In the first in vitro model, we used a human lung epithelial cell line (A549) activated by a stable synthetic double-stranded RNA (poly-(I:C)) that can bind to toll-like receptor 3 (TLR3) with high affinity [34] to stimulate the pathophysiological viral disease state and reproduce the cell signaling pathways typical of the cytokine storm in terms of IL-6 overproduction. This evidence concerns the gene TLR3 and viral load.