IL1B and infection: In both the B.1.351 model and the AAV-hACE2-WA1 model, intranasal SARS-CoV-2 infection resulted in increases in pro-inflammatory cytokines (e.g., IL-1β, IFNβ, CXCL10, IFNγ, IL-6, and CCL11) in the hippocampus and cerebrospinal fluid at 7 days post-infection [38,75,82,83].