Research has demonstrated that the extracellular nucleoprotein of influenza virus activates the expression of TLR2 and TLR4 and that there is an increased expression of TLR2, TLR3, and TLR9 in human patients infected with H1N1, leading to the production of pro-inflammatory cytokines such as IL-2, IL-6, IFN-γ, and TNF-α, and their overexpression mediates ARDS pathogenesis [60]. This evidence concerns the gene TLR2 and acute respiratory distress syndrome.