☣First up for the final session is ☣Nathan Bartlett (ncbi.nlm.nih.gov/pubmed/?term=B…), Hunter Medical Research Institute, Uni of Newcastle, NSW talking on TLR2 agonist treatment suppresses rhinovirus infection of human epithelial cells in vitro

☣modify host immunity to tackle *any* virus; boost innate immunity
☣grand plan
☣TLR the sentinel activators/regulators of innate immunity
☣any old virus can be a huge problem if you are immunosuppressed (vax less effective)
☣TLRs on the surface facing out, and those inside in endosomes (the antiviral TLRs) inducing lots of IFN and inflammation
☣used as a last resort to avoid immunopathology that can be associated with their activation; too inflammatory
☣the surface facing TLRs may be a better target for a therapeutic to tune innate immunity?
☣in collaboration with Ena therapeutics
☣TLR2 is one such target
☣use this to contain virus in the nose
☣Primary BEC ALI system again
☣first from asthma and COPD donors - reduced viral load in pretreated cells using TLR2 agonist - not huge, better control of the infection
☣not proinflammatory
☣to uncover mechanisms, immune transcriptomics using nanostring
☣clear upregulation of innate immunity in pretretaed ALIs, before infection
☣untreated cells had not yet recognised virus after 8h
☣early IFNλ was key prior to controlling infection (limits inflammation; if not controlled, need to make a more aggressive IFNβ-driven inflammation that is damaging-think some #flu)

☣may work well with #fluoride vaccine when rollout timing is a consideration
☣RV gets in, but from 24h reduction starts; looks to be about more efficiently sensing, and then killing off, the infected cells
*#flu, you evil autocompleting device!
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