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