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IMIN 324 > Antiviral defense I > Flashcards

Antiviral defense I Flashcards

1
Q

What are some innate and adaptive factors used in response to virus infection?

A

Innate:
- PRR, PAMPS and Nf-kB
- NK cells
- cytokines (type I IFN)
- complement

Adaptive:
- CTLs
- Ab production by B cells

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2
Q

What is the innate immune system of bacteria and some archae against phages?

A

CRISPR (clustered regularly interspaced short palindromic repeats)

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3
Q

What is the innate immune system of plants against viruses?

A

RNA interference is mediated by RISC and DICER to degrade viral genomes

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4
Q

What is the activating component of the vertebrate innate immune system?

A

PRRs and PAMPs

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5
Q

What can be said about the evolutionary importance of the Toll-NF-kB pathway?

A
  • Toll-Nf-kB pathway is involved in immune defense in many species, from flies to humans
  • believe that the activation of Nf-kB is the original and central signaling pathway of activation in innate immunity
  • toll pathway of Nf-kB is evolutionary conserved
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6
Q

Why are kinase pathways advantageous (say compared to proteolytic pathways or having only one activation even)?

A
  1. kinases can be easily tuned on and off
  2. kinase pathway are fast in comparison to proteolytic pathway
  3. lots of steps
    - better control of immune response
    - amplification
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7
Q

What are the two pathways of how IFN induces an anti-viral state?

A
  1. oligo adenylate synthesis
  2. protein kinase R
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8
Q

Describe the structure and function of oligoadenylate synthetase, what’s it regulated by?

A
  • structure: contains and RNA binding domain + a catalytic domain
  • function: polymerizes ATP into 2’5’ ATP oligomers (2’5’ oligo adenylic acid)
  • regulated by dsRNA
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9
Q

Describe the oligoadenylate synthetase IFN pathway

A

dsRNA activates OAS1 –> oligoadenylate synthetase production –> converts ATP into 2’5’ Adenylic acid which binds to endoribonuclease L –> endoribonuclease L dimerizes –> activation of endoribonuclease L –> degradation of viral and cellular ssRNA

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10
Q

What is protein kinase R, where is it found, how does IFN affect it, what activates it?

A
  • PKR = dsRNA-dep-protein kinase
  • found = cytoplasm
  • IFN results in upregulation of PKR at the ts level
  • PKR is activates via interactions with dsRNA
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11
Q

Describe the protein kinase R IFN pathway

A

PKR is phosphorylated to its active form by RNA-dep auto-phosphorylation –> phosphorylated tl initiation factor ElF-2 –> translation of viral and cellular protein blocked

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12
Q

How does adenovirus evade the IFN pathway?

A

inhibits PKR activation:

  1. produces an RNA called VA-RNA1
  2. VA-RNA1 binds directly to PKR and inhibits interaction of dsRNA with PKR and the activation of PKR
  3. PKR doesn’t become activated –> viral tl occurs
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13
Q

What is the red queen hypothesis?

A

evolutionary pressure exerted by a pathogen on a given host species will promote mutation of the host for the purpose of survival, not to confer a reproductive advantage

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14
Q

How does vaccina virus (a poxvirus) inhibit IFN?

A
  1. secreted IFNgR like M-T7
  2. production of the viral protein E3L that binds dsRNA
  3. production of the viral protein K3L which acts a substrate for PKR
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15
Q

what are some characterisitics of poxviruses’ M-T7

A
  • M-T7 has homolgy to cellular IFNR
  • M-T7 is secreted from infected cells
  • binds to cellular IFN and prevents interaction with the cellular R
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16
Q

What are some characterisitics of vaccina virus’ E3L?

A
  • E3L binds dsRNA produced during virus infection
  • E3L has an RNA binding domain
  • prevents dsRNA from interacting with PKR and inducing its activaton
17
Q

What are the differences between CD4+ and CD8+ T cells?

A

CD4:
- helper functions for the immune system
- synthesize cytokine and growth factors

CD8:
- kill virus infected cells
- “CTL”

18
Q

Describe MHC-I components, and what size of peptides it binds to

A
  1. heavy chain (alpha) with transmembrane anchor
  2. beta 2M associated with heavy chain non-covalently

size of peptides = 9-13 a.a

19
Q

Describe how MHC-1 assemebly occurs

A
  1. MHC alpha chain and B2M are transported into the ER due to the presence of a hydrophobic signal sequence at the (N)-term of the protein
  2. they assemble in the ER with help of a cellular chaperone called calnexin
  3. viral peptides are ubiquitylated and degraded in proteasomes
  4. TAP transports viral peptides into the ER where they associate with MHC-1
20
Q

Describe how the adenovirus E3 19K protein blocks MHC-I presentation

A
  1. expressed from the virus and localizes into the ER
  2. retained in the ER by the presence of an ER retention sequence
  3. E3 19K binds the cellular MHC heavy chain, inhibiting the expression of MHC-I on the surface of the cell
21
Q

Describe how HSV-I inhibits MHC-I expression

A
  1. ICP47-IE gene
  2. associates with TAP
  3. blocks transport of peptides into the ER
22
Q

Describe how HCMV inhibits MHC-I expression

A
  • US6 inhibits peptides from entering into the ER
  • US3 retains MHC in the ER
  • US2, 11 translocate MHC-I to the cytoplasm where MHC-I undergoes degradation
23
Q

What are the two mechanisms by which CTLs kill infected cells

A
  1. degranulation
  2. ligation of FAS
24
Q

What R family does FAS belong to, what is a characteristic of this family, how does FAS work?

A
  • FAS is a member of teh TNFR superfamily
  • have extracellular cysteine-rich repeats
  • not all members signal for apoptosis
  • TNFR1 and FAS signal for apoptosis -> both have a cytoplasmic domain called death domain which is essential for apoptosis
25
Q

What are the adaptor proteins of FAS and TNFR1, what protein do they both ultimately activate?

A

FAS: adaptor = FADD –> caspase 8
TNFR1: adaptor = TRADD + FADD –> caspase 8

26
Q

How can viruses inhibit Fas and TNF killing?

A
  1. caspase 8 inhibitors
    - adenovirus 14.7K
    - HCMV UL36
  2. virus encoded DED containing proteins
  3. down regulation of FAS from the surface of infected cell
    - adenovirus
27
Q

How have caspase 8 inhibitors shaped the evolution of mammalian cells?

A

in the absence of casp 8 mammalian cells undergo necroptosis

28
Q

How does adenovirus E3 10.4K and 14.5K induce the loss of FAS from the surface of cells? Are both necessary? Do any other viruses use this mechanism?

A

E3 10.4K and 14.5K form a complex that’s expressed at the surface of the cell –> results in the endocytosis of FAS from the p.m –> FAS degradation in lysosomes

  • both are necessary
  • adenovirus is the only virus known to do this

IMIN 324 (14 decks)

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