Host Immunity And Pathogen Evasion Flashcards

1
Q

What 4 agents can be infectiois

A

Opportunists , pathogenic , commensals or transposable retrovirus elements

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2
Q

What is virus tropism

A

Ability for viruses to infect a cell type successfully

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3
Q

What is this dependant on

A

Host factors eg diabetes link to covid

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4
Q

What 2 major things did diabetes do as a severe comorbidity of covid

A

Impair ifna production which is antiviral

Upregulste ace2 receptors

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5
Q

What are the diff ways viruses can be cytopathic to cells

A

Hi Jack cells and stop protein synthesis

Cause cell death after utilising them

Can cause cell cell fusion forming giant synctium which eventually cause cell death and allows viral spread

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6
Q

Do non cytopathic viruses exist

A

Yea eg lcmv but still cause cell stress

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7
Q

Explain the cycle of tissue damage from both virus and inflammation

A

Infection

Detected by prr

Also cause cytopathicity = tissue damage

Pamps and damps now detected both

Cause inflammation which causes even more tissue damage eg via mmp, ros

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8
Q

How does vessel leakage eventually occur and immune cell influx

A

Selectins , cams upreg

And vessel leakage via cytokines eg TNFa but also others like pg

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9
Q

If defences are successful, what is the course of innate then adaptive

A

2 weeks inmate
Then adaptive with igm to start.
Long term protection from igG and iga

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10
Q

Which chemokines which are triggered in innate by ifn type 1 and y allow adaptive immunity link

A

Cxcl9,10,11

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11
Q

What do they attract

A

Cells with cxcr3 which are mainly T cells, memory t , NK cells and apc

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12
Q

What sort of ifn responsive genes are upreg by ifn antiviral

A

Pkr - blocks translation

OAS 2’5’ - degrade mrna

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13
Q

How do they also allow for viral infected cell - T cell interaction

A

MHC 1 and II upreg

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14
Q

What sort of prr can stimulate type 1 ifn production

A

Rig 1 and mda5 recognising dsrna

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15
Q

Why is it said type 1 might cause persistent infection even if they’re antiviral acutely

A

Induce il10 producing tregs

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16
Q

What sort of things do cd8 cells have to promote death

A

Fas L binding to fas on infected cells

Granzymes

Perforin
Antiviral ifnY

17
Q

What does il2 do

A

Promote expansion of CD8 via growth signals

18
Q

How do NK cells recognise downregulated MHC

A

Kir inhibitory recetor

19
Q

Which isotype can be switched by th1 which is why it’s the most common

A

Igga2

20
Q

Which th17 cytokines promotes sustained cd8 in chronic infection

A

Il21

21
Q

Which cd4 cell needed for plasma cell maturation and memory b cell

A

Tfh

22
Q

What sorts of things are antibodies needed for

A

Adcc via fc receptors eg on NK cells

Binding complement c1q

Neutralisation

23
Q

Why would fast replication of small viruses cause immune evasion

A

Immunity not kicked in fast enough

24
Q

How can viruses evolve

A

Mutations eg to stop hla from presenting

25
Q

Give 2 examples of hikacking cytokines responses

A

Can inhibit ifn eg covid

Can produce homolog of il10 (ebv)

26
Q

Despite persistent ifn response being suppressive eg via il10 or ido. How does it still cause chronic inflam

A

Via TNFa etc cytokines

27
Q

How has cytomegalovirus dealt with the fact downregulated MHC can activate NK

A

They produce a decoy MHC which mimics MHC on surface so NK not activated

28
Q

What is clonal exhaustion

A

When excessive viral ag is presented to overstimulate tcr to cause peripheral deletion or anergy

29
Q

How can infection in thymus cause immune tolerance eg congenital rubella

A

It causes central deletion of virus specific T cells