In the cases of bacterial and viral infections and bleomycin toxicity, an IL-1- and IL-17A-associated mechanism is activated to propagate the TGF-β1 pathway, forming an IL-1–IL-17–TGF-β1 axis that serves as a major driver of fibrosis during sustained type 1- and Th17-driven inflammatory responses (45). This evidence concerns the gene IL1A and viral infectious disease.