For example, respiratory syncytial virus infection could upregulate the expression of TLR3, resulting in the overexpression and release of downstream inflammatory factors through the TLR3/NF-κB/IRF3 pathway in asthmatic mice; this process also enhances extracellular matrix synthesis, further aggravating asthma symptoms (67). This evidence concerns the gene TLR3 and respiratory syncytial virus infectious disease.