In addition, SARS-CoV-2 (MA10) infection increased blood-brain barrier permeability, evidenced by reduced claudin 5 mRNA expression in C57BL/6, BALB/c, and Rag2−/− mice and increased GFAP mRNA expression indicating astrogliosis, which broadly supports the hypothesis that SARS-CoV-2 induces a neuroinflammatory phenotype as found in previous studies using the hACE2 over-expressing K18 mouse model [26,27,28], rendering the brain susceptible to infection-induced dysfunction. The gene discussed is KRT18; the disease is infection.