Aim
To investigate whether HBV-miR-3 is involved in HBV immune evasion.
Background
Hepatitis B virus (HBV) evades the innate immunity and leads to persistent chronic infection, but the molecular mechanism is still not well known.
Conclusion
HBV-miR-3 plays an important role in HBV immunity evasion by targeting cGAS 3'-UTR and interfering with cGAS-Sting-IFN pathway.
Methods
HBV-miR-3 agomir and antagomir were employed to verify the effectiveness of HBV-miR-3 on cGAS-Sting-IFN pathway through the experiments on relative luciferase activity, cGAS protein expression, Sting phosphorylation and interferon (IFN) production.
Results
HBV-miR-3 down-regulates cGAS protein expression post-transcriptionally by inhibition of cGAS 3'-untranslated region (3'-UTR) activity, which results in lower Sting phosphorylation and IFN production. HBV-miR-3 antagomir rescued cGAS protein expression, Sting phosphorylation and IFN-β production.