This observation was previously made in epithelial cells and suggests that viral sensing by TLR3 during influenza or SARS-CoV-2 infections may modulate the response toward other microorganisms, such as gram-negative and gram-positive bacteria during secondary infections, whose derivatives may activate TLR2 and TLR4 signaling (Takeuchi et al., 1999; Melkamu et al., 2013; Morris et al., 2017; Zhou et al., 2020). This evidence concerns the gene TLR4 and influenza.