virus does Mx2 inhibit

67
Q
  • Mx can form multimers which …..
A

wrap around the nucleocapsids of incoming viruses

68
Q

how long does an IFN response last

69
Q

How does an IFN response get suppressed

A
  • SOCS (suppressor of cytokine signalling) genes turn off the response
70
Q

What genes suppress IFNs

A
  • SOCS (suppressor of cytokine signalling) genes turn off the response
71
Q

7 ways viruses evade IFN response?

A
  1. Avoid detection by hiding the PAMP
  2. Interfere globally with host cell gene expression and/or protein synthesis
  3. Block IFN induction cascades by destroying or binding components of the cascade
  4. Inhibit IFN signalling
  5. Block the action of individual IFN induced antiviral enzymes
  6. Activate SOCS
  7. Replication strategy that is insensitive to IFN because they’re so quick that neighbouring cells haven’t had the time to respond to interferon.
72
Q

How does hep C evade the IFN response

A

NS3/4 protease acts as an antagonist to interferon induction by cleaving MAVS from the mitochondria so it can no longer start a signal

73
Q

What virus has NS3/4 protease which acts as an antagonist to interferon induction by cleaving MAVS from the mitochondria so it can no longer start a signal

74
Q

How does influenza evade the IFN response

A

NS1 (non-structural 1) protein acts as an antagonist to interferon induction by binding to RIG-I /TRIM25/RNA complex and preventing activation of signalling pathway, and also prevents nuclear processing of newly induced genes

75
Q

What virus has NS1 (non-structural 1) protein which acts as an antagonist to interferon induction by binding to RIG-I /TRIM25/RNA complex and preventing activation of signalling pathway, and also prevents nuclear processing of newly induced genes

76
Q

How does POX virus evade the IFN response

A

POX viruses encode soluble cytokine receptors (vaccinia virus B18) which mops up cytokines - being developed as possible future immunoregulatory therapies

77
Q

Which viruses encode soluble cytokine receptors (vaccinia virus B18) which mops up cytokines - being developed as possible future immunoregulatory therapies

A

POX viruses

78
Q

How does ebola virus evade the IFN response (2)

A

Encode these proteins:
 VP35 is a protein which blocks RIG-I and MDA5 signalling to the nucleus of infected cells
 VP24 blocks the signal from the IFN receptor into the nucleus so no ISGs are made

79
Q

2 ways we end up with viral pathology

A

We can end up with viral pathology because of damage of infected cells by virus OR damage of infected and bystander cells by the immune response

80
Q

What can cause a cytokine storm

A

Viruses modulating the immune response

81
Q

What does the protective/immunopathological effects of IFN response depend on

A

Concentration of IFN, if you give too much IFN or if a virus stimulates a lot of production of IFN, you get a pro-inflammatory IL-6 response

82
Q

Describe the events leading to a cytokine storm

A
  • So virus gets into cell, triggers IFN-β release, but this doesn’t help kill the virus due to evasion mechanisms so escapes, finds another cell, IFN released and this causes cytokine storm.
83
Q

6 mediators of a cytokine storm?

A
  • TNF, type I and II IFN. IL1-β, IL6 and other chemokines (CCL2 and CXCL10).
84
Q

What does a cytokine storm result in

A
  • This makes endothelium leaky resulting in hemorrhaging, huge inflammatory responses and pulmonary fibrosis
85
Q

RoA of IFN for IFN therapy

A

has to be injected

86
Q

What is necessary of a virus before it can be used in vaccines?

A
  • Viruses deficient in control of IFN are attenuated in IFN competent cells
87
Q

How can viruses be used in cancer therapy?

A

Oncolytic viruses take advantage of the IFN deficient state of cancer cells We hope to be able to engineer oncolytic viruses to cure cancers

88
Q

IFN response of cancer cells?

A

Cancer cells don’t make healthy IFN responses

Microbiology Y2 (6 decks)

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