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- W2016404508 abstract "Redox homeostasis is an important host factor determining the outcome of infectious disease. Enterovirus 71 (EV71) infection has become an important endemic disease in Southeast Asia and China. We have previously shown that oxidative stress promotes viral replication, and progeny virus induces oxidative stress in host cells. The detailed mechanism for reactive oxygen species (ROS) generation in infected cells remains elusive. In the current study, we demonstrate that mitochondria were a major ROS source in EV71-infected cells. Mitochondria in productively infected cells underwent morphologic changes and exhibited functional anomalies, such as a decrease in mitochondrial electrochemical potential ΔΨ(m) and an increase in oligomycin-insensitive oxygen consumption. Respiratory control ratio of mitochondria from infected cells was significantly lower than that of normal cells. The total adenine nucleotide pool and ATP content of EV71-infected cells significantly diminished. However, there appeared to be a compensatory increase in mitochondrial mass. Treatment with mito-TEMPO reduced eIF2α phosphorylation and viral replication, suggesting that mitochondrial ROS act to promote viral replication. It is plausible that EV71 infection induces mitochondrial ROS generation, which is essential to viral replication, at the sacrifice of efficient energy production, and that infected cells up-regulate biogenesis of mitochondria to compensate for their functional defect." @default.
- W2016404508 created "2016-06-24" @default.
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- W2016404508 creator A5032551978 @default.
- W2016404508 creator A5037904452 @default.
- W2016404508 creator A5079773948 @default.
- W2016404508 date "2014-11-17" @default.
- W2016404508 modified "2023-10-18" @default.
- W2016404508 title "Enterovirus 71 Induces Mitochondrial Reactive Oxygen Species Generation That is Required for Efficient Replication" @default.
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- W2016404508 doi "https://doi.org/10.1371/journal.pone.0113234" @default.
- W2016404508 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4234665" @default.
- W2016404508 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25401329" @default.
- W2016404508 hasPublicationYear "2014" @default.
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