Role of STAT1 in the resistance of HBV to IFN-α

Bingfa Xu; Bo Tang; Jiajia Wei

doi:10.3892/etm.2021.9982

Role of STAT1 in the resistance of HBV to IFN-α

Exp Ther Med. 2021 Jun;21(6):550. doi: 10.3892/etm.2021.9982. Epub 2021 Mar 24.

Authors

Bingfa Xu¹, Bo Tang², Jiajia Wei³

Affiliations

¹ Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230061, P.R. China.
² Department of Pharmacy, Huainan First People's Hospital, Huainan, Anhui 232007, P.R. China.
³ Department of Pharmacy, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China.

Abstract

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.

Keywords: Hepatitis B virus; drug resistance; interferon α-2b; phosphorylation; signal transducer and activator of transcription 1.

Grants and funding

Funding: The present study was supported by grants from National Natural Science Foundation of China (grant no. 81470165).