As shown previously in Figure 7, the blockade of IFNAR1 resulted in protection from early hepatitis, yet it subsequently led to exacerbated concentrations of ALT 12 days after infection, coinciding with improved virus control that was likely driven by T cells (Figure S5C) (Teijaro et al., 2013, Wilson et al., 2013). This evidence concerns the gene IFNAR1 and hepatitis A virus infection.