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Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

Caffeic acid inhibits HCV replication via induction of IFN α antiviral response through p62-mediated Keap1/Nrf2 signaling pathway
In this study, we showed that CA could notably inhibit HCV replication. Mechanism study demonstrated that CA could induce HO-1 expression, which would trigger the IFNα antiviral response, and the antiviral effect of CA was attenuated when HO-1 activity was inhibited by SnPP (an HO-1 inhibitor). CA could also increase erythroid 2-related factor 2 (Nrf2) expression. When Nrf2 was knocked down by specific siRNA, HO-1 expression was concomitantly decreased while HCV expression was restored. Further study indicated that kelch-like ECH-associated protein 1 (Keap1) expression was decreased by CA in a p62/Sequestosome1 (p62)-depe...
Source: Antiviral Therapy - April 14, 2018 Category: Virology Source Type: research

Caffeic acid inhibits HCV replication via induction of IFN α antiviral response through p62-mediated Keap1/Nrf2 signaling pathway.
In this study, we showed that CA could notably inhibit HCV replication. Mechanism study demonstrated that CA could induce HO-1 expression, which would trigger the IFNα antiviral response, and the antiviral effect of CA was attenuated when HO-1 activity was inhibited by SnPP (an HO-1 inhibitor). CA could also increase erythroid 2-related factor 2 (Nrf2) expression. When Nrf2 was knocked down by specific siRNA, HO-1 expression was concomitantly decreased while HCV expression was restored. Further study indicated that kelch-like ECH-associated protein 1 (Keap1) expression was decreased by CA in a p62/Sequestosome1 (p62)-depe...
Source: Antiviral Research - April 12, 2018 Category: Virology Authors: Shen J, Wang G, Zuo J Tags: Antiviral Res Source Type: research

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