Herpes simplex virus type 1 infection induces oxidative stress and the release of bioactive lipid peroxidation by-products in mouse P19N neural cell cultures
| Autor: | Vaibhav Tiwari, Jerry H. Kavouras, Tibor Valyi-Nagy, Emese Prandovszky, S. Krisztian Kovacs, Mária Kovács, Klara Valyi-Nagy, Deepak Shukla |
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| Rok vydání: | 2007 |
| Předmět: |
Herpesvirus 1
Human Biology medicine.disease_cause Virus Replication Lipid peroxidation Cellular and Molecular Neuroscience chemistry.chemical_compound Tissue culture Mice Viral entry Virology medicine Animals Cells Cultured chemistry.chemical_classification Neurons Reactive oxygen species Herpes Simplex Malondialdehyde Molecular biology Oxidative Stress Neurology Viral replication chemistry Biochemistry Cell culture Neurology (clinical) Lipid Peroxidation Reactive Oxygen Species Oxidative stress |
| Zdroj: | Journal of neurovirology. 13(5) |
| ISSN: | 1355-0284 |
| Popis: | To determine whether herpes simplex virus type 1 (HSV-1) infection causes oxidative stress and lipid peroxidation in cultured neural cells, mouse P19 embryonal carcinoma cells were differentiated into cells with neural phenotypes (P19N cells) by retinoic acid and were then infected with HSV-1. Cellular levels of reactive oxygen species (ROS) and the release of lipid peroxidation by-products into the tissue culture medium were then measured by the generation of fluorescent markers hydroxyphenyl fluorescein and a stable chromophore produced by lipid peroxidation products, malondialdehyde (MDA) and hydroxyalkenals (4-HAEs; predominantly 4-hydroxy-2-nonenal [HNE]), respectively. HSV-1 infection increased ROS levels in neural cells as early as 1 h post infection (p.i.) and ROS levels remained elevated at 24 h p.i. This viral effect required viral entry and replication as heat- and ultraviolet light-inactivated HSV-1 were ineffective. HSV-1 infection also was associated with increased levels of MDA/HAE in the culture medium at 2 and 4 h p.i., but MDA/HAE levels were not different from those detected in mock infected control cultures at 1, 6, and 24 h p.i. HSV-1 replication in P19N cells was inhibited by the antioxidant compound ebselen and high concentrations of HNE added to the cultures, but was increased by low concentrations of HNE. These findings indicate that HSV-1 infection of neural cells causes oxidative stress that is required for efficient viral replication. Furthermore, these observations raise the possibility that soluble, bioactive lipid peroxidation by-products generated in infected neural cells may be important regulators of HSV-1 pathogenesis in the nervous system. |
| Databáze: | OpenAIRE |
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