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Year 2 MCD Microbiology > 3: Interferon > Flashcards

3: Interferon Flashcards

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1
Q

What is an interferon?

A

soluble Polypeptide produced by virus infected cells that signal self and neighboring cells to switch on defence mechanism

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2
Q

What kind of molecule is a Type I interferon?

A

Polypeptides

(soulouble cytokine)

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3
Q

What is the function of a type one interferon?

A
  1. Switch on antimicrobial state in infected and neighbouring cells
  2. Mudulating immune response by
    • Innate: promote Antigen presentation and Natural Killer cells
    • Adaptive: Activate the adaptive immune response
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4
Q

Name examples of Type I interferons

A

IFN beta and IFN alpha

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5
Q

Which cells produce IFN ß?

What is its taget (and where is it present)?

A

IFN ß is secreted by all (infected) cells and

  • bind to IFNAR (Interferon-alpha-Receptor) also present on all cells
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6
Q

Which cells produce IFN alpha?

A

14 different types Produced by Plasmacytoid dendritic cells

  • exepcially involved in immune cell modulation
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7
Q

Which cells produce Type II interferons? Name an example

What do they bind to?

A

E.g. IFN gamma

  • produced by activated T cells and NK cells
  • bind to different IFNGR
    • regulation/modulation of adaptive immune response
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8
Q

Which cells produce Type III interferons? Name an example

What do they bind to?

A

E.g. INF lambda

  • produced by endothelial cells (not immune cells)
  • bind to IL28 and IL10ß receptors
    • increase barrier function of epithelial surfaces
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9
Q

Summarist how an Interferon response gets activated

A

Viral PAMS (Pattern Associated Molecular Patterns) get recogised by PRR (Pattern recognitiion receptors)

–> Set off dowonstream mechanism in cell modulating transcription

–> TF produce Interferon

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10
Q

What are the PAMS that are recognised in Viral infections?

What are thex recognised by?

A

Different types of viral genome in places where is would normally not be found are recognised

  1. RNA
    • in Cytoplasm: RIG-I like Receptors (RLRs)
    • In endosomes: Toll like receptors (TLRs)
  2. DNA: cGAS
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11
Q

Explain the downstream Mechanism that is set off by activation of RIG-I like Receptors (RLR)

A

Get activated by ssRNA in the cytoplasm

  • RLR foreign genome and
  • actiate MAVS (mitochondrial antiviral signaling protein)
    • leads to activation of downstream kinase cascasde leading to
    • phosphorylation of Irf3
    • Irf3 phosphoarylation causes dimerisation and activation of the Transcriptionfactor
      • Expression of Interferon gene
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12
Q

Explain the downstream Mechanism that is set off by activation of TLRs (Toll-Like Receptors)

A

TLRs= sense RNA in endosomes (mainly on dendritic cells)

  1. Activation of Tlr3
    • Trif
    • Irf3
  2. Activation of TLR 7+8 (expecially on dendritic cells)
    • Activation of Myd88
    • NF-kb and Irf7

Activation of Transcription Factors lead to INF Type I production!

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13
Q

Explain the effects of activation of cGAS

A

cGas are activated by dsDNA in the cytoplasm leading to

  • activation of cGAMP which
  • activate STING
  • STING (similar to MAVS) activate Irf3 (interferon regulatory factor 3)
    • induced expression of type I IFN
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14
Q

What are the effects of IFN binding to a cell?

A

Leading to: activation of downstream mechanism and induces transcription of 100s of antiviral mediators

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15
Q

How does INF binding to INFAR lead to transcription of antiviral mediators?

A
  1. INF binding caues dimerisation of INFAR
  2. Via adaptor protein JAK –> phosphorylation of STAT
    • STAT phosphorylation causes STAT dimerisation which forms the Transcription factor
      • migrates to nucleus and causes stimmulation of production of many genes
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16
Q

What are the effects of expression of the ISG (interferon stimmulated Geners?

A

Many hundret genes expressed–> widely varied antiviral effects e.g.

  • inhibition of (viral and host) translation (Protein Kinase R)
  • Destruction of ssRNA (via RNAse L) (host and viral)
  • Inhibition of incoming viral genome (Mx)
  • Errors during viral replication (ADAR)
  • Protease Activation
  • Inhibition of viral budding
    • MANY RESPONSES THAT ARE TOXIC FOR CELL AND VIRUS
17
Q

What kind of protein is IFITM3?

What does it cause?

A

IFITM3= ISG (interferon stimulated gene)

  • Restict the virus entry through the endosome (inhibits endosome budding)
18
Q

Explain the role of Mx1 and Mx2 in antiviral defence

A

Mx1+2 are ISG (INF stimmulated genes) causing

  • multimer formation that wraps around and inhibits nucleocapsids of incoming viruses
19
Q

Explain why and how INF response is regulated

A

It can only be obtained for several hours because

  • of strong, toxic effects of INF on the cells
  • Turned off via negative regulation
    • SOCS (suppressor of cytokine signalling) genes turn off the response
20
Q

Explain why it is important for Viruses to evade the INF response

A

Because it is so powerful and otherwise Viruses would not have a chance to be virulent

21
Q

What are general mechanisms by which virused can evade the INF system?

A
  • Avoid detection by hiding the PAMP
  • Interfere globally with host cell gene expression and/or protein synthesis
  • Interfere directly with IFN
    • Block IFN induction cascades by destroying or binding
    • Inhibit IFN signalling
    • Block the action of individual IFN induced antiviral enzymes
    • End IFN response by Activate SOCS
  • Replication strategy that is insensitive to IFN (e.g. very fast)
22
Q

Explain how Hepatitis C can evade the IFN response

A
  • Hep C interferes with downstream mechanism that would cause IFN activation

NS3/4 protease acts as antagonist to interferon induction by cleaving MAVS

23
Q

Explain how Influenza can evade the IFN repsonse

A
  1. NS1 inhibits IFN activation by
    • antagonisingby binding to RIG-I /TRIM25/RNA complex and preventing activation of signalling pathway
  2. and also prevents nuclear processing of newly induced genes (inhibits some newly formed genes that are needed for production of IFNß)
24
Q

Explain how POX viruses and Herpes evade the IFN pathway

A

Is a large DNA virus

  • have accessory genes that modify host immune system
    • e.g. expression of soluble cytokine receptors
25
Q

How do viruses cause damage to the host?

A

Damage due to a viral infection is a combination of

  • direct viral damage to the cell
  • damage from immune response
26
Q

What happens during a cytokine storm?

What are typical infections that might induce one?

A

E.g. Dengue haemorrhagic fever, severe influenza infections and Ebola

It is a overproduction of Cytokines (Interferons) which can lead to

  • various outcomes (also depends on age)
  • can lead to severe complications
27
Q

Explain how IFN can be used therapeutically

A
  1. As antiviral treatement
    • but: immune resonse leading to (flue like) unpleasant side-effects
    • new solution: IFN lambda used that does not activate the immune cells (aka no side effects) but increase epithelial barrier function
  2. Attenuated Vaccines
    • if viruses cannot interfere with IFN –> no chance of invastion –> attenuated virus can be used for vaccines (if suspect immunocompetent)
  3. Cancer
    • many cancer cells can’t make IFN
      • attenuated viruses could only infect/kill cancer cells and not the healthy host cells (that can fight the virus with IFN)

Year 2 MCD Microbiology (8 decks)

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