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Virology > 12 Viruses vs Host cell – interferon response > Flashcards

12 Viruses vs Host cell – interferon response Flashcards

1
Q

what is innate immunity from

A

non-specific, all antigens attacked equally. Genetically based, pass to offspring

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2
Q

what is adaptive immunity from

A

develops when exposed to various antigens and builds defence that is specific to antigen

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3
Q

what are the nonspecific defences

A

anatomic barriers, inhibitors, phagocytosis, fever, inflammation, and IFN

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4
Q

what are the specific defences

A

antibody and cell-mediated immunity

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5
Q

what are the properties of interferon

A
  • cytokines
  • induction is rapid and transient
  • bind to receptors (IFN receptors) then cause signal transduction cascade-inducing cytokine and antiviral state – some viruses are sensitive, and some are resistant to IFN
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6
Q

what are very sensitive to interferon

A

VSV

NDV

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7
Q

what are very resistant to interferon

A

influenza

HSV

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8
Q

what is a signal transduction cascade

A

signal from outside cell binds to receptor and turns on transcription genes

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9
Q

what are interferons released as

A

soluble factor from virally infected tissues

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10
Q

what do interferons do when released

A

protect neighbouring cells from infection

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11
Q

when do cells synthesis IFNs

A

when activated by IFN-inducing agent

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12
Q

what is an IFN-inducing agent

A

virus most common

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13
Q

what are the major biological actions of interferons

A
  • induce class I and II MHC antigens
  • activate monocytes/macrophages, NK, cytotoxic T cells
  • modulation of Ig synthesis in B cells
  • induction of Fc receptors in monocytes
  • inhibition of growth of non-viral intracellular pathogens
  • pyrogenic action (fever)
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14
Q

what does the interferon system do

A

Cellular mechanism to limit virus infection to first infected cell
Is a cytokine (IFN) binds to front receptor on the host cell receptor activates other proteins that turn on genes – interferon stimulated genes

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15
Q

what do all interferon stimulated genes have in common

A

have in their promoter interferon stimulated response element in their nucleus

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16
Q

what does PRR recognise

A

dsRNA

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17
Q

how do interferons induce antiviral state

A

Interferon released into second cell
Interferon bind to interferon receptor on outside of the cell
Signal transduction – IFN goes from outside of the cell and induces interferon stimulated genes
Genes are activated and suppresses viral replication

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18
Q

what does PKR do

A

stops translation – inhibition of protein synthesis

19
Q

what does OAS do

A

degrade mRNA

20
Q

what is STAT

A

Signal transductor and activator of transcription

21
Q

what turns on transcription

A

STAT1-STAT2 travel from cytoplasm to nucleus = turn on transcription

22
Q

what does virus induce

A

ISGs – interferon stimulates genes (cell is in ‘antiviral state’)

23
Q

what happens when virus is induces ISGs

A

New virus comes in and activates
PKR binds
OAS made
Shutting down protein synthesis by degrading mRNA and blocking translation

24
Q

how does PKR block translation

A

Will trap eIF2B and block translation

As at the end of translation eIF2 needs to be changed from GDP to GTP

25
Q

how are virus infected cells translationally controlled

A
  • viral messages are translated while cellular messages are not
  • mechanism whereby lytic or fast-growing viruses take over cell for own benefit, hijack translational machinery
  • adenovirus eIF2-alpha (VA RNA) and eIF4F (TPL)
26
Q

what blocks the initiation of eIF2-GDP

A

PKR

27
Q

how does PKR phosphorylate the eIF2-GDP

A

PKR dimerizes (2 subunits) on dsRNA molecule – phosphorylates each other and eIF2

28
Q

what does VA RNA, TAR and EBERS bind to

A

monomers not dimers

29
Q

why can VA RNA, TAR and EBERS not bind to dimers

A

Viruses make short RNA

Bind PKR monomers and cause dimerization

30
Q

what makes VA RNA

A

adenovirus

31
Q

what makes EBERS

A

EBV

32
Q

what makes TAR

A

HIV

33
Q

what are the mechanisms involving prevention of dimers - HCV

A

HCV encodes a protein NS5A – binds to PKR

34
Q

what are the mechanisms involving prevention of dimers - FLU

A

activates cellular inhibitor which recruits heat shock protein 70

35
Q

what are the mechanisms involving prevention of dimers - involving PKR

A

mechanisms involving PKR expression/stability

36
Q

what are the mechanisms involving prevention of dimers - involving dsRNA

A

mechanisms involving sequestering dsRNA

37
Q

what are the mechanisms involving prevention of dimers - involving substrate

A

mechanisms involving substrate interaction

38
Q

how do viruses block PKR

A
  • block dimerization (bind dsRNA, Protein)
  • block phosphorylation of eIF2 (pseudosubstate)
  • degrade PKR (brute force)
  • sequester dsRNA (keeps activator away)
39
Q

translational control, regulation of eIF4E phosphorylation

A
  • eIF4F remains dephosphorylated in adenovirus infected cells inactivated cap binding protein
  • eIF4E and cap binding complex (4F) scanning cellular translation stopped – displacement of
  • eIF4G associated MnK kinase thus host translation shut off
40
Q

what does the adenovirus late transcripts (L1-5) tripartite leader do

A

employs ribosome shunting method to translate cap independently

41
Q

what makes coat proteins

A

Adenovirus late messages

42
Q

what allows cap independent translation

A

Have a little RNA segment

43
Q

what does the ribosome shunt do

A

binds near cap-(At TPL) but scans short sequence then jumps secondary structure to AUG

Virology (15 decks)

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