After infection, c-Jun and c-Fos bind to the AP-1 binding sites in the miR-21 promoter and evoke AP-1 mediated miR-21 induction, leading to the silencing of MyD88 and IRAK1, which play a major role in the initiation of the antiviral response in host cells and increased virus production (Figure 12). This evidence concerns the gene JUN and infection.