AZI, as opposed to PTX and especially DEX, did not affect R848-induced IFN-α production in newborn cord blood, and may therefore provide an approach to selectively and potently inhibit the pro-inflammatory mediators IL-1β and TNF in the context of infections that engage the TLR8 and inflammasome pathways (eg, influenza and HIV infection), while preserving endogenous antiviral IFN-α responses [55]. The gene discussed is IL1B; the disease is influenza.