2-o-methylhonokiol suppresses hcv replication via traf6-mediated nf-kb activation

Suyun Jeong, Young Seok Lee, Kiyoon Kim, Ji Su Yoon, Sungsoo Kim, Joohun Ha, Insug Kang, Wonchae Choe

Research output: Contribution to journalArticlepeer-review

Abstract

Hepatitis C virus (HCV) is associated with various liver diseases. Chronic HCV infection is characterized by an abnormal host immune response. Therefore, it is speculated that to suppress HCV, a well-regulated host immune response is necessary. 2-O-methylhonokiol was identified by the screening of anti-HCV compounds using Renilla luciferase assay in Huh 7.5/Con 1 genotype 1b replicon cells. Here, we investigated the mechanism by which 2-O-methylhonokiol treatment inhibits HCV replication using real-time PCR. Our data shows that treatment with 2-O-methylhonokiol activated innate immune responses via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) pathway. Additionally, the immunoprecipitation result shows that treatment with 2-O-methylhonokiol augmented tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) by preventing p62 from binding to TRAF6, resulting in reduced autophagy caused by HCV. Fi-nally, we reproduced our data with the conditioned media from 2-O-methylhonokiol-treated cells. These findings strongly suggest that 2-O-methylhonokiol enhances the host immune response and suppresses HCV replication via TRAF6-mediated NF-kB activation.

Original languageEnglish
Article number6499
JournalInternational Journal of Molecular Sciences
Volume22
Issue number12
DOIs
Publication statusPublished - 2 Jun 2021

Keywords

  • 2-O-methylhonokiol
  • Hepatitis C virus
  • Innate immune response
  • Nuclear factor kappa-light-chain-enhancer of activated B cells

Fingerprint

Dive into the research topics of '2-o-methylhonokiol suppresses hcv replication via traf6-mediated nf-kb activation'. Together they form a unique fingerprint.

Cite this