ArticleArchives of virology2025
Inhibition of hepatitis C virus replication in HepG2 cells via modulation of the Raf-1 and interferon-alpha signaling pathways by thymoquinone.
Article in Archives of virology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Hypermethylation of lysosomal-associated genes LAMP1 and LAMP2 compromises lysosome function in patients with acute lymphoblastic leukemia.Immunologic research · 2025Article
- A novel mechanistic study on inhibiting influenza A virus replication by a newly extracted polypeptide targeting host autophagy.Archives of microbiology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) infection is a significant global health concern, as both acute and chronic hepatitis caused by HCV can lead to liver cancer and long-term liver damage. Thymoquinone (TQ), the active compound found in the remarkable herb Nigella sativa, has various anti-inflammatory and antiproliferative effects. In this study, we investigated the effect of TQ on the interferon-alpha (IFN-α) pathway and its ability to prevent HCV replication in the HepG2 cell line. Our findings showed no significant alterations in cell viability or lactate dehydrogenase (LDH) production in TQ-treated cells, while significant alteration in both factors was detected in cells treated with Sovaldi, the most commonly used drug for treatment of HCV infection. Interestingly, the level of the HCV NS5A protein was significantly reduced in infected cells treated with either TQ or Sovaldi in a dose-dependent manner. The expression of phosphorylated Raf-1 (phospho-Raf-1) and phospho-Mek-1 in infected cells was inhibited by TQ treatment, and the potential interaction between TQ and Ref-1 was confirmed by a molecular docking simulation. Unlike autophagy-related 12 (Atg12), the expression of LC3B in infected cells was also inhibited in a dose-dependent manner by TQ treatment. Conversely, the levels of interleukin-27 (IL-27) and interferon-alpha (IFN-α) in infected cells were significantly increased in a time- and dose-dependent manner by TQ treatment. These data suggest that TQ exerts antiviral effects in HepG2 cells by disrupting HCV replication through targeting of the Raf-1 signaling pathway and promoting the overproduction of IL-27 and IFN-α in infected cells.
Indexed as
Identifiers
40317342What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.