Andrea Knight, MD, MSCE
Hospital for Sick Children
Toronto, ON, Canada
Disclosure(s): Pfizer: Speaker/Honoraria (includes speakers bureau, symposia, and expert witness) (Terminated, May 27, 2023)
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Carla Cuda, PhD
Northwestern University
Chicago, Illinois, United States
Disclosure information not submitted.
Innate immune responses are essential for host defense from viral pathogenesis and cellular damage and must be tightly regulated to avoid excessive inflammation or autoimmunity. Recent scientific discovery has shown that fibrinogen deposits in the lungs and brains of patients with SARS-CoV-2 infection correlate with disease severity and predict long COVID cognitive deficits. Fibrin promotes innate immune activation by binding to the SARS-CoV-2 spike protein and activating thrombin, which contributes to neuronal loss after infection. Alternative innate immune mechanisms regulating type 1 interferon responses to SARS-CoV-2 include transposons. Transposons are alternative splicing of exons derived from transposable elements that can control immune cell signaling in humans. In SARS-CoV-2 infection, the transposon-derived isoform of IFNAR2 is highly expressed and functions as a decoy receptor that inhibits interferon signaling. This pathway may be dysregulated in autoimmunity and/or could be a novel therapeutic target for autoinflammatory disease.
Speaker: Zhaoqi Yan, PhD – Gladstone Institute of Neurological Disease
Speaker: Linda Geng, MD, PhD – Stanford University
