Role of STAT1 in the resistance of HBV to IFN‑α
- Bingfa Xu
- Bo Tang
- Jiajia Wei
Affiliations: Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, P.R. China, Department of Pharmacy, Huainan First People's Hospital, Huainan, Anhui 232007, P.R. China, Department of Pharmacy, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China
- Published online on: March 24, 2021 https://doi.org/10.3892/etm.2021.9982
Copyright: © Xu
et al. This is an open access article distributed under the
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The objective of the present study was to explore the mechanism of hepatitis B virus (HBV) resistance to interferon (IFN), and the role of signal transducer and activator of transcription 1 (STAT1). HepG2.2.15 cells were stimulated with a long‑term (6‑24 weeks) low‑dose interferon (IFN)α‑2b (10‑70 IU/ml), so as to construct and screen a HepG2.2.15 cell model resistant to IFNα‑2b. The changes of STAT1 and other proteins in the JAK‑STAT signaling pathway, before and after drug resistance, were compared. The phosphorylation of STAT1 in HepG2.2.15 cells resistant to IFNα‑2b was significantly decreased, and the expression level of 2',5'‑oligoadenylate synthetase 1 was downregulated. Decreased phosphorylation of STAT1 in the JAK‑STAT signaling pathway a contributor to the development of resistance to IFN‑α in HBV.