
pmid: 27640443
We have recently reported that bovine herpesvirus 1 (BoHV-1)-induced overproduction of reactive oxygen species (ROS) partially depends on NADPH oxidases (Noxs). In this study, we found that the decreased levels of main intracellular non-enzymatic antioxidant glutathione (GSH) during BoHV-1 infection also contributed to ROS production. Exogenous GSH administration dramatically inhibited BoHV-1 replication, indicating the critical role of decreased GSH for BoHV-1 replication. Interestingly, GSH synergistically enhanced the antiviral effects of acyclovir (ACV) against BoHV-1 infection in vitro. This study not only illuminates the effect of GSH on BoHV-1 infection but also provides evidence that pharmacological modulation of GSH-mediated ROS production in combination with specific antiviral drugs is a viable therapeutic approach to fighting virus infection.
Dose-Response Relationship, Drug, Acyclovir, Drug Synergism, Virus Replication, Antiviral Agents, Glutathione, Madin Darby Canine Kidney Cells, Dogs, Animals, Drug Therapy, Combination, Herpesvirus 1, Bovine
Dose-Response Relationship, Drug, Acyclovir, Drug Synergism, Virus Replication, Antiviral Agents, Glutathione, Madin Darby Canine Kidney Cells, Dogs, Animals, Drug Therapy, Combination, Herpesvirus 1, Bovine
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