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YR2: MCD Microbiology > Interferon > Flashcards

Interferon Flashcards

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Biology 101 flashcards
1
Q

What is the most common cause of sporadic encephalitis worldwide? Which subset of the population is this most common in?

A

Herpes simplex encephalitis

Children: affecting previously healthy individuals on primary infection with HSV-1

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2
Q

What is interferon?

A

Transferrable factor produced when cells are exposed to virus

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3
Q

What is the effect of interferon binding to interferon receptors on cells?

A

Signals the de novo transcription of 100s of interferon stimulated genes (ISG)

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4
Q

What are the 3 functions of type I interferons?

A

Induce antimicrobial state in infected + neighbouring cells
Modulate innate immune response to promote antigen presentation + NK cells
Activate the adaptive immune response

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5
Q

What are the type I interferons?

A

IFN alpha + IFN beta

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6
Q

What is the first interferon to be produced in a viral infection?
Which cells produce this?

A

IFN beta

All cells produce IFN beta + all tissues have IFNAR receptors

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7
Q

What is IFN beta induction triggered by?

A

IRF-3

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8
Q

Name a cell type that is specialised for producing IFN alpha. What do these cells express high levels of?

A

Plasmacytoid dendritic cells

IRF-7

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9
Q

How many genes are there for IFN alpha and IFN beta?

A

Alpha: 13/14 isotypes
Beta: 1

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10
Q

Which IFN comes under type II interferon?

Which cells produce this? Which receptor do these signal through?

A

IFN-gamma: specialist immune signalling molecule
Produced by activated T cells+ NK cells
IFNGR

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11
Q

Which IFN falls under type III IFN? Which receptors do type III IFNs signal through?

A

IFN-lambda
L-28 receptors
IL-10 beta receptors

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12
Q

Where are L-28 and IL-10 beta receptors mainly present?

A

Epithelial surfaces

E.g. respiratory epithelium

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13
Q

Which organ is IFN lambda very important in?

A

Liver

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14
Q

How does the innate immune system recognise non-self?

A

PRRs (pattern recognition receptors) on innate immune cells recognise PAMPs (pathogen-associated molecular patterns)
Often sense nucleic acids

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15
Q

Name two receptors that are involved in detecting the presence of viruses and state where they are found.

A

RIG-I like receptor (RLRs): cytoplasmic

Toll-like receptors (TLRs): plasma membrane + endosomal membrane, mainly found in Plasmacytoid dendritic cells

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16
Q

Describe RIG-I signalling.

A

RIG-I like receptors recognise ssRNA in the cytoplasm + signal through MAVS (mitochondrial)
Signals downstream, leading to phosphorylation of IRF3 which then dimerises + acts as a TF for generation of IFN-beta

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17
Q

Describe TLR signalling.

A

TLR detects nucleic acids in the endosome (not normal)
Signals to molecules outside the endosome (MyD88) + sends various TF’s to the nucleus
Results in switching on of expression of IFN alpha + beta

18
Q

Describe DNA sensing.

A

Mainly done by cGAS
= enzyme that binds to dsDNA in the cytoplasm + synthesises cGAMP (2nd messenger)
cGAMP binds to STING (found on endoplasmic reticulum)
Triggers phosphorylation of IRF3, IRF3 dimerises, enters nucleus as TF, promotes synthesis of IFN beta

19
Q

Describe the structure of IFN receptors for IFN alpha and IFN beta

A

Heterodimers of IFNAR 1 + IFNAR 2

20
Q

Describe the signalling from IFNAR receptors

A

Binding leads to signalling cascade involving JAK + STAT
Results in phosphorylation of STAT molecules
STAT molecules dimerise + enter nucleus
Bind to a promoter + regulates transcription of 100s of new genes

21
Q

What is IFITM3? What does lack of IFITM3 result in?

A

Sits on membrane of endosomes
Prevent fusion of virus membrane with endosomal membrane so virus gets trapped in the endosome
Lacking IFITM3 results in more severe influenza

22
Q

What are Mx1 and Mx2?

A

Mx can form multimers that wrap around nucleocapsids of incoming viruses: nullifies the viral genomes
Mx1: inhibits influenza
Mx2: inhibits HIV

23
Q

Describe the actions of Protein Kinase R. When is PKR activated by cells?

A

Prevents ribosomes from binding to mRNA so NO NEW genes will be TRANSLATED
An extreme measure + a last resort – only activated when the cell has no other option

24
Q

Name a family of genes that suppress the cytokine signalling and turn off the response.

A

SOCS

25
Q

State 6 mechanisms of viral evasion of the IFN response.

A 
Avoid detection by hiding the PAMP  
Interfere globally with host cell gene expression +/or protein synthesis 
Block IFN induction cascades  
Inhibit IFN signalling  
Activate SOCS  
Replication strategy insensitive to IFN
26
Q

Explain how hepatitis C controls the interferon response.

A

NS3/4 protease cleaves MAVS
MAVS is important in detecting Hep C through the RIG-I pathway
Thus Hep C is not detected

27
Q

Explain how influenza controls the interferon response.

A

NS1 protein
Acts an antagonist to IFN induction by binding to the RIG-I complex + preventing activation of the signalling pathway
Also prevents nuclear processing of newly induced genes

28
Q

What type of virus are Pox and Herpes viruses? What does this allow them to encode?

A

Large DNA viruses

Encode accessory genes to evade immune responses

29
Q

What do Pox viruses encode that helps deal with the interferon response?

A

Encode soluble cytokine receptors that mop up IFN + prevent it from reaching its receptors

30
Q

Describe a potential therapeutic use of the soluble cytokine receptors encoded by Pox viruses

A

Could be useful in AI or inflammatory conditions where IFN + other cytokines are produced in abundance

31
Q

What can result from viruses interfering with the immune response?

A

Skewing of immune response resulting in immunopathology

32
Q

Describe how viral infections can cause cytokine storm.

A

Lots of virus propagation, induces high IFN production

accompanied by massive release of TNF alpha + other cytokines

33
Q

What is a serious consequence of cytokine storm?

A

Pulmonary fibrosis – due to accumulation of immune cells in the lungs

34
Q

Explain why viruses that can’t control interferon can be used as the next generation of live attenuated vaccines.

A

They’re able to infect cells + will replicate sufficiently to be able to mount an immune response but won’t replicate to the extent where it causes disease

35
Q

Viruses that can’t control interferon can’t be propagated in normal healthy cells. What is the solution to this issue?

A

Propagate in cells deficient in IFN response

36
Q

Explain why interferons are not frequently used as an antiviral therapy.

A

Stimulate production of several cytokines which cause unpleasant side effects

37
Q

What disease has IFN been used to treat?

A

Hepatitis C

38
Q

Explain the reasoning behind using IFN-lambda as a treatment for influenza.

A

Receptors for IFN lambda are only found on epithelial surfaces (site of infection of influenza)
IFN lambda can’t signal through immune cells + cause immunopathology
Only induces an antiviral state in epithelial cells

39
Q

Explain how oncolytic viruses would work.

A

Viruses engineered to uniquely replicate in tumour cells + kill them
Cancer cells are unable to mount a proper IFN response
So, a virus unable to control the IFN response will NOT be able to replicate in healthy cells but will be able to infect + replicate in cancer cells

40
Q

What can lead to increased susceptibility to herpes simplex virus, thus resulting in encephalitis?

A

Inborn errors of certain genes result in lack of CNS intrinsic interferon response

41
Q

Give 2 examples of viruses that can trigger a cytokine storm

A

Dengue haemorrhage fever

Sever influenza

YR2: MCD Microbiology (8 decks)

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