Abstract
Aim: USP18 is a type of IFN-stimulated gene, which is associated with virological responses to IFN therapy in HBV (hepatitis B virus). However, its detailed molecular mechanism needs to be explored. Materials & methods: With HBV replication cells and mouse models, the USP18 was overexpressed or inhibited, followed by treatment with IFN or Poly (I:C). The expressions of HBV DNA, HBsAg, HBeAg and protein factors in the samples were detected. Results: Overexpression of USP18 attenuates anti-HBV effect of IFN in vitro and in vivo by inhibiting JAK-STAT pathway and reducing the expression of MX1 and OAS. While, the inhibition of USP18 can promote to activate JAK-STAT pathway to enhance the antiviral effect of IFN. Conclusion: USP18 negatively regulates the anti-HBV effect of IFN by regulating JAK-STAT pathway. It may provide new insights into innate immunity mechanisms in CHB patients receiving IFN treatment.
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