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Immunology 3 > HOst response to viruses > Flashcards

HOst response to viruses Flashcards

1
Q

Order of Innate early resposne:

Day 1 and 2

A

rise in INFs, TNFs and IL-12

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2
Q

Innater early resposne;

day 2 and 3

A

NK cell medated killin

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3
Q

Innate early response

Day 5-10

A

T cell mediated killing

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4
Q

What immune system branch does a lot of killing off in the early stage of viral infection

A

INNATE… adaptive comes in later

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5
Q

NK activity is 20-100 X better when _____ are present

A

IFNs adn IL-12

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6
Q

Parts of innate immunity

A

Innate Immunity
Recognition of pattens by PRRs
Type I INF secreation
Secreation of sobule mediators: Cytokines—IL-1, TNFα, IFNγ chemokines
Complement
NK cells for direct killing of virusese and a source of INFγ

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7
Q

Parts of adaptive immunity

A

Adaptive immunity
Cytokines
Cytocotoxic T cells (granule exocytosis, Fas L-induced apoptosis)
B cells and Antibiodies (neutralization, opsonization and phagocytosis)

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8
Q

REview for cell cycle.. not that important

A
  1. Virus enters and binds—enters epithelial cells—causes epi cells to release INFαand β to activate NK cells
  2. NK cells upreguated by INFs and IL-12 (which is released by DC cell)
  3. DC take processed host cell and viral proteins and releaes IL-6 and IL-1 to CD4 TH0 cells
  4. THO cells release IL-2 and INF to CDH TH1
  5. CDH TH1 will induce B cell, CD4 emmory, CD8 and CTL
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9
Q

used to tx chronic hep C and for tx of melanoma, hairy cell leukemia, chrnoic myelogenous leukemina, Kaposi’s sarcoma

A

INFα

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10
Q

Given the importantce of INFγ in driving _____immune response, woud INFs be useful for tx of virus infecion

A

Th1

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11
Q

INF___ to tx MS

A

β

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12
Q

Issues with interferuons

A

-Flu like symptoms after each injection (msl aches, pains, malaise) Pt on INF have issue with thinking and conc and can reduce bood counts

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13
Q

Vira products (ssDNA, ds RNA and CpG DNA)→ sensed by PRRs→ cascade of signaling through adaptors and kinases→ activate TFs → these will activate:

A

IRFs or Intrferon response factors

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14
Q

Once Interferoun response activators are activated… they will

A

bind to the Interferon stimulated response element and make INFapha/beta and secreate to nearby cells

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15
Q

What is the benefit of an infected cell secreating INFa/b

A

inducts and antiviral state in the nearby cells by binding to INF-a/b receptor

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16
Q

Type I receptor

A

INF a/b receptor that activates the PKR path

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17
Q

Protein kinase R (PKR) is induced in nearby cell by

A

IFN

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18
Q

PKF binds to dsRNA, autophosphorylated to phosphorylate :

A

elF-2

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19
Q

when elF is P’d it wil do what to translation

A

prevent it

20
Q

2’5 OAS is induced by

A

IFN

21
Q

like PKR it binds to and is activated by

A

dsRNA

22
Q

once activated, OAS cat syntehsis of lolgoadenylate form ATP into :

A

oligoAAAA

23
Q

oligoAAAA that was adenylated from activated OAS will activate

A

RNAase L

24
Q

RNAase L is

A

endoribonucleus

25
Q

purpose of RNAaseL

A

binds to oligoAAA and dimerizes = active whith then degrades mRNA

26
Q

whats the point of the OAS path

A

to get oligoAAAA to activate and dimerize with RNAse L to degrade mRNA = NO viral protein synthesis

27
Q

INFbeta/alpha induce

A

anti-viral state

28
Q

Antiviral state will

A

decrease viral produciton
increase MHC I expression
increase NK cells

29
Q

Path of anitival state

A 
a. increaes MHC class I expression→ Increase PKR expression→ 2’5’ synthase expression → increase 2’5’ oligo A (A-A) → increase viral mRNA degredation
OVERALL: decrease viral protein synthesis and increase class I MCH
30
Q

pyrogens to induce fever

A

TNF and IL-1b

31
Q

made by activated macros, CD4 T cells and NK cells

A

TNF

32
Q

major pro-inflammatory cytokine

A

(TNF, IL-1, IL-6)

33
Q

ILB

A

can induce fever
major pro-inflammaory cytokine
produced and secreated by activated macrophages

34
Q

What cytokine is produced and secreated by activated macrophages

A

IL-1B

35
Q

IL-6 is

A

pro-inflammatory cytokine

36
Q

induce death signaling

A

TNF

37
Q

Mouse story: not that important… see twice

A

Mice infected with vaccinia virus (strain to make small pox) didn’t devo fever
Poxvirus recombiants lacking the IL-1β binding protein have been generated…when mice are infectd w/ these, no fever
Thus viral IL-1β proteins will seqester IL-1β and ≠ it’s pyrogenic activity (need fever to fight off virus)

38
Q

NK response

1. cytotoxic… kills targets after assessing the balance between:

A

inhibitory signals from class I and activating signals from NK activating ligands

39
Q

In “first response” to virus infection, cells upregulate

A

Type I IFNs and upregulate NK activating ligands

40
Q 
NK sees a class I MHC \_\_\_\_\_
sees a class I MHC + NK activating ligang\_\_\_\_
A

leave it be

DEATH!

41
Q

Recap on class MHC1

A

proteasome chews up protein→ TAP brings it in, assembles MHC with it’s β2m subunit and processes protein + MHC I through ER and golgi→ to cell surface

42
Q

Whos responsible for the early ‘anti-viral’ host defense?

A

innate

early symptoms of viral infection happen before adaptive immune system comes into play

43
Q

key for neutralizing a virus before it enters a cell

A

B cells or antiBodies

44
Q

Infected cells will often undergo

A

apoptosis
from withing
and from without

45
Q

signals for apoptosis without

A

Fas, TNF=alpha, CTL, NK

46
Q

Mech of apoptosis

A

go pro-capsase 9→ capsase 9→ which takes pro-cap3 to capsase-3 == end result is activated capsase 3 and you get DNA fragmentation and death

Immunology 3 (20 decks)

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