ArticleJournal of virology2008
Mitochondrial dysfunction in lyssavirus-induced apoptosis.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- Oncolytic Effects of S89K Matrix Protein of Vesicular Stomatitis Virus in Cervical Cancer.Advanced biomedical research · 2026Article
- TRIM72 restricts lyssavirus infection by inducing K48-linked ubiquitination and proteasome degradation of the matrix protein.PLoS pathogens · 2024Article
- Evaluation of Taxonomic Characteristics of Matlo and Phala Bat Rabies-Related Lyssaviruses Identified in South Africa.Viruses · 2023Article
- Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis.Viruses · 2021Review
- Rabies Infection: An Overview of Lyssavirus-Host Protein Interactions.Iranian biomedical journal · 2021Review
- Review
- Animal and human RNA viruses: genetic variability and ability to overcome vaccines.Archives of microbiology · 2021Review
- Lyssaviruses and the Fatal Encephalitic Disease Rabies.Frontiers in immunology · 2021Review
- Article
- Article
- Lyssavirus phosphoproteins increase mitochondrial complex I activity and levels of reactive oxygen species.Journal of neurovirology · 2017Article
- Regulation of NF-κB by the p105-ABIN2-TPL2 complex and RelAp43 during rabies virus infection.PLoS pathogens · 2017Article
- Serine residues at positions 162 and 166 of the rabies virus phosphoprotein are critical for the induction of oxidative stress in rabies virus infection.Journal of neurovirology · 2017Article
- Phosphoprotein Gene Contributes to the Enhanced Apoptosis Induced by Wild-Type Rabies Virus GD-SH-01Frontiers in microbiology · 2017Article
- The matrix protein of rabies virus binds to RelAp43 to modulate NF-κB-dependent gene expression related to innate immunity.Scientific reports · 2016Article
- Subversion of the Immune Response by Rabies Virus.Viruses · 2016Review
- Involvement of ROS-mediated mitochondrial dysfunction and SIRT3 down-regulation in tris(2-chloroethyl)phosphate-induced cell cycle arrest.Toxicology research · 2016Article
- Rabies virus phosphoprotein interacts with mitochondrial Complex I and induces mitochondrial dysfunction and oxidative stress.Journal of neurovirology · 2015Article
- Mitochondrial dysfunction in rabies virus infection of neurons.Journal of neurovirology · 2013Article
- Chandipura virus induces neuronal death through Fas-mediated extrinsic apoptotic pathway.Journal of virology · 2013Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lyssaviruses are highly neurotropic viruses associated with neuronal apoptosis. Previous observations have indicated that the matrix proteins (M) of some lyssaviruses induce strong neuronal apoptosis. However, the molecular mechanism(s) involved in this phenomenon is still unknown. We show that for Mokola virus (MOK), a lyssavirus of low pathogenicity, the M (M-MOK) targets mitochondria, disrupts the mitochondrial morphology, and induces apoptosis. Our analysis of truncated M-MOK mutants suggests that the information required for efficient mitochondrial targeting and dysfunction, as well as caspase-9 activation and apoptosis, is held between residues 46 and 110 of M-MOK. We used a yeast two-hybrid approach, a coimmunoprecipitation assay, and confocal microscopy to demonstrate that M-MOK physically associates with the subunit I of the cytochrome c (cyt-c) oxidase (CcO) of the mitochondrial respiratory chain; this is in contrast to the M of the highly pathogenic Thailand lyssavirus (M-THA). M-MOK expression induces a significant decrease in CcO activity, which is not the case with M-THA. M-MOK mutations (K77R and N81E) resulting in a similar sequence to M-THA at positions 77 and 81 annul cyt-c release and apoptosis and restore CcO activity. As expected, the reverse mutations, R77K and E81N, introduced in M-THA induce a phenotype similar to that due to M-MOK. These features indicate a novel mechanism for energy depletion during lyssavirus-induced apoptosis.
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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.