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RESEARCH PRODUCT
Role of mitochondria in parvovirus pathology.
Matti VuentoLeona GilbertJonna Nykkysubject
PathologyvirusesCelllcsh:MedicineMitochondrionSignal transductionERK signaling cascadeMolecular cell biologyInner mitochondrial membraneExtracellular Signal-Regulated MAP Kinaseslcsh:SciencepatologiaCellular Stress ResponsesMembrane Potential MitochondrialMultidisciplinarybiologyCell DeathCanine parvovirusapoptosisSignaling cascadesCellular StructuresCell biologyMitochondriaHost-Pathogen Interactionmedicine.anatomical_structureMitochondrial MembranesResearch Articlemedicine.medical_specialtyViral EntryParvovirus CanineMAP Kinase Signaling SystemmitokondriotMicrobiologyCell LineParvoviridae InfectionsDogsViral entryVirologymedicineAnimalsBiologysoluviestintäParvovirusta1183parvoviruslcsh:Rta1182biology.organism_classificationMolecular biologyEnzyme ActivationViral replicationSubcellular OrganellesApoptosisCatsCalciumlcsh:QReactive Oxygen SpeciesViral Transmission and Infectiondescription
Proper functioning of the mitochondria is crucial for the survival of the cell. Viruses are able to interfere with mitochondrial functions as they infect the host cell. Parvoviruses are known to induce apoptosis in infected cells, but the role of the mitochondria in parvovirus induced cytopathy is only partially known. Here we demonstrate with confocal and electron microscopy that canine parvovirus (CPV) associated with the mitochondrial outer membrane from the onset of infection. During viral entry a transient depolarization of the mitochondrial transmembrane potential and increase in ROS level was detected. Subsequently, mitochondrial homeostasis was normalized shortly, as detected by repolarization of the mitochondrial membrane and decrease of ROS. Indeed, activation of cell survival signalling through ERK1/2 cascade was observed early in CPV infected cells. At 12 hours post infection, concurrent with the expression of viral non-structural protein 1, damage to the mitochondrial structure and depolarization of its membrane were apparent. Results of this study provide additional insight of parvovirus pathology and also more general information of virus-mitochondria association. peerReviewed
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2014-01-21 | PLoS ONE |