ArticleJournal of virology2009
Arsenic trioxide inhibits hepatitis C virus RNA replication through modulation of the glutathione redox system and oxidative stress.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 40 citations in OpenAlex.
- Arsenic trioxide impacts hepatitis B virus core nuclear localization and efficiently interferes with HBV infection.Microbiology spectrum · 2024Article
- Arsenic trioxide: applications, mechanisms of action, toxicity and rescue strategies to date.Archives of pharmacal research · 2024Review
- Arsenic in medicine: past, present and future.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Review
- Down-regulation of RdRp complex and activated immune response due to increased arsenic level leads to decreased corona virus replication.Current research in microbial sciences · 2022Article
- Interplay between RNA Viruses and Promyelocytic Leukemia Nuclear Bodies.Veterinary sciences · 2021Review
- ATO (Arsenic Trioxide) Effects on Promyelocytic Leukemia Nuclear Bodies Reveals Antiviral Intervention Capacity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Hepatitis C: From inflammatory pathogenesis to anti-inflammatory/hepatoprotective therapy.World journal of gastroenterology · 2018Review
- Isolation and characterization of hepatitis C virus resistant to a novel phenanthridinone derivative.Antiviral chemistry & chemotherapy · 2015Article
- PML/TRIM19-Dependent Inhibition of Retroviral Reverse-Transcription by Daxx.PLoS pathogens · 2015Article
- Establishment of chronic hepatitis C virus infection: translational evasion of oxidative defence.World journal of gastroenterology · 2014Review
- Arsenic trioxide stabilizes accumulations of adeno-associated virus virions at the perinuclear region, increasing transduction in vitro and in vivo.Journal of virology · 2013Article
- Hepatitis C virus-induced mitochondrial dysfunctions.Viruses · 2013Review
- Interplay between Hepatitis C Virus and Redox Cell Signaling.International journal of molecular sciences · 2013Article
- Curcumin inhibits HCV replication by induction of heme oxygenase-1 and suppression of AKT.International journal of molecular medicine · 2012Article
- Hepatitis C virus hijacks P-body and stress granule components around lipid droplets.Journal of virology · 2011Article
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- Alcohol and hepatitis C virus--interactions in immune dysfunctions and liver damage.Alcoholism, clinical and experimental research · 2010Review
- Ethanol enhances hepatitis C virus replication through lipid metabolism and elevated NADH/NAD+.The Journal of biological chemistry · 2010Article
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arsenic trioxide (ATO), a therapeutic reagent used for the treatment of acute promyelocytic leukemia, has recently been reported to increase human immunodeficiency virus type 1 infectivity. However, in this study, we have demonstrated that replication of genome-length hepatitis C virus (HCV) RNA (O strain of genotype 1b) was notably inhibited by ATO at submicromolar concentrations without cell toxicity. RNA replication of HCV-JFH1 (genotype 2a) and the release of core protein into the culture supernatants were also inhibited by ATO after the HCV infection. To clarify the mechanism of the anti-HCV activity of ATO, we examined whether or not PML is associated with this anti-HCV activity, since PML is known to be a target of ATO. Interestingly, we observed the cytoplasmic translocation of PML after treatment with ATO. However, ATO still inhibited the HCV RNA replication even in the PML knockdown cells, suggesting that PML is dispensable for the anti-HCV activity of ATO. In contrast, we found that N-acetyl-cysteine, an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively. In this context, it is worth noting that we found an elevation of intracellular superoxide anion radical, but not hydrogen peroxide, and the depletion of intracellular glutathione in the ATO-treated cells. Taken together, these findings suggest that ATO inhibits the HCV RNA replication through modulation of the glutathione redox system and oxidative stress.
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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 OpenQuestion graph.