ArticleThe Journal of biological chemistry2007
The hepatitis E virus Orf3 protein protects cells from mitochondrial depolarization and death.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 84 citations in OpenAlex.
- Integrated Transcriptomics Reveals a SHEV ORF3-Mediated circRNA Network That Disrupts Riboflavin Metabolism and Activates the ko05212 Pathway.Veterinary sciences · 2026Article
- Elevated serum mtDNA in COVID-19 patients is linked to SARS-CoV-2 envelope protein targeting mitochondrial VDAC1, inducing apoptosis and mtDNA release.Apoptosis : an international journal on programmed cell death · 2024Article
- Decoding Cancer through Silencing the Mitochondrial Gatekeeper VDAC1.Biomolecules · 2024Review
- Multiple Functions of Hepatitis E Virus ORF3.Microorganisms · 2024Review
- Quantification of host proteomic responses to genotype 4 hepatitis E virus replication facilitated by pregnancy serum.Virology journal · 2023Article
- Characteristics and Functions of HEV Proteins.Advances in experimental medicine and biology · 2023Article
- Structural aspects of hepatitis E virus.Archives of virology · 2022Review
- Dysregulation of host cell calcium signaling during viral infections: Emerging paradigm with high clinical relevance.Molecular aspects of medicine · 2021Review
- Structural and molecular biology of hepatitis E virus.Computational and structural biotechnology journal · 2021Review
- VDAC1 at the Intersection of Cell Metabolism, Apoptosis, and Diseases.Biomolecules · 2020Review
- Mitochondria Targeted Viral Replication and Survival Strategies-Prospective on SARS-CoV-2.Frontiers in pharmacology · 2020Review
- Mitochondria in the biology, pathogenesis, and treatment of hepatitis virus infections.Reviews in medical virology · 2019Review
- Mitochondrial electron transport chain complex III sustains hepatitis E virus replication and represents an antiviral target.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress.Cell stress · 2017Article
- The Mitochondrial Voltage-Dependent Anion Channel 1, CaFrontiers in oncology · 2017Review
- Hepatitis E Virus Mutations: Functional and Clinical Relevance.EBioMedicine · 2016Review
- The ORF3 Protein of Genotype 1 Hepatitis E Virus Suppresses TLR3-induced NF-κB Signaling via TRADD and RIP1.Scientific reports · 2016Article
- Molecular Biology and Infection of Hepatitis E Virus.Frontiers in microbiology · 2016Review
- Therapeutic targets for the treatment of hepatitis E virus infection.Expert opinion on therapeutic targets · 2015Review
- Antiviral strategies for hepatitis E virus.Antiviral research · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The biology and pathogenesis of hepatitis E virus are poorly understood due to the lack of an in vitro culture or infection models. The viral Orf3 protein activates the cellular mitogen-activated protein kinase pathway and is likely to modulate the host cell environment for efficient viral replication. We screened for cellular genes whose transcription was differentially up-regulated in an Orf3-expressing stable cell line (ORF3/4). The gene for mitochondrial voltage-dependent anion channel (VDAC) was one such candidate. The up-regulation of VDAC in ORF3/4 cells was confirmed by Northern and Western blotting in various cell lines. Transfection of ORF3/4 cells with an ORF3-specific small interfering RNA led to a reduction in VDAC protein levels. VDAC is a critical mitochondrial outer membrane protein, and its overexpression results in apoptosis. Surprisingly, Orf3-expressing cells were protected against staurosporine-induced cell death by preservation of mitochondrial potential and membrane integrity. A small interfering RNA-mediated reduction in Orf3 and VDAC levels also made cells sensitive to staurosporine. Chemical cross-linking showed Orf3-expressing cells to contain higher levels of oligomeric VDAC. These cells also contained higher levels of hexokinase I that directly interacted with VDAC. This interaction is known to preserve mitochondrial potential and prevent cytochrome c release. We report here the first instance of a viral protein promoting cell survival through such a mechanism.
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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.