{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T03:49:09Z","timestamp":1788320949660,"version":"build-2803163510"},"reference-count":32,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2021,1,4]],"date-time":"2021-01-04T00:00:00Z","timestamp":1609718400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Italian Ministry of Health"},{"DOI":"10.13039\/501100004359","name":"Swedish Research Council","doi-asserted-by":"publisher","award":["2017-00915"],"award-info":[{"award-number":["2017-00915"]}],"id":[{"id":"10.13039\/501100004359","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002565","name":"Alzheimer Drug Discovery Foundation","doi-asserted-by":"publisher","award":["RDAPB-201809-2016615"],"award-info":[{"award-number":["RDAPB-201809-2016615"]}],"id":[{"id":"10.13039\/100002565","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Swedish Alzheimer Foundation","award":["grant number AF-742881"],"award-info":[{"award-number":["grant number AF-742881"]}]},{"name":"Hj\u00e4rnfonden, Sweden","award":["FO2017-0243"],"award-info":[{"award-number":["FO2017-0243"]}]},{"DOI":"10.13039\/501100000781","name":"European Research Council","doi-asserted-by":"publisher","award":["681712"],"award-info":[{"award-number":["681712"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000781","name":"European Research Council","doi-asserted-by":"publisher","award":["201809-2016862"],"award-info":[{"award-number":["201809-2016862"]}],"id":[{"id":"10.13039\/501100000781","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,11,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Recent findings indicated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-related neurological manifestations involve cytokine release syndrome along with endothelial activation, blood brain barrier dysfunction, and immune-mediated mechanisms. Very few studies have fully investigated the cerebrospinal fluid (CSF) correlates of SARS-CoV-2 encephalitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Patients with polymerase chain reaction (PCR)-confirmed SARS-CoV-2 infection and encephalitis (COV-Enc), encephalitis without SARS-CoV-2 infection (ENC), and healthy controls (HC) underwent an extended panel of CSF neuronal (neurofilament light chain [NfL], T-tau), glial (glial fibrillary acidic protein [GFAP], soluble triggering receptor expressed on myeloid cells 2 [sTREM2], chitinase-3-like protein 1 [YKL-40]) and inflammatory biomarkers (interleukin [IL]-1\u03b2, IL-6, Il-8, tumor necrosis factor [TNF] \u03b1, CXCL-13, and \u03b22-microglobulin).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Thirteen COV-Enc, 21 ENC, and 18 HC entered the study. In COV-Enc cases, CSF was negative for SARS-CoV-2 real-time PCR but exhibited increased IL-8 levels independently from presence of pleocytosis\/hyperproteinorracchia. COV-Enc patients showed increased IL-6, TNF- \u03b1, and \u03b22-microglobulin and glial markers (GFAP, sTREM2, YKL-40) levels similar to ENC but normal CXCL13 levels. Neuronal markers NfL and T-tau were abnormal only in severe cases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>SARS-CoV-2-related encephalitis were associated with prominent glial activation and neuroinflammatory markers, whereas neuronal markers were increased in severe cases only. The pattern of CSF alterations suggested a cytokine-release syndrome as the main inflammatory mechanism of SARS-CoV-2-related encephalitis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cid\/ciaa1933","type":"journal-article","created":{"date-parts":[[2021,1,1]],"date-time":"2021-01-01T15:08:32Z","timestamp":1609513712000},"page":"e3019-e3026","source":"Crossref","is-referenced-by-count":152,"title":["Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Encephalitis Is a Cytokine Release Syndrome: Evidences From Cerebrospinal Fluid Analyses"],"prefix":"10.1093","volume":"73","author":[{"given":"Andrea","family":"Pilotto","sequence":"first","affiliation":[{"name":"Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy"},{"name":"Parkinson\u2019s Disease Rehabilitation Centre, FERB ONLUS\u2014S. 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