Hepatitis C Virus Core Protein Enhances NF-κB Signal Pathway Triggering by Lymphotoxin-β Receptor Ligand and Tumor Necrosis Factor Alpha

• DOI: 10.1128/jvi.73.2.1672-1681.1999
• Publication Date: 2019-12-31T18:23:47Z
• Authors: Li-Ru You; Chun-Ming Chen; Yan-Hwa Wu Lee
• Keywords: Lymphotoxin beta receptor; Lymphotoxin alpha

ABSTRACT Our previous study indicated that the core protein of hepatitis C virus (HCV) can associate with tumor necrosis factor receptor (TNFR)-related lymphotoxin-β (LT-βR) and this protein-protein interaction plays a modulatory effect on cytolytic activity recombinant form LT-βR ligand (LT-α1β2) but not alpha (TNF-α) in certain cell types. Since both TNF-α/TNFR LT-α1β2/LT-βR are also engaged transcriptional activator NF-κB activation or c-Jun N-terminal kinase (JNK) activation, biological effects HCV these regards were elucidated study. As demonstrated by electrophoretic mobility shift assay, expression prolonged enhanced TNF-α LT-α1β2-induced DNA-binding HuH-7 HeLa cells. The presence cells without cytokine treatment NF-κB-dependent reporter plasmid activity, was more strongly seen than Western blot analysis suggested modulation part due to elevated nuclear retention p50 p65 species protein-producing treatment. Furthermore, IκB-β degradation triggering LT-α1β2 In contrast IκB-β, increased IκB-α occurred only LT-α1β2-treated core-producing TNF-α-treated Therefore, cytokines, though mechanism particular regulation IκB degradation, is rather line specific. Studies had no TNF-α-stimulated JNK These findings, together our study, suggest among three signaling pathways triggered TNF-α-related potentiates most types, which turn may contribute chronically activated, persistent state HCV-infected