ArticleJournal of neurovirology2013
Mitochondrial dysfunction in rabies virus infection of neurons.
Article in Journal of neurovirology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 53 citations in OpenAlex.
- Role of mitochondrial translation in modulating inflammatory disease outcome: Current knowledge and future perspectives.The Journal of biological chemistry · 2026Review
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- Demise of the Milwaukee Protocol for Rabies.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2025Article
- Viruses and psychiatric disorders: We have not crossed the borderline from hypothesis to proof yet (Review).Molecular medicine reports · 2025Review
- Mitochondrial quality control and transfer communication in neurological disorders and neuroinflammation.Frontiers in immunology · 2025Review
- Review
- Review
- Molecular Mechanisms Associated with Neurodegeneration of Neurotropic Viral Infection.Molecular neurobiology · 2024Review
- SARS-CoV-2 Nsp7 plays a role in cognitive dysfunction by impairing synaptic plasticity.Frontiers in neuroscience · 2024Article
- Review
- Bardoxolone methyl inhibits the infection of rabies virus via Nrf2 pathway activation in vitro.Virology journal · 2023Article
- Rabies virus infection is associated with variations in calbindin D-28K and calretinin mRNA expression levels in mouse brain tissue.Archives of virology · 2023Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- Review
- Mitochondrial Dysfunction in Rabies Virus-Infected Human and Canine Brains.Neurochemical research · 2022Article
- Rotenone-Induced 4-HNE Aggresome Formation and Degradation in HL-1 Cardiomyocytes: Role of Autophagy Flux.International journal of molecular sciences · 2022Article
- Thermal dysregulation in patients with multiple sclerosis during SARS-CoV-2 infection. The potential therapeutic role of exercise.Multiple sclerosis and related disorders · 2022Review
- A One Medicine Mission for an Effective Rabies Therapy.Frontiers in veterinary science · 2022Article
- Rabies Infection: An Overview of Lyssavirus-Host Protein Interactions.Iranian biomedical journal · 2021Review
- Lyssavirus phosphoproteins increase mitochondrial complex I activity and levels of reactive oxygen species.Journal of neurovirology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Infection with the challenge virus standard-11 (CVS) strain of fixed rabies virus induces neuronal process degeneration in adult mice after hindlimb footpad inoculation. CVS-induced axonal swellings of primary rodent dorsal root ganglion neurons are associated with 4-hydroxy-2-nonenal protein adduct staining, indicating a critical role of oxidative stress. Mitochondrial dysfunction is the major cause of oxidative stress. We hypothesized that CVS infection induces mitochondrial dysfunction leading to oxidative stress. We investigated the effects of CVS infection on several mitochondrial parameters in different cell types. CVS infection significantly increased maximal uncoupled respiration and complex IV respiration and complex I and complex IV activities, but did not affect complex II-III or citrate synthase activities. Increases in complex I activity, but not complex IV activity, correlated with susceptibility of the cells to CVS infection. CVS infection maintained coupled respiration and rate of proton leak, indicating a tight mitochondrial coupling. Possibly as a result of enhanced complex activity and efficient coupling, a high mitochondrial membrane potential was generated. CVS infection reduced the intracellular ATP level and altered the cellular redox state as indicated by a high NADH/NAD+ ratio. The basal production of reactive oxygen species (ROS) was not affected in CVS-infected neurons. However, a higher rate of ROS generation occurred in CVS-infected neurons in the presence of mitochondrial substrates and inhibitors. We conclude that CVS infection induces mitochondrial dysfunction leading to ROS overgeneration and oxidative stress.
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What OpenQuestion 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 OpenQuestion graph.