{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T23:23:08Z","timestamp":1792797788156,"version":"4.5.0"},"reference-count":29,"publisher":"American Society for Microbiology","issue":"20","license":[{"start":{"date-parts":[[2012,10,15]],"date-time":"2012-10-15T00:00:00Z","timestamp":1350259200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2012,10,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Beta interferon (IFN-\u03b2) is a major component of innate immunity in mammals, but information on the\n                    <jats:italic>in vivo<\/jats:italic>\n                    source of this cytokine after pathogen infection is still scarce. To identify the cell types responsible for IFN-\u03b2 production during viral encephalitis, we used reporter mice that express firefly luciferase under the control of the IFN-\u03b2 promoter and stained organ sections with luciferase-specific antibodies. Numerous luciferase-positive cells were detected in regions of La Crosse virus (LACV)-infected mouse brains that contained many infected cells. Double-staining experiments with cell-type-specific markers revealed that similar numbers of astrocytes and microglia of infected brains were luciferase positive, whereas virus-infected neurons rarely contained detectable levels of luciferase. Interestingly, if a mutant LACV unable of synthesizing the IFN-antagonistic factor NSs was used for challenge, the vast majority of the IFN-\u03b2-producing cells in infected brains were astrocytes rather than microglia. Similar conclusions were reached in a second series of experiments in which conditional reporter mice expressing the luciferase reporter gene solely in defined cell types were infected with wild-type or mutant LACV. Collectively, our data suggest that glial cells rather than infected neurons represent the major source of IFN-\u03b2 in LACV-infected mouse brains. They further indicate that IFN-\u03b2 synthesis in astrocytes and microglia is differentially affected by the viral IFN antagonist, presumably due to differences in LACV susceptibility of these two cell types.\n                  <\/jats:p>","DOI":"10.1128\/jvi.01093-12","type":"journal-article","created":{"date-parts":[[2012,8,9]],"date-time":"2012-08-09T01:34:12Z","timestamp":1344476052000},"page":"11223-11230","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":86,"title":["Visualizing Production of Beta Interferon by Astrocytes and Microglia in Brain of La Crosse Virus-Infected Mice"],"prefix":"10.1128","volume":"86","author":[{"given":"Carsten","family":"Kallfass","sequence":"first","affiliation":[{"name":"Department of Virology, University of Freiburg, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Ackerman","sequence":"additional","affiliation":[{"name":"Department of Virology, University of Freiburg, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"Lienenklaus","sequence":"additional","affiliation":[{"name":"Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Siegfried","family":"Weiss","sequence":"additional","affiliation":[{"name":"Molecular Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernd","family":"Heimrich","sequence":"additional","affiliation":[{"name":"Institute of Anatomy and Cell Biology, University of Freiburg, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Staeheli","sequence":"additional","affiliation":[{"name":"Department of Virology, University of Freiburg, Freiburg, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni736"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20051395"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1186\/1743-422X-5-25"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01933-06"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.79.16.10420-10428.2005"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2010.05.007"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-05-023770"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1089\/jir.2004.24.687"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1023\/A:1008942828960"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0602460103"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-09-03445.2002"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20071365"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.154.2.347"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1159\/000086657"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/icb.2011.109"},{"key":"e_1_3_2_17_2","first-page":"447","article-title":"Mechanisms of bunyavirus virulence. 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