A randomized clinical trial of peginterferon alpha-2b with or without entecavir in patients with HBeAg-negative chronic hepatitis B: Role of host and viral factors associated with treatment response

2015 ◽  
Vol 23 (6) ◽  
pp. 427-438 ◽  
Author(s):  
P. Tangkijvanich ◽  
S. Chittmittraprap ◽  
K. Poovorawan ◽  
U. Limothai ◽  
A. Khlaiphuengsin ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Treatment Response ◽  
Randomized Clinical Trial ◽  
Chronic Hepatitis B ◽  
Factors Associated ◽  
Negative Chronic Hepatitis

scholarly journals Expression of Interferon Effector Gene SART1 Correlates with Interferon Treatment Response against Hepatitis B Infection

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Yong Li ◽  
Chuanlong Zhu ◽  
Faxi Wang ◽  
Tiantian Zhu ◽  
Jun Li ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Antiviral Activity ◽  
Treatment Response ◽  
Chronic Hepatitis B ◽  
Hepg2 Cells ◽  
Hbv Dna ◽  
Stat Signaling ◽  
Ifn Treatment

Interferon-α (IFN-α) has limited response rate in the treatment of chronic hepatitis B (CHB). The underlying mechanism of differential responsiveness to IFN remains elusive. It has been recently reported that SART1 mediates antiviral effects of IFN-α in the hepatitis C virus (HCV) cell culture model. In this study, we investigated the role of SART1 in antiviral activity of IFN-α against hepatitis B virus (HBV) using blood and liver biopsy samples from chronic hepatitis B patients treated with pegylated IFN-α and HepG2 cells transfected with cloned HBV DNA. We observed that the basal SART1 expression in liver and PBMCs before IFN treatment was significantly higher in responders than in nonresponders. Furthermore, baseline SART1 expression level positively correlated with the degree of HBV DNA and HBeAg decline after IFN treatment. Mechanistically, silencing SART1 abrogated the antiviral activity of IFN-α, reduced the expression of IFN-stimulated genes (ISGs) Mx, OAS, and PKR, and attenuated JAK-STAT signaling in HepG2 cells, suggesting that SART1 regulates IFN-mediated antiviral activity through JAK-STAT signaling and ISG expression. Our study elucidates the important role of SART1 in IFN-mediated anti-HBV response and provides new insights into understanding variation of IFN treatment response in CHB patients.

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