TGFB1 and infection: Pathogens may also directly promote activation of TGF-β, as was found in the case of influenza A neuraminidase activating the latent TGF-β complex in epithelial cells and tissues [79]; furthermore, the consequent upregulation of extracellular matrix proteins facilitated the adhesion and infection with streptococcal bacteria, thereby promoting secondary infection of the host.