{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T08:01:06Z","timestamp":1773734466346,"version":"3.50.1"},"reference-count":52,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2007,8,6]],"date-time":"2007-08-06T00:00:00Z","timestamp":1186358400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2007,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Herpes simplex virus (HSV) can enter the central nervous system and cause encephalitis (HSV\u20101) or meningitis (HSV\u20102). 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\u20101 during pathological events, leading to increased microglial glutamate uptake and glutathione synthesis. This study aims to address the role of GLT\u20101 and glutathione, a major antioxidant with antiviral properties, during HSV infections. Using neuron\u2010enriched 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\u2010\u03b1 (TNF\u2010\u03b1) and upregulating GLT\u20101 after 24 h incubation with 1 PFU\/cell HSV\u20101 or HSV\u20102. Furthermore, the microglial glutathione levels were not significantly diminished after 24 h. Inhibition of the microglial glutathione synthesis with 200 \u03bcM buthionine sulfoximide (BSO) led to significantly more infected cells after 24 h incubation with 1 PFU\/cell HSV\u20101 or HSV\u20102. These data indicate that the higher resistance in microglia against HSV infections may be due to the expression of GLT\u20101, which can maintain the glutathione levels and provide a mechanism for microglial self\u2010defense against HSV. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20560","type":"journal-article","created":{"date-parts":[[2007,8,6]],"date-time":"2007-08-06T18:19:34Z","timestamp":1186424374000},"page":"1449-1458","source":"Crossref","is-referenced-by-count":23,"title":["Microglial GLT\u20101 is upregulated in response to herpes simplex virus infection to provide an antiviral defence via 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