Author: Remsik, J.; Wilcox, J. A.; Babady, N. E.; McMillen, T.; Vachha, B. A.; Halpern, N. A.; Dhawan, V.; Rosenblum, M.; Iacobuzio-Donahue, C. A.; Avila, E. K.; Santomasso, B.; Boire, A.
Title: Inflammatory leptomeningeal cytokines mediate delayed COVID-19 encephalopathy Cord-id: 5cltw11t Document date: 2020_9_18
ID: 5cltw11t
Snippet: SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction. Here we show that a particularly vulnerable population with neurologic manifestations of COVID-19 harbor an influx of inflammatory cytokines within the cerebrospinal fluid in the absence of viral neuro-invasion. The majority of these inflammatory mediators are driven by type 2 interferon and are known to induce neuronal injury in other disease models. Levels of matrix metalloproteinase-10 within the spinal fluid correlate wi
Document: SARS-CoV-2 infection induces a wide spectrum of neurologic dysfunction. Here we show that a particularly vulnerable population with neurologic manifestations of COVID-19 harbor an influx of inflammatory cytokines within the cerebrospinal fluid in the absence of viral neuro-invasion. The majority of these inflammatory mediators are driven by type 2 interferon and are known to induce neuronal injury in other disease models. Levels of matrix metalloproteinase-10 within the spinal fluid correlate with the degree of neurologic dysfunction. Furthermore, this neuroinflammatory process persists weeks following convalescence from the acute respiratory infection. These prolonged neurologic sequelae following a systemic cytokine release syndrome lead to long-term neurocognitive dysfunction with a wide range of phenotypes.
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