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Virology 11-20 > #17 innate immunity and virus evasion > Flashcards

#17 innate immunity and virus evasion Flashcards

(42 cards)

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1
Q

what immune cells have PRRs?

A

monocytes, DCs, macrophages

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2
Q

what part of the immune system is PRRs?

A

innate

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3
Q

what is the first line of defence?

does it need to be activated?

A
  • skin
  • mucous
  • gastric juice
  • normal body flora etc.
    these are passive barriers and do not need activation
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4
Q

what is in the second line of defence

do they need activating?

A
  • monocytes
    -DCs
    -macrophages
    -cytokines
    need activating but quick response active within hours
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5
Q

what do TLRs recognise

A

PAMPS

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6
Q

what does TLR3 recognise

A

dsRNA

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7
Q

what does TLR7 recognise

A

ssRNA

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8
Q

what does TLR8 recognise

A

ssRNA

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9
Q

what does TLR9 recognise

A

CpG unmethylated dinucleotides and herpesviruses

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10
Q

where are TLRs for viruses found mostly?

A

endosome

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11
Q

explain the process of TLR recognition of virus

A
  • TLR interacts with ligand PAMP
  • TLR will dimerise and activate
  • adaptor molecule MyD88 or Triff will associate with the TLR
  • the adaptor molecule will activate transcription factors such as IRF3, IRF7, NFkB that enter the nucleus to drive gene transcription
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12
Q

what adaptor molecule does TLR3 associate with?

A

just TRIFF

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13
Q

what adaptor molecules does TLR7, TLR8 and TLR9 associate with?

A

just MyD88

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14
Q

what transcription factors does adaptor molecule MyD88 activate

A
  • NFkB and IRF7
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15
Q

what transcription factors does adaptor molecule TRIFF activate

A
  • NFkB, IRF7 and IRF3
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16
Q

what type of response does transcription factor NFkB drive?

what cytokines are produces

A

a pro-inflammatory response.
Pro-inflammatory cytokines TNFa and IL-6 are made
this is a more general response but still helpful

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17
Q

what type of response does transcription factors IRF3 and IRF7 drive?
what cytokines are produced

Study These Flashcards
A

a type 1 interferon response
IFNa and IFNb
these are specific antiviral cytokines

18
Q

what is RIG-I?
where is it located?
what does RIG-I recognise?

Study These Flashcards
A

it is a cytosolic helicase
cytosol
recognises triphosphate RNAs in the cytoplasm (RNA that doesnt have a 5’ CAP)

19
Q

what is MDA-5?
where is it located?
what does MDA-5 recognise?

Study These Flashcards
A

it is a cytosolic helicase
located in the cytosol
recognises dsRNA in the cytosol

20
Q

what viruses does RIG-I generally recognise?

Study These Flashcards
A

most -ssRNA viruses

and flaviviruses

21
Q

what viruses does MDA-5 mostly recognise?

Study These Flashcards
A

most +ssRNA viruses

22
Q

explain the signalling process of cytosolic helicases MDA-5 and RIG-I

Study These Flashcards
A
  • they will interact with dsRNA or triphosphate RNAs in the cytoplasm
  • will dimerise and activate
  • will interact with adaptor protein MAVS on the mitochondrial membrane
  • MAVS will induce dimerisation and phosphorylation of transcription factors IRF3 and IRF7. MAVS also activates NFkB
  • pro-inflammatory cytolines TNFa and IL-6 will be produced along with type 1 interferons IFNa and IFNb
23
Q

what adaptor molecule does RIG-I and MDA-5 use

24
Q

what does MAVS activate?

Study These Flashcards
A
  • MAVS will induce dimerisation and phosphorylation of transcription factors IRF3 and IRF7.
    MAVS also activates NFkB
25
what are some DNA receptors in the cytoplasm?
AIM2, DAI, cGAS!
26
what does activation of the DNA in the cytoplasm induce?
- inflammasome mediated death - DNA should NOT be in the cytosol - if it is this is a DANGER signal
27
describe the pathway of cGAS/STING and what it recognises
- cGAS detects DNA in the cytoplasm - from virus or self - cGAS will generate cAMP that will bind to the adaptor molecule STING molecule on the ER - cAMP bound to sting will activate transcription factors NFkB, IRF3, TBK1 which will drive production of IFN and cytokines
28
how do cytokines work | what do they do
they bind to receptors on cells they alter gene expression in cells - they are important regulatory molecules
29
what is autocrine cytokine function?
- cell will produce cytokines and the cytokines will act on itself
30
what is paracrine cytokine function
- virus infected cell produces cytokines that will act on near by cells
31
what is endocrine cytokine function
cell will produce cytokines - they will spread systemically to act on cells far away!
32
describe the JAK/STAT signalling pathway for type 1 interferons
- type 1 interferons will use the JAK/STAT pathway - they will bind to the receptor and activate it - Jak1 and Tyk2 (adaptor molecule) will associate with the receptor, become phosphorylated and phosphorylate the receptor itself - the transcription factors STAT1 and STAT2 will associate and phosphorylate in the cytosol - they will dimerise and form a heterodimer, then translocate into the nucleus where they drive gene expression of multiple genes
33
describe the JAK/STAT signalling pathway for type II interferons
- IFNy will use the JAK/STAT pathway - IFNy will bind to the receptor and activate it - Jak1 and Jak2 (adaptor molecule) will associate with the receptor, become phosphorylated and phosphorylate the receptor itself - the transcription factors STAT1 and STAT2 will associate and phosphorylate in the cytosol - they will dimerise and form a homodimer, then translocate into the nucleus where they drive gene expression of multiple genes
34
what genes do interferons drive production of?
interferon stimulated genes a range of them up to 1000 genes ISGs are only made in response to IFN
35
what is MxA protein
it is a ISG - it will recognise and bind to viral capsids, it will sequester them up so they cannot be used by virus - attenuates virus
36
what is OAS and RNaseL - what do they do
- they are ISGs they are made in response to IFN - OAS will interact with RNA and activate -OAS will form a tetramer and then make 2'-5' adenylic acid which will induce the RNAseL monomer to dimerise making it active - the RNAseL will then degrade viral RNA!
37
what is PKR? how does it work
it is a ISG - it will bind to dsRNA and become active - PKR will then phosphorylate ElF2a stopping its activity therefore host cell totally stops host cell translation this is a TOTAL shut down mechanism
38
what are some viruses that modulate TLR signalling pathways?
HCV and poxviruses | they have a number of proteins that interfere with the TLR signalling
39
what viruses degrade adaptor signaller MAVS?
picornaviridae and Hep. C
40
what does west nile virus do to inhibit interferon signalling?
- prevents phosphorylation of Jak1/Tyk2 - it redistributes cholesterol from the PM, inactivating the IFN receptor - is shields itself from the MxA protein
41
what viruses inhibit PKR | why?
almost every virus has a way of inhibiting PKR activation and activity because PKR shuts down all translation in the cell Polio cuts up PKR Pox, HSV and HCV prevent phosphorylation of EIF2a however nornovirus can use PKR as an immune evasion method
42
how do SARs, measles and mumps prevent interferon signalling
they prevent nuclear import of the transcription factors STAT1 and STAT2 - so they cannot drive gene transcription

Virology 11-20 (8 decks)

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