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Alandijany 2013 J Neurovirol
Additional label Labels  + , 2018-10  +
Coupling states LEAK  + , OXPHOS  + , ET  +
Diseases Infectious  +
Enzyme Complex I  + , Complex II;succinate dehydrogenase  + , Complex III  + , Complex IV;cytochrome c oxidase  +
Has abstract Infection with the challenge virus standar
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.
o ROS overgeneration and oxidative stress.  +
Has editor [[Plangger M]]  +
Has info [https://www.ncbi.nlm.nih.gov/pubmed/24277436 PMID: 24277436]  +
Has publicationkeywords Oxidative stress  + , Pathogenesis  + , Rabies  + , Rabies virus  + , Reactive oxygen species  +
Has title Alandijany T, Kammouni W, Roy Chowdhury SK, Fernyhough P, Jackson AC (2013) Mitochondrial dysfunction in rabies virus infection of neurons. J Neurovirol 19:537-49.  +
Instrument and method Oxygraph-2k  +
Mammal and model Rat  +
MiP area Respiration  +
Pathways N  + , CIV  + , ROX  +
Preparation Permeabilized cells  +
Stress Oxidative stress;RONS  +
Tissue and cell Nervous system  +
Was published by MiPNetLab CA Winnipeg Banerji V + , CA Winnipeg Fernyhough P +
Was published in journal J Neurovirol +
Was published in year 2013  +
Was written by Alandijany T + , Kammouni W + , Roy Chowdhury SK + , Fernyhough P + , Jackson AC +
Categories Publications
Modification date
"Modification date" is a predefined property that corresponds to the date of the last modification of a subject and is provided by Semantic MediaWiki.
14:41:04, 16 October 2018  +
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