Host Immunity And Pathogen Evasion Flashcards
What 4 agents can be infectiois
Opportunists , pathogenic , commensals or transposable retrovirus elements
What is virus tropism
Ability for viruses to infect a cell type successfully
What is this dependant on
Host factors eg diabetes link to covid
What 2 major things did diabetes do as a severe comorbidity of covid
Impair ifna production which is antiviral
Upregulste ace2 receptors
What are the diff ways viruses can be cytopathic to cells
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
Do non cytopathic viruses exist
Yea eg lcmv but still cause cell stress
Explain the cycle of tissue damage from both virus and inflammation
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
How does vessel leakage eventually occur and immune cell influx
Selectins , cams upreg
And vessel leakage via cytokines eg TNFa but also others like pg
If defences are successful, what is the course of innate then adaptive
2 weeks inmate
Then adaptive with igm to start.
Long term protection from igG and iga
Which chemokines which are triggered in innate by ifn type 1 and y allow adaptive immunity link
Cxcl9,10,11
What do they attract
Cells with cxcr3 which are mainly T cells, memory t , NK cells and apc
What sort of ifn responsive genes are upreg by ifn antiviral
Pkr - blocks translation
OAS 2’5’ - degrade mrna
How do they also allow for viral infected cell - T cell interaction
MHC 1 and II upreg
What sort of prr can stimulate type 1 ifn production
Rig 1 and mda5 recognising dsrna
Why is it said type 1 might cause persistent infection even if they’re antiviral acutely
Induce il10 producing tregs
What sort of things do cd8 cells have to promote death
Fas L binding to fas on infected cells
Granzymes
Perforin
Antiviral ifnY
What does il2 do
Promote expansion of CD8 via growth signals
How do NK cells recognise downregulated MHC
Kir inhibitory recetor
Which isotype can be switched by th1 which is why it’s the most common
Igga2
Which th17 cytokines promotes sustained cd8 in chronic infection
Il21
Which cd4 cell needed for plasma cell maturation and memory b cell
Tfh
What sorts of things are antibodies needed for
Adcc via fc receptors eg on NK cells
Binding complement c1q
Neutralisation
Why would fast replication of small viruses cause immune evasion
Immunity not kicked in fast enough
How can viruses evolve
Mutations eg to stop hla from presenting
