This allows the influx of lipopolysaccharides into the liver, triggering cytokine production (e.g., IL-8 and TGF-β1) in the liver and initiating a cascade that exacerbates hepatitis and promotes liver fibrosis (Albillos et al., 2020; Liu et al., 2022). This evidence concerns the gene CXCL8 and hepatitis A virus infection.