Chronic inflammation, triggered by bacterial or viral infections or autoimmune processes, generates an environment rich in pro-inflammatory cytokines, such as interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), which directly impact cerebral endothelial cells [11,12,13]. This evidence concerns the gene TNF and viral infectious disease.