Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling

Figure 3 Impact of hepatitis B virus-miR-3 on Sting phosphorylation and IFN-β production. A: CGAS protein expression, Sting phosphorylation, and IFN-β production in HepG2.2.15 cells compared to HepG2 cells; B: CGAS protein expression, Sting phosphorylation, and IFN-β production in HepG2-NTCP cells treated with hepatitis B virus (HBV) from HepG2.2.15 cell supernatant; C: CGAS protein expression, Sting phosphorylation, and IFN-β production in HepG2-NTCP cells treated with HBV from HepG2.2.15 cell supernatant; D: Co-treatment with HBV-miR-3 agonist and salmon sperm DNA increased cGAS protein expression, Sting phosphorylation, and IFN-β production in HepG2 cells. Each experiment was repeated three times. Data are presented as mean ± SD.