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Microglial GLT-1 is upregulated in response to herpes simplex virus infection to provide an antiviral defence via glutathione.

Journal article
Authors Mikael Persson
Mona Brantefjord
Jan-Åke Liljeqvist
Tomas Bergström
Elisabeth Hansson
Lars Rönnbäck
Published in Glia
Volume 55
Issue 14
Pages 1449-58
ISSN 0894-1491
Publication year 2007
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Biomedicine, Department of Infectious Medicine
Pages 1449-58
Language en
Keywords Animals, Animals, Newborn, Brain, immunology, metabolism, virology, Cells, Cultured, Encephalitis, Herpes Simplex, immunology, metabolism, physiopathology, Excitatory Amino Acid Transporter 2, metabolism, secretion, Glutamic Acid, metabolism, Glutathione, metabolism, Herpesvirus 1, Human, immunology, Herpesvirus 2, Human, immunology, Immunity, Innate, physiology, Microglia, immunology, metabolism, virology, Rats, Rats, Sprague-Dawley, Tumor Necrosis Factor-alpha, metabolism, secretion, Up-Regulation, physiology
Subject categories Microbiology in the medical area


Herpes simplex virus (HSV) can enter the central nervous system and cause encephalitis (HSV-1) or meningitis (HSV-2). Microglia, the immunocompetent cells of the central nervous system, are potentially able to detect viral infections. Microglia have been shown to express the glutamate transporter GLT-1 during pathological events, leading to increased microglial glutamate uptake and glutathione synthesis. This study aims to address the role of GLT-1 and glutathione, a major antioxidant with antiviral properties, during HSV infections. Using neuron-enriched mixed primary cultures from rat, it was found that microglia have higher resistance to HSV infections than neurons or astrocytes after 24 h incubation with HSV. Purified microglia in culture were used to further address this. It was found that microglia were able to detect HSV and responded by releasing tumor necrosis factor-alpha (TNF-alpha) and upregulating GLT-1 after 24 h incubation with 1 PFU/cell HSV-1 or HSV-2. Furthermore, the microglial glutathione levels were not significantly diminished after 24 h. Inhibition of the microglial glutathione synthesis with 200 microM buthionine sulfoximide (BSO) led to significantly more infected cells after 24 h incubation with 1 PFU/cell HSV-1 or HSV-2. These data indicate that the higher resistance in microglia against HSV infections may be due to the expression of GLT-1, which can maintain the glutathione levels and provide a mechanism for microglial self-defense against HSV.

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